From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
Identifieur interne : 000739 ( Istex/Corpus ); précédent : 000738; suivant : 000740From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
Auteurs : Monique Dubois-Dalcq ; Anna Williams ; Christine Stadelmann ; Bruno Stankoff ; Bernard Zalc ; Catherine LubetzkiSource :
- Brain [ 0006-8950 ] ; 2008.
Abstract
In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.
Url:
DOI: 10.1093/brain/awn076
Links to Exploration step
ISTEX:C2CA6E337E425395BB40CEA63368993F4A8FCEA1Le document en format XML
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sortKey="Williams, Anna" sort="Williams, Anna" uniqKey="Williams A" first="Anna" last="Williams">Anna Williams</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stadelmann, Christine" sort="Stadelmann, Christine" uniqKey="Stadelmann C" first="Christine" last="Stadelmann">Christine Stadelmann</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stankoff, Bruno" sort="Stankoff, Bruno" uniqKey="Stankoff B" first="Bruno" last="Stankoff">Bruno Stankoff</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Zalc, Bernard" sort="Zalc, Bernard" uniqKey="Zalc B" first="Bernard" last="Zalc">Bernard Zalc</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Lubetzki, Catherine" sort="Lubetzki, Catherine" uniqKey="Lubetzki C" first="Catherine" last="Lubetzki">Catherine Lubetzki</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:C2CA6E337E425395BB40CEA63368993F4A8FCEA1</idno><date when="2008" year="2008">2008</date><idno type="doi">10.1093/brain/awn076</idno><idno type="url">https://api.istex.fr/ark:/67375/HXZ-K7JKPH5G-5/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">000739</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000739</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title><author><name sortKey="Dubois Dalcq, Monique" sort="Dubois Dalcq, Monique" uniqKey="Dubois Dalcq M" first="Monique" last="Dubois-Dalcq">Monique Dubois-Dalcq</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mdalcq@pasteur.fr</mods:affiliation></affiliation></author><author><name sortKey="Williams, Anna" sort="Williams, Anna" uniqKey="Williams A" first="Anna" last="Williams">Anna Williams</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stadelmann, Christine" sort="Stadelmann, Christine" uniqKey="Stadelmann C" first="Christine" last="Stadelmann">Christine Stadelmann</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Stankoff, Bruno" sort="Stankoff, Bruno" uniqKey="Stankoff B" first="Bruno" last="Stankoff">Bruno Stankoff</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Zalc, Bernard" sort="Zalc, Bernard" uniqKey="Zalc B" first="Bernard" last="Zalc">Bernard Zalc</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author><author><name sortKey="Lubetzki, Catherine" sort="Lubetzki, Catherine" uniqKey="Lubetzki C" first="Catherine" last="Lubetzki">Catherine Lubetzki</name><affiliation><mods:affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Brain</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><publisher>Oxford University Press</publisher><date when="2008-07">2008</date><date type="e-published" when="2008-05-12">2008</date><biblScope unit="vol">131</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="1686">1686</biblScope><biblScope unit="page" to="1700">1700</biblScope></imprint><idno type="ISSN">0006-8950</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0006-8950</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.</div></front></TEI><istex><corpusName>oup</corpusName><keywords><teeft><json:string>remyelination</json:string><json:string>myelin</json:string><json:string>oligodendrocyte</json:string><json:string>axon</json:string><json:string>myelination</json:string><json:string>demyelination</json:string><json:string>axonal</json:string><json:string>demyelinated</json:string><json:string>opcs</json:string><json:string>multiple sclerosis</json:string><json:string>neurosci</json:string><json:string>node</json:string><json:string>receptor</json:string><json:string>spinal</json:string><json:string>precursor</json:string><json:string>sclerosis</json:string><json:string>glia</json:string><json:string>immune</json:string><json:string>ranvier</json:string><json:string>myelin 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Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string><json:string>E-mail: mdalcq@pasteur.fr</json:string></affiliations></json:item><json:item><name>Anna Williams</name><affiliations><json:string>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Christine Stadelmann</name><affiliations><json:string>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Bruno Stankoff</name><affiliations><json:string>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Bernard Zalc</name><affiliations><json:string>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item><json:item><name>Catherine Lubetzki</name><affiliations><json:string>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</json:string></affiliations></json:item></author><subject><json:item><value>multiple sclerosis</value></json:item><json:item><value>nodes of Ranvier</value></json:item><json:item><value>enhancing repair</value></json:item><json:item><value>animal models</value></json:item><json:item><value>transparent fish</value></json:item></subject><articleId><json:string>awn076</json:string></articleId><arkIstex>ark:/67375/HXZ-K7JKPH5G-5</arkIstex><language><json:string>unknown</json:string></language><originalGenre><json:string>review-article</json:string></originalGenre><abstract>In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.</abstract><qualityIndicators><score>7.203</score><pdfWordCount>11897</pdfWordCount><pdfCharCount>75853</pdfCharCount><pdfVersion>1.4</pdfVersion><pdfPageCount>15</pdfPageCount><pdfPageSize>613 x 791 pts</pdfPageSize><pdfWordsPerPage>793</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>128</abstractWordCount><abstractCharCount>860</abstractCharCount><keywordCount>5</keywordCount></qualityIndicators><title>From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title><pmid><json:string>18474520</json:string></pmid><genre><json:string>review-article</json:string></genre><host><title>Brain</title><language><json:string>unknown</json:string></language><issn><json:string>0006-8950</json:string></issn><eissn><json:string>1460-2156</json:string></eissn><publisherId><json:string>brainj</json:string></publisherId><volume>131</volume><issue>7</issue><pages><first>1686</first><last>1700</last></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Review Article</value></json:item></subject></host><namedEntities><unitex><date><json:string>2008-05-12</json:string><json:string>1965</json:string><json:string>1961</json:string></date><geogName></geogName><orgName><json:string>NINDS</json:string><json:string>Nagoya University</json:string><json:string>Porter Neuroscience Center</json:string><json:string>National Institute of Neurological Disorders and Stroke</json:string><json:string>Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK</json:string><json:string>Vanderbilt University</json:string><json:string>National Academy of Sciences, USA</json:string><json:string>Porter Neuroscience Research Center, Bdg</json:string><json:string>Congo Red</json:string><json:string>National Institutes of Health</json:string><json:string>Institute of Neuropathology, University Medical Center</json:string><json:string>Oxford University</json:string><json:string>European Leukodystrophy Foundation</json:string><json:string>Department of Biological Sciences, Vanderbilt University, Tennessee, USA</json:string><json:string>National Institutes of Health, Bethesda, MD</json:string><json:string>Stroke</json:string><json:string>National Institute for Neurological Disorders</json:string><json:string>NINDS</json:string></orgName><orgName_funder><json:string>Stroke</json:string><json:string>National Institute for Neurological Disorders</json:string><json:string>NINDS</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>B. Stankoff</json:string><json:string>J.L. Thomas</json:string><json:string>Bruce Appel</json:string><json:string>S. Ghandour</json:string><json:string>Lymphotoxin</json:string><json:string>C. Lubetzki</json:string><json:string>R. Franklin</json:string><json:string>B. Zalc</json:string><json:string>E. Chadzopollou</json:string><json:string>Norio Takada</json:string><json:string>Thus Schwann</json:string><json:string>Bruno Stankoff</json:string><json:string>Catherine Lubetzki</json:string><json:string>Heinz Arnheiter</json:string><json:string>Monique Dubois-Dalcq</json:string><json:string>Manuel Koch</json:string><json:string>Marie Curie</json:string><json:string>The</json:string><json:string>S. Fancy</json:string><json:string>Y. Wakamatsu</json:string><json:string>Anna Williams</json:string><json:string>D. Rowitch</json:string><json:string>M. Schumacher</json:string><json:string>Bernard Zalc</json:string><json:string>Christine Stadelmann</json:string><json:string>Monique Dubois</json:string></persName><placeName><json:string>Paris</json:string><json:string>France</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Hu et al., 2006</json:string><json:string>Perier and Gregoire, 1965</json:string><json:string>Calderon et al., 2006</json:string><json:string>Arnett and Viney, 2007</json:string><json:string>Voas et al., 2007</json:string><json:string>Howell et al., 2006</json:string><json:string>Zalc and Colman, 2000</json:string><json:string>Stankoff et al., 2006</json:string><json:string>Fortin et al., 2005</json:string><json:string>Bagnato et al., 2007</json:string><json:string>Cahoy et al., 2008</json:string><json:string>Greenberg and Calabresi, 2008</json:string><json:string>Pogoda et al., 2006</json:string><json:string>Schafer et al., 2006</json:string><json:string>Woods et al., 2006</json:string><json:string>Wolburg, 1981</json:string><json:string>Dupree et al., 2005</json:string><json:string>Seifert et al., 2007</json:string><json:string>Tozer et al., 2005</json:string><json:string>Lee et al., 2007</json:string><json:string>Plant et al., 2007</json:string><json:string>Eshed et al., 2007</json:string><json:string>Sim et al., 2006</json:string><json:string>Lin et al., 2006</json:string><json:string>reviewed by Hannila and Filbin, 2008</json:string><json:string>Schumacher et al., 2007</json:string><json:string>Barkhof et al., 2003</json:string><json:string>Merkler et al., 2006</json:string><json:string>Zhao et al., 2008</json:string><json:string>Patrikios et al., 2006</json:string><json:string>Hall, 1972</json:string><json:string>Ludwin, 1978</json:string><json:string>Lubetzki et al., 2005</json:string><json:string>Zapata et al., 2006</json:string><json:string>Kristensson et al., 1986</json:string><json:string>Windrem et al., 2004</json:string><json:string>Barres and Raff, 1993</json:string><json:string>Schwab et al., 2006</json:string><json:string>Patani et al., 2007</json:string><json:string>NaitOumesmar et al., 2007</json:string><json:string>Brain (2008)</json:string><json:string>Rogister et al., 1999</json:string><json:string>Aguirre et al., 2004</json:string><json:string>Song et al., 2002, 2005</json:string><json:string>Schweitzer et al., 2003</json:string><json:string>Miller and Mi, 2007</json:string><json:string>reviewed in Waxman, 2006</json:string><json:string>Karadottir and Attwell, 2007</json:string><json:string>Coman et al., 2006</json:string><json:string>Sarchielli et al., 2007</json:string><json:string>Wakamatsu et al., 2001</json:string><json:string>Woodruff and Franklin, 1999</json:string><json:string>Zhou et al., 2006</json:string><json:string>Butzkueven et al., 2002, 2006</json:string><json:string>Deloire-Grassin et al., 2000</json:string><json:string>Kirby et al., 2006</json:string><json:string>Le Bihan et al.</json:string><json:string>Nona et al. (2000)</json:string><json:string>Albert et al., 2007</json:string><json:string>Honmou et al., 1996</json:string><json:string>discussed in Arnett and Viney, 2007</json:string><json:string>Duyn et al., 2007</json:string><json:string>Fancy et al., 2004</json:string><json:string>Magliozzi et al., 2007</json:string><json:string>Li et al., 2006</json:string><json:string>Barbin et al., 2004</json:string><json:string>Chen et al., 2005</json:string><json:string>Charles et al., 2002</json:string><json:string>Colognato et al., 2007</json:string><json:string>Rodriguez, 2007</json:string><json:string>Laule et al., 2006</json:string><json:string>Kaplan et al., 1997, 2001</json:string><json:string>Delaunay et al., 2008</json:string><json:string>reviewed in Sherman and Back, 2008</json:string><json:string>Dubois-Dalcq et al., 2005</json:string><json:string>Neema et al., 2007</json:string><json:string>Lazarini et al., 2003</json:string><json:string>Vanderlocht et al., 2006</json:string><json:string>Compston et al., 2006</json:string><json:string>Coman et al., 2005</json:string><json:string>Zhang et al., 2006</json:string><json:string>Taveggia et al., 2008</json:string><json:string>Felts and Smith, 1992</json:string><json:string>Nave and Salzer, 2006</json:string><json:string>Utzschneider et al., 1994</json:string><json:string>Vana et al., 2007a</json:string><json:string>Stankoff et al.</json:string><json:string>Xiang et al., 2005</json:string><json:string>Zalc et al., 2008</json:string><json:string>Mi et al., 2007</json:string><json:string>Armstrong et al., 1990</json:string><json:string>Kerschensteiner et al., 2004</json:string><json:string>Nucifora et al., 2007</json:string><json:string>Mc Farland, 2008</json:string><json:string>Spassky et al., 2002</json:string><json:string>Rossignol et al., 2007</json:string><json:string>Klein et al., 2002</json:string><json:string>Wu et al., 2006</json:string><json:string>Krumbholz et al., 2006</json:string><json:string>Glaser et al., 2007</json:string><json:string>Lubetzki and Zalc, 2001</json:string><json:string>Nait-Oumesmar et al., 2007</json:string><json:string>M. Dubois-Dalcq et al.</json:string><json:string>Zhao et al., 2005</json:string><json:string>Kazakova et al., 2006</json:string><json:string>Larsen et al., 2003</json:string><json:string>Aguirre et al., 2007</json:string><json:string>Sasaki et al., 2006</json:string><json:string>Balabanov et al., 2006</json:string><json:string>Funch and Faber (1984)</json:string><json:string>Dziembowska et al., 2005</json:string><json:string>Arnett et al., 2004</json:string><json:string>reviewed in Franklin and Hinks, 1999</json:string><json:string>Dutta et al., 2007</json:string><json:string>Gold et al., 2006</json:string><json:string>Doetsch et al., 2002</json:string><json:string>Maertens et al., 2007</json:string><json:string>Black et al., 2006</json:string><json:string>Bunge et al., 1961</json:string><json:string>Nunes et al., 2003</json:string><json:string>Zujovic et al., 2007</json:string><json:string>Zivadinov, 2007</json:string><json:string>Marriott et al., 2008</json:string><json:string>Pearse et al., 2007</json:string><json:string>Stankoff et al., 2002</json:string><json:string>Setzu et al., 2006</json:string><json:string>Kotter et al., 2005</json:string><json:string>Kukley et al., 2007</json:string><json:string>Armstrong et al., 2002, 2006</json:string><json:string>Stevens et al., 2002</json:string><json:string>Michaelov et al., 2004</json:string><json:string>reviewed in Smith, 2006</json:string><json:string>Ishibashi et al., 2006</json:string><json:string>Sim et al., 2002</json:string><json:string>Demerens et al., 1996</json:string><json:string>Zhang et al., 2004</json:string><json:string>discussed by Arnett and Viney, 2007</json:string><json:string>Smith, 2006</json:string><json:string>Blakemore, 1973</json:string><json:string>Kohwi et al., 2007</json:string><json:string>Padovani-Claudio et al., 2006</json:string><json:string>Mc Kinnon et al., 1993</json:string><json:string>reviewed by Miller and Mi, 2007</json:string><json:string>Arnett et al., 2003</json:string><json:string>Mi et al., 2005</json:string><json:string>reviewed in Zawadzka and Franklin, 2007</json:string><json:string>reviewed in Scolding and Dubois-Dalcq, 2008</json:string><json:string>Back et al., 2005</json:string><json:string>Fujiyoshi et al., 2007</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/HXZ-K7JKPH5G-5</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - neurosciences</json:string><json:string>2 - clinical neurology</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - neurology & neurosurgery</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Clinical Neurology</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences biologiques fondamentales et appliquees. psychologie</json:string></inist></categories><publicationDate>2008</publicationDate><copyrightDate>2008</copyrightDate><doi><json:string>10.1093/brain/awn076</json:string></doi><id>C2CA6E337E425395BB40CEA63368993F4A8FCEA1</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-K7JKPH5G-5/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/HXZ-K7JKPH5G-5/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/HXZ-K7JKPH5G-5/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><licence>Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</licence></availability><date when="2008-07">2008</date><date type="e-published" when="2008-05-12">2008</date><date type="Copyright" when="2008">2008</date></publicationStmt><notesStmt><note type="content-type" source="review-article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</note><note type="publication-type" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main" xml:lang="en">From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title><author xml:id="author-0000" role="corresp"><persName><surname>Dubois-Dalcq</surname><forename type="first">Monique</forename></persName><affiliation><orgName type="institution">1National Institute for Neurological Disorders and Stroke 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Neurological Disorders and Stroke (NINDS)</orgName><address><addrLine>Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</addrLine><country key="MD" xml:lang="en">MOLDOVA, REPUBLIC OF</country><country key="US" xml:lang="en">UNITED STATES</country><country key="GB" xml:lang="en">UNITED KINGDOM</country><country key="DE" xml:lang="en">GERMANY</country><country key="FR" xml:lang="en">FRANCE</country></address></affiliation><email>mdalcq@pasteur.fr</email><email>dalcqm@mail.nih.gov</email></author><author xml:id="author-0002"><persName><surname>Stadelmann</surname><forename type="first">Christine</forename></persName><affiliation><orgName type="institution">1National Institute for Neurological Disorders and Stroke (NINDS)</orgName><address><addrLine>Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</addrLine><country key="MD" xml:lang="en">MOLDOVA, REPUBLIC OF</country><country key="US" xml:lang="en">UNITED STATES</country><country key="GB" xml:lang="en">UNITED KINGDOM</country><country key="DE" xml:lang="en">GERMANY</country><country key="FR" xml:lang="en">FRANCE</country></address></affiliation><email>mdalcq@pasteur.fr</email><email>dalcqm@mail.nih.gov</email></author><author xml:id="author-0003"><persName><surname>Stankoff</surname><forename type="first">Bruno</forename></persName><affiliation><orgName type="institution">1National Institute for Neurological Disorders and Stroke (NINDS)</orgName><address><addrLine>Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</addrLine><country key="MD" xml:lang="en">MOLDOVA, REPUBLIC OF</country><country key="US" xml:lang="en">UNITED STATES</country><country key="GB" xml:lang="en">UNITED KINGDOM</country><country key="DE" xml:lang="en">GERMANY</country><country key="FR" xml:lang="en">FRANCE</country></address></affiliation><email>mdalcq@pasteur.fr</email><email>dalcqm@mail.nih.gov</email></author><author xml:id="author-0004"><persName><surname>Zalc</surname><forename type="first">Bernard</forename></persName><affiliation><orgName type="institution">1National Institute for Neurological Disorders and Stroke (NINDS)</orgName><address><addrLine>Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</addrLine><country key="MD" xml:lang="en">MOLDOVA, REPUBLIC OF</country><country key="US" xml:lang="en">UNITED STATES</country><country key="GB" xml:lang="en">UNITED KINGDOM</country><country key="DE" xml:lang="en">GERMANY</country><country key="FR" xml:lang="en">FRANCE</country></address></affiliation><email>mdalcq@pasteur.fr</email><email>dalcqm@mail.nih.gov</email></author><author xml:id="author-0005"><persName><surname>Lubetzki</surname><forename type="first">Catherine</forename></persName><affiliation><orgName type="institution">1National Institute for Neurological Disorders and Stroke (NINDS)</orgName><address><addrLine>Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</addrLine><country key="MD" xml:lang="en">MOLDOVA, REPUBLIC OF</country><country key="US" xml:lang="en">UNITED STATES</country><country key="GB" xml:lang="en">UNITED KINGDOM</country><country key="DE" 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<journal-id journal-id-type="publisher-id">brainj</journal-id>
<journal-title>Brain</journal-title>
<issn pub-type="ppub">0006-8950</issn>
<issn pub-type="epub">1460-2156</issn>
<publisher>
<publisher-name>Oxford University Press</publisher-name>
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<article-id pub-id-type="doi">10.1093/brain/awn076</article-id>
<article-id pub-id-type="publisher-id">awn076</article-id>
<article-categories>
<subj-group>
<subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author" corresp="yes">
<name><surname>Dubois-Dalcq</surname><given-names>Monique</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>1</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Williams</surname><given-names>Anna</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>2</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Stadelmann</surname><given-names>Christine</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>3</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Stankoff</surname><given-names>Bruno</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>4</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>5</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>6</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Zalc</surname><given-names>Bernard</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>4</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>5</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>6</sup></xref>
</contrib>
<contrib contrib-type="author">
<name><surname>Lubetzki</surname><given-names>Catherine</given-names></name>
<xref ref-type="aff" rid="AFF1"><sup>4</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>5</sup></xref>
<xref ref-type="aff" rid="AFF1"><sup>6</sup></xref>
</contrib>
</contrib-group>
<aff id="AFF1"><sup>1</sup>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, <sup>2</sup>Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, <sup>3</sup>Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, <sup>4</sup>Inserm, U711, 75013 Paris, <sup>5</sup>Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and <sup>6</sup>AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</aff>
<author-notes>
<corresp>Correspondence to: Monique Dubois-Dalcq, MD, National Institute of Neurological Disorders and Stroke, Porter Neuroscience Research Center, Bdg 35, Pod 2A106, 35 Convent Drive MSC3706, Bethesda MD 20892-3706, USA E-mail: <email>mdalcq@pasteur.fr</email>; <email>dalcqm@mail.nih.gov</email></corresp>
</author-notes>
<pub-date pub-type="ppub">
<month>7</month>
<year>2008</year>
</pub-date>
<pub-date pub-type="epub">
<day>12</day>
<month>5</month>
<year>2008</year>
</pub-date>
<volume>131</volume>
<issue>7</issue>
<fpage>1686</fpage>
<lpage>1700</lpage>
<history>
<date date-type="received">
<day>31</day>
<month>1</month>
<year>2008</year>
</date>
<date date-type="rev-recd">
<day>18</day>
<month>3</month>
<year>2008</year>
</date>
<date date-type="accepted">
<day>26</day>
<month>3</month>
<year>2008</year>
</date>
</history>
<permissions>
<copyright-statement>Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement>
<copyright-year>2008</copyright-year>
</permissions>
<abstract>
<p>In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.</p></abstract>
<kwd-group><kwd>multiple sclerosis</kwd><kwd>nodes of Ranvier</kwd><kwd>enhancing repair</kwd><kwd>animal models</kwd><kwd>transparent fish</kwd></kwd-group>
</article-meta>
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<sec sec-type="intro"><title>Introduction</title>
<p>Confronted with the urgency of combating the loss of function in multiple sclerosis (MS) patients, neuroscientists and neurologists have generated a wealth of new data on mechanisms of remyelination which restores rapid saltatory conduction along myelinated tracts and prevents axonal loss. These data come from gene expression analysis of MS neural tissues and experiments in a variety of animal models. Discoveries regarding the molecular basis of myelination and the biology of adult neural stem cells have also influenced views on myelin repair in the adult central nervous system (CNS) (reviewed in Dubois-Dalcq <italic>et al</italic>., <xref ref-type="bibr" rid="B35">2005</xref>; Miller and Mi, <xref ref-type="bibr" rid="B91">2007</xref>). Here, we present our viewpoint on these studies by apposing observations in man and human tissues to results obtained in experimental models. We particularly want to draw attention to the importance of restoring fast conduction in demyelinated axons by rapid remyelination in man and of developing strategies to enhance remyelination at the early stages of MS based on visualization of ongoing, recent demyelinating events by imaging.</p>
<p>Endogenous remyelination occurs in white and grey matter in MS and fully remyelinated areas are often referred to as ‘shadow plaques’ by neuropathologists (Patrikios <italic>et al</italic>., <xref ref-type="bibr" rid="B103">2006</xref>; Albert <italic>et al</italic>., <xref ref-type="bibr" rid="B4">2007</xref>; Patani <italic>et al</italic>., <xref ref-type="bibr" rid="B102">2007</xref> among others). Newly made myelin sheaths are indeed thinner than normal, have shorter internodes and variability in nodal length (Perier and Grégoire, <xref ref-type="bibr" rid="B105">1965</xref>). These variations in myelin thickness and internode distance in shadow plaques might decrease the robustness of saltatory conduction along myelinated axons. Yet, in animal models, the conduction velocity increases during remyelination. For instance, grafting of embryonic glial cells into the dorsal columns of myelin-deficient rats resulted in a significant increase in conduction velocity compared to non-transplanted regions, provided a sufficient density of sodium channels is restored at the nodes of Ranvier (Utzschneider <italic>et al</italic>., <xref ref-type="bibr" rid="B133">1994</xref>).</p>
<p>Unexpectedly, extensive remyelination has been observed not only in the early phase of MS, but also in patients with long-standing disease (Patrikios <italic>et al</italic>., <xref ref-type="bibr" rid="B103">2006</xref>). An important question is whether genes modulating disease severity influence myelin repair. A case to study is HLA-G which is involved in materno-foetal tolerance and expressed in the CNS in inflammatory conditions. In women with relapsing-remitting MS, levels of expression of HLA-G in blood mononuclear cells and in serum during pregnancy and postpartum inversely correlate with disease activity (Airas <italic>et al</italic>., <xref ref-type="bibr" rid="B3">2007</xref>). Discovery of genes modulating repair will expand our understanding of the physiological and molecular basis of endogenous CNS remyelination. It will likely provide clues as to how to develop strategies to enhance this spontaneous repair process that has been preserved by evolutionary pressure since the appearance of myelin in the first gnatostomes, the placoderms. This is a highly successful fish group that arose about 425 million years ago, and was a dominant organism in the ocean during the Devonian period (Zalc and Colman, <xref ref-type="bibr" rid="B148">2000</xref>; Zalc, <xref ref-type="bibr" rid="B147">2006</xref>; Zalc <italic>et al</italic>., <xref ref-type="bibr" rid="B149">2008</xref> in press).</p></sec>
<sec><title>An ancient neural regeneration programme, starting in fish</title>
<p>It is rather fascinating to browse through papers on fish CNS regeneration as they outline many of the processes occurring during axonal regeneration and remyelination in mammals. The process of axonal regeneration is also relevant to MS in view of the extensive axonal damage, including transection, which occurs in this disease. The optic nerve, a frequent site of the first clinical manifestation of MS, has been the focus of several early fish studies. Murray (<xref ref-type="bibr" rid="B92">1976</xref>) studied cytoskeletal and organelle changes during regeneration of goldfish retinal axons after optic nerve transection, reporting that ‘the regenerating axons gradually increase in diameter but do not reach preoperative sizes’ while ‘remyelination is delayed and proceeds slowly’. Wolburg's study (<xref ref-type="bibr" rid="B142">1981</xref>) of goldfish optic nerve crush described that the regenerating axons acquired thinner myelin sheaths. The author proposed that ‘a neuron is capable of inducing a normally developed myelin sheath when its axon contacts an oligodendrocyte for the first time whereas a neuron whose axon contacts an oligodendrocyte the second time is not capable of forming a normal myelin sheath in the adult animal’. Nona <italic>et al</italic>. (<xref ref-type="bibr" rid="B96">2000</xref>) later found that, after optic nerve injury in fish, remyelination only occurred after the regenerating axons had reached the tectum where the axon terminals refine their map. Myelin repair was synchronous throughout the optic nerve and exacted by both Schwann cells and oligodendrocytes. Myelin protein zero, the major myelin protein in the mammalian peripheral nervous system (PNS), is present in zebrafish optic nerve and spinal cord where its expression increases during regeneration (Schweitzer <italic>et al</italic>., <xref ref-type="bibr" rid="B116">2003</xref>). These fish studies therefore underline the requirement of connectivity of damaged CNS axons before axons can be remyelinated. This is in keeping with developmental studies in the mouse showing the crucial role of electrical activity along axons to induce myelination (Demerens <italic>et al</italic>., <xref ref-type="bibr" rid="B33">1996</xref>; Stevens <italic>et al</italic>., <xref ref-type="bibr" rid="B129">2002</xref>). It may also be important in MS where the maintenance or re-establishment of connectivity of demyelinated axons may be a prerequisite for remyelination.</p>
<p>In recent years, zebrafish mutant screens have identified genes essential to the development of myelinated axons (Kazakova <italic>et al</italic>., <xref ref-type="bibr" rid="B60">2006</xref>; Pogoda <italic>et al</italic>., <xref ref-type="bibr" rid="B144">2006</xref>). Most of these have homologues in higher vertebrates but, in some cases, new unexpected functions linked to myelination were discovered as in the case of NSF, a protein essential for vesicular fusion at synapses and ion channel clustering on axons (Woods <italic>et al</italic>., <xref ref-type="bibr" rid="B144">2006</xref>). We advocate the use of fish models not only for studying neurite regeneration but also for remyelination in view of the rapid, convenient mutant analysis and the possibility to follow oligodendrocyte movement and activities in the living animal.</p></sec>
<sec><title>A see-through fish in lieu of a mouse?</title>
<p>The recognition of axons by migrating oligodendrocytes processes has been visualized in intact nearly transparent zebrafish larvae in which oligodendrocytes—and some axons—of the spinal cord expressed membrane-localized GFP under the control of the nkx2.2 promoter (Kirby <italic>et al</italic>., <xref ref-type="bibr" rid="B62">2006</xref>). A continuous process of oligodendrocyte extension and branching precedes the final positioning and wrapping of the axon by oligodendrocytes. When such oligodendrocytes were ablated by laser microsurgery, other oligodendrocytes compensated for the loss by rapidly extending new processes and migrating towards the region abandoned by the dying oligodendrocyte (<xref ref-type="fig" rid="F1">Fig. 1</xref>). After all oligodendrocytes were ablated in five hemi-segments of the spinal cord, oligodendrocyte precursor cells (OPCs) from the intact hemi-segments rapidly migrated toward the lesion site whilst dividing. The result was that 50% of oligodendrocytes had already been replaced on the lesion side at 1 day (ibidem).
<fig id="F1"><label><bold>Fig. 1</bold></label><caption><p>Time-lapse recording and OPC ablation experiment in transgenic <italic>olig2 EGFP</italic> zebrafish larva (at 60 h post fertilization) which expresses EGFP both in axons and OPCs. Image of spinal cord (dorsal side up) before and after laser ablation. Membrane bound GFP + oligodendrocyte-lineage cells which had migrated dorsally were targeted by their fluorescence and ablated using approximately five pulses of 440 nm light generated by a Photonics Micropoint Laser System. At time zero after ablation, the oligodendrocyte (arrow) extends new processes into the area vacated by the ablated cell (arrowhead) and later starts to enwrap axons between 3 and 8 h. The larvae were anaesthesized during both ablation and time lapse and then placed on their side on glass-bottomed 35 mm Petri dishes. The time lapse images were captured using 40 × oil-immersion objectives mounted on a motorized Zeiss Axiovert 200 microscope equipped with a Perkin Elmer ERS spinning disk confocal system with a heated stage and chamber to maintain embryos at 28.5oC (Kirby <italic>et al</italic>., <xref ref-type="bibr" rid="B62">2006</xref>). <italic>Figure and Methodology</italic>: Courtesy of Norio Takada and Bruce Appel, Vanderbilt University, Tennessee, USA. Scale bar: 24 µm.</p></caption><graphic xlink:href="awn076f1"></graphic></fig></p>
<p>Imaging such repair processes could be done in mutant medaka fish that are transparent throughout life (Wakamatsu <italic>et al</italic>., <xref ref-type="bibr" rid="B138">2001</xref>). GFP-expressing transgenics of this fertile fish have been made, allowing non invasive studies of internal organs (ibidem). If nkx2.2-GFP transgenics could be obtained in medaka as in zebrafish, one could possibly succeed in performing multiple oligodendrocyte laser ablation in the spinal cord (a close equivalent to focal chemical lesions in rodent, discussed below) and imaging demyelination/remyelination in the living animal. As in demyelinated mammals, one would predict that fish-activated macrophages and lymphoid cells (Zapata <italic>et al</italic>., <xref ref-type="bibr" rid="B150">2006</xref>) would be attracted to the lesion site. The transparent medaka fish stock of Nagoya University are available to interested scientists (Y. Wakamatsu, personal communication).</p>
<p>Whatever progress is made in fish, however, must be translated to mammals, which have an immune system that is more similar to that of humans.</p></sec>
<sec><title>Animal models of remyelination in mammals</title>
<p>A variety of rodent animal models has helped to elucidate some of the mechanisms involved in CNS remyelination. As there is no perfect model for MS, one particular animal model may be chosen to examine one specific aspect of MS to be investigated. These models include the induction of a focal demyelinated lesion by a toxin such as lysolecithin or ethidium bromide (Hall, <xref ref-type="bibr" rid="B51">1972</xref>; Woodruff and Franklin, <xref ref-type="bibr" rid="B143">1999</xref>). A cuprizone diet causes demyelination in major myelinated tracts such as the corpus callosum and cerebellar peduncles and is followed by myelin repair when the diet is stopped (Blakemore, <xref ref-type="bibr" rid="B18">1973</xref>; Ludwin, <xref ref-type="bibr" rid="B80">1978</xref>).</p>
<p>The value of viral-mediated and auto-immune demyelination lies mostly in their modelling of the immune cells in MS lesions. Some neurotropic strains of mouse corona virus induce demyelinating lesions mostly in the spinal cord followed by immune-mediated clearing of the virus, remyelination and recovery (Kristensson <italic>et al</italic>., <xref ref-type="bibr" rid="B67">1986</xref>; Armstrong <italic>et al</italic>., <xref ref-type="bibr" rid="B5">1990</xref>). Another viral model is the Theiler virus-induced murine encephalomyelitis whose chronic inflammation in gray and white matter mimics some aspects of MS and where natural IgM autoantibodies were shown to enhance remyelination (discussed in Arnett and Viney, <xref ref-type="bibr" rid="B9">2007</xref>; Rodriguez, <xref ref-type="bibr" rid="B108">2007</xref>).</p>
<p>Injection of a CNS-specific myelin protein such as myelin oligodendrocyte glycoprotein with adjuvants induces experimental autoimmune encephalitis (EAE) which mimics different clinical presentations of MS and its multifocal inflammatory lesions more closely. EAE has been extensively used to identify immunoregulators for preclinical trial in MS (reviewed in Gold <italic>et al</italic>., <xref ref-type="bibr" rid="B49">2006</xref>) and also to assay remyelination as in a study on the role of Notch in repair (Seifert et al., <xref ref-type="bibr" rid="B118">2007</xref>). Recently, cortical demyelination was induced by focal injection of pro-inflammatory cytokines in subclinically MOG-immunized rats, a model originally developed in the spinal cord (Kerschensteiner <italic>et al</italic>., <xref ref-type="bibr" rid="B61">2004</xref>; Merkler <italic>et al</italic>., <xref ref-type="bibr" rid="B87">2006</xref>). After cortical inflammation subsided, rapid remyelination occurred, mimicking extensive remyelination observed in MS cortical lesions (Albert <italic>et al</italic>., <xref ref-type="bibr" rid="B4">2007</xref>). Mice deficient in neural and immune system genes have been used extensively in these models to study their impact on remyelination.</p>
<p>To understand how remyelination is initiated, a series of studies have characterized the precursors of remyelinating cells in rodent and man.</p></sec>
<sec><title>Origin of remyelinating cells in the adult mammalian CNS</title>
<p>The first event in myelin repair is the recruitment of OPCs to the demyelinated lesions (reviewed by Chandran <italic>et al</italic>., 2008). In rodents, there are at least two known sources of remyelinating oligodendrocytes in the adult mammalian CNS: the first is the large pool of OPCs expressing the proteoglycan NG2 and/or PDGF-receptor alpha, the second comes from precursors in the adult subventricular zone (SVZ) (Menn <italic>et al</italic>., <xref ref-type="bibr" rid="B86">2006</xref>; reviewed in Zhao <italic>et al</italic>., <xref ref-type="bibr" rid="B155">2008</xref>). Both rodent and MS white matter OPCs express Olig 2, Nkx2.2 and Myt1 transcription factors when recruited to demyelinating lesions (Sim <italic>et al</italic>., <xref ref-type="bibr" rid="B122">2002</xref>; Fancy <italic>et al</italic>., <xref ref-type="bibr" rid="B41">2004</xref>; Nait-Oumesmar <italic>et al</italic>., <xref ref-type="bibr" rid="B93">2007</xref>; Vana <italic>et al</italic>., <xref ref-type="bibr" rid="B135">2007<italic>b</italic></xref>). In mouse SVZ, some OPC markers such as NG2 and olig 2 are sometimes expressed in type C precursors which are derived from GFAP-expressing neural stem cells (Doetsch <italic>et al</italic>., <xref ref-type="bibr" rid="B34">2002</xref>; Aguirre <italic>et al</italic>., <xref ref-type="bibr" rid="B1">2004</xref>). The finding of OPC markers in some SVZ precursors may be due to the rapid commitment to an oligodendrocyte fate when precursors move out of the SVZ or a pre-commitment of these precursors to this fate within the SVZ (Delaunay <italic>et al</italic>., <xref ref-type="bibr" rid="B31">2008</xref>) as described also in the case of neurons (Kohwi <italic>et al</italic>., <xref ref-type="bibr" rid="B64">2007</xref>).</p>
<p>Of important relevance to CNS remyelination in man, OPCs have been isolated from normal appearing white matter obtained in the course of surgery for epilepsy and found to be multipotential <italic>in vitro</italic> (Nunes <italic>et al</italic>., <xref ref-type="bibr" rid="B98">2003</xref>). When grafted into dysmyelinating shiverer mice—which lack myelin basic protein—these human OPCs extensively migrate and remyelinate the mouse white matter (Windrem <italic>et al</italic>., <xref ref-type="bibr" rid="B141">2004</xref>). As remyelination occurs in MS, it is presumed that OPCs recruited from normal appearing white matter to lesions have similar remyelinating properties. The transcriptional profile of freshly sorted human OPCs was compared to that of the white matter from which they were isolated. The results indicate that adult human OPCs are responsive to local factors triggering distinct signaling pathways either regulating their self maintenance or inducing their differentiation (Sim <italic>et al</italic>., <xref ref-type="bibr" rid="B121">2006</xref>).</p>
<p>Another source of remyelinating cells in the CNS is Schwann cells. In some MS cases, Schwann cells were found in the spinal cord and hindbrain where they synthesize PNS myelin around demyelinated CNS axons (reviewed in Compston <italic>et al</italic>., <xref ref-type="bibr" rid="B30">2006</xref>). Importantly, the Schwann cells that migrate and remyelinate CNS lesions after experimental demyelination of rat dorsal columns by ethidium bromide (EB) restore fast conduction ‘within normal limits’ (Felts and Smith, <xref ref-type="bibr" rid="B42">1992</xref>). Moreover, a normal pattern of sodium and potassium channels at the nodes of Ranvier was maintained 1 year after a similar EB lesion was made (Black <italic>et al</italic>., <xref ref-type="bibr" rid="B17">2006</xref>). Normal conduction velocity was also restored after grafting labelled cultured Schwann cells into EB-treated, glial free dorsal columns (Honmou <italic>et al</italic>., <xref ref-type="bibr" rid="B53">1996</xref>). These observations strongly suggest that PNS myelin made by remyelinating Schwann cells may restore conduction of CNS axons also in MS. Thus Schwann cell migration into the CNS is a remarkable natural repair mechanism. However, we do not know how extensive this is and what attract these repair cells to the CNS. Could it be the same factors that attract OPCs?</p></sec>
<sec><title>Regulators of OPCs mitosis/migration may help remyelination</title>
<p>Epidermal growth factor (EGF) and platelet-derived growth factor A (PDGFA) stimulate OPCs to divide and migrate during CNS development (reviewed in Rogister <italic>et al</italic>., <xref ref-type="bibr" rid="B109">1999</xref>). Experiments in transgenic mice have also revealed a role for these factors in remyelination. Indeed, mouse OPCs overexpressing human EGF-R showed increased mitotic and migratory activity toward a corpus callosum lesion and this resulted in acceleration of remyelination and functional recovery (Aguirre <italic>et al</italic>., <xref ref-type="bibr" rid="B2">2007</xref>). Transgenic mice overexpressing the human PDGF A gene and submitted to a cuprizone diet that caused chronic demyelination, showed enhanced remyelination and oligodendrocyte numbers after removal of the diet (Vana <italic>et al</italic>., <xref ref-type="bibr" rid="B134">2007<italic>a</italic></xref>). The migration response of OPCs to PDGF is enhanced <italic>in vitro</italic> by the polysialylated form of the neural adhesion molecule (PSA-NCAM) (Zhang <italic>et al</italic>., <xref ref-type="bibr" rid="B152">2004</xref>). In response to a demyelinating event in the corpus callosum, some SVZ precursors expressing PDGFR alpha and PSA-NCAM divide, migrate away from the SVZ and generate OPCs in the lesion (Menn <italic>et al</italic>., <xref ref-type="bibr" rid="B86">2006</xref>). Accordingly, the SVZ of MS patients shows a significant increase in PSA-NCAM expressing precursors which also appear to migrate toward lesions (Nait-Oumesmar <italic>et al</italic>., <xref ref-type="bibr" rid="B93">2007</xref>). Interestingly, both OPCs and Schwann cells engineered to overexpress PSA on N-CAM show enhanced migratory properties in the rodent CNS (Lavdas <italic>et al</italic>., <xref ref-type="bibr" rid="B72">2006</xref>; Glaser <italic>et al</italic>., <xref ref-type="bibr" rid="B48">2007</xref>).</p>
<p>Semaphorins, a class of molecules providing guidance cues for developing neurons, have been shown to also regulate developing OPC migration. Semaphorins 3A and F are repulsive or attractive, respectively for embryonic OPCs (Spassky <italic>et al</italic>., <xref ref-type="bibr" rid="B126">2002</xref>). In MS, Sema3A and Sema3F expression is elevated in glial cells in and around active lesions and also in neurons whose axons have been demyelinated. There is a differential expression pattern, so that more Sema3F (attractive) expression is seen around and within those plaques which are very active with a dense inflammatory infiltrate, compared to more Sema3A (repulsive) expression around and within less active plaques (Williams <italic>et al</italic>., <xref ref-type="bibr" rid="B140">2007</xref>). These results suggest that repulsive or attractive properties of different semaphorins can influence OPC migration, a prerequisite for MS plaque remyelination. In addition, these observations are in good agreement with several reports on the pro-remyelinating influence of inflammation.</p></sec>
<sec><title>A link between inflammation and remyelination</title>
<p>There have been several recent studies on MS tissues that argue convincingly for a link between components of the inflammatory milieu in and around the lesions and myelin repair, a concept that has been reinforced by animal studies of remyelination, including gain or loss of function experiments (discussed in Zhao <italic>et al</italic>., <xref ref-type="bibr" rid="B154">2005</xref>).</p>
<p>Nervous tissue inflammation generally implies the presence of T and/or B cells with macrophages/microglia showing signs of activation, leading to the local release of immune mediators. Abundance of T cells and activated macrophages/microglia are frequently observed in areas of active remyelination. Foamy macrophages and CD3 and CD8-positive T cells are often present in early MS lesions that at the same time show striking signs of remyelination (<xref ref-type="fig" rid="F2">Fig. 2</xref>). Further evidence for a link between inflammation and remyelination comes from the presence of HLA-DR positive microglial cells close to areas of remyelination in MS shadow plaques (Patani <italic>et al</italic>., <xref ref-type="bibr" rid="B102">2007</xref>). Accordingly, loss of function experiments have shown that MHC type II antigens are necessary for efficient remyelination in mice (Arnett <italic>et al</italic>., <xref ref-type="bibr" rid="B10">2003</xref>).
<fig id="F2"><label><bold>Fig. 2</bold></label><caption><p>Early remyelination of a demyelinated lesion with abundant inflammation in a brain biopsy from an MS patient. Pictures were taken from adjacent, sequential sections; the first section (<bold>A</bold>) was stained with luxol fast blue for myelin and PAS (nuclei are stained blue by hematoxylin) while all other sections were stained by peroxidase immunolabelling for different antigens (<bold>B</bold>–<bold>F</bold>). (<bold>A</bold>) Extensive demyelination with scarce, thin and irregular remyelinated fibres in light blue (arrows). (<bold>B</bold>) Proteolipid protein antibody stains abundant thin, apparently newly formed myelin sheaths. (<bold>C</bold>) Oligodendrocytes in the lesion are strongly immunolabelled (in brown) for TPPP/p25, the brain-specific tubulin polymerization promoting protein (Kovacs <italic>et al</italic>., <xref ref-type="bibr" rid="B66">2004</xref>). <italic>Source:</italic> Antibody kindly provided by Poul H. Jensen, Aarhus, Denmark. (<bold>D</bold>–<bold>F</bold>) Abundant immune cells are detected in the same remyelinating lesion and identified as foamy macrophages (KiM1P in <bold>D</bold>) as well as T cells stained for CD3 (<bold>E</bold>) and CD8 (<bold>F</bold>). Scale bar: 50 µm.</p></caption><graphic xlink:href="awn076f2"></graphic></fig></p>
<p>The cause–effect relationship between myelin repair and macrophage activation/tissue invasion in MS was confirmed by experiments in rodent focal demyelination models showing that macrophage depletion impairs remyelination (Kotter <italic>et al</italic>., <xref ref-type="bibr" rid="B65">2005</xref>; reviewed in Zhao <italic>et al</italic>., <xref ref-type="bibr" rid="B154">2005</xref>). The clearing of myelin debris by macrophages may contribute to create an environment favourable to OPC recruitment for repair (ibidem). Moreover, induction of acute inflammation in chronically demyelinated tissue triggers remyelination in spinal cord (Foote and Blakemore, <xref ref-type="bibr" rid="B43">2005</xref>) and acute inflammation also enhances myelination of retinal axons by OPCs grafted in the eye (Setzu <italic>et al</italic>., <xref ref-type="bibr" rid="B119">2006</xref>).</p>
<p>Could antibodies detected in lesions also have a role in myelin repair? The evidence that accumulation of B cells in submeningeal follicles is associated with extensive demyelination in some MS patients argues against this possibility (Magliozzi <italic>et al</italic>., <xref ref-type="bibr" rid="B82">2007</xref>). Unfortunately, the natural auto-antibodies that enhance remyelination in the mouse Theiler virus model (Rodriguez, <xref ref-type="bibr" rid="B108">2007</xref>) have not been detected in MS tissues or correlated with remyelination in the human disease.</p>
<p>Many chemokines, which are potent mediators of immune cell migration, are released by lymphocytes and macrophages in MS tissues. Three alpha chemokine receptors CXCR1, CXCR2, CXCR3, expressed by OPCs and oligodendrocytes in the normal adult CNS, showed enhanced expression in MS but also in other CNS diseases. Yet, their respective ligands, chemokines CXCL8, 1 and 10, were specifically detected in reactive astrocytes at the edge of active MS lesions (Omari <italic>et al</italic>., <xref ref-type="bibr" rid="B99">2005</xref>). It was proposed that CXCL1 could stop OPC migration as it does during development (reviewed by Miller and Mi, <xref ref-type="bibr" rid="B91">2007</xref>). CXCL12, which is essential to immune and nervous system development (Lazarini <italic>et al</italic>., <xref ref-type="bibr" rid="B73">2003</xref>), was detected in astrocytes around MS lesions as well as in the CSF of relapsing-remitting MS patients (Calderon <italic>et al</italic>., <xref ref-type="bibr" rid="B23">2006</xref>; Krumbholz <italic>et al</italic>., <xref ref-type="bibr" rid="B68">2006</xref>). During mouse embryonic development, CXCL12 is an attractant for rodent neural precursors and OPCs expressing its CXCR4 receptor (Dziembowska <italic>et al</italic>., <xref ref-type="bibr" rid="B39">2005</xref>). As CXCR4 is downregulated on mature oligodendrocytes and has not been described on adult rodent and human OPCs, the role of CXCL12 in MS lesions is presently unclear.</p>
<p>Two haemopoietic cytokines are released in MS inflammatory lesions. Leukemia inhibitory factor (LIF) is produced by myelin reactive T cells infiltrating demyelinating lesions (Vanderlocht <italic>et al</italic>., <xref ref-type="bibr" rid="B136">2006</xref>). Interleukin 11 is expressed by astrocytes at lesion edges while its receptor is detected on nearby oligodendrocytes (Zhang <italic>et al</italic>., <xref ref-type="bibr" rid="B153">2006</xref>). Both cytokines promote oligodendrocyte survival and myelination <italic>in vitro</italic> and LIF promotes remyelination in EAE (Butzkueven <italic>et al</italic>., <xref ref-type="bibr" rid="B21">2002</xref>, <xref ref-type="bibr" rid="B20">2006</xref>; Stankoff <italic>et al</italic>., <xref ref-type="bibr" rid="B127">2002</xref>; Zhang <italic>et al</italic>., <xref ref-type="bibr" rid="B153">2006</xref>). LIF has therefore emerged as a potential therapy to enhance remyelination.</p>
<p>Collectively, these human and experimental studies strengthen the proposal that some immune mediators, either membrane bound or secreted by T cells and macrophages, may positively influence endogenous remyelination in MS. Yet other components of the inflammatory cascade such as nitric oxide production and free radicals can damage axons, underlining the importance of protecting demyelinated axons from degeneration.</p></sec>
<sec><title>Neuroprotection: the first line of defence before remyelination</title>
<p>Even if remyelination is the best way to provide axon protection, this process takes time during which recently demyelinated axons risk exposure to nitric oxide, oxidative stress, glutamate-induced excitotoxicity as well as calcium influx and alterations of mitochondrial function (reviewed in Smith, <xref ref-type="bibr" rid="B123">2006</xref>; Greenberg and Calabresi, <xref ref-type="bibr" rid="B50">2008</xref>). Therefore, it would be beneficial to ‘protect’ axons at this time to enhance their survival, maintain axon connectivity and facilitate re-emergence of myelinating signals whilst OPCs are being recruited to the lesion site (reviewed in Scolding and Dubois-Dalcq, <xref ref-type="bibr" rid="B117">2008</xref>). Some neurotrophic factors released either by immune cells or neurons may act locally to protect demyelinated axons in MS lesions. First, the synthesis of ciliary neurotrophic factor (CNTF) or brain-derived neurotrophic factor (BDNF) by immune cells is increased in MS patients treated with glatiramer acetate (a synthetic peptide mimicking MBP structure and inhibiting T cell peptide binding) or interferon (IFN) beta1a, the two major immunomodulators used to treat relapsing-remitting MS (Sarchielli <italic>et al</italic>., <xref ref-type="bibr" rid="B111">2007</xref>). Thus these treatments are also potentially neuroprotective. Second, cortical neurons in MS showed increased expression of CNTF, its tripartite receptor complex composed of CNTR alpha, LIFR beta and gp130, and their phosphorylated downstream products (Dutta <italic>et al</italic>., <xref ref-type="bibr" rid="B37">2007</xref>).</p>
<p>In the neuropharmaceutical world, a number of neuroprotective agents have been successfully used in EAE to target ion channels or NMDA/AMPA receptors, and some are being tested in clinical trials. Molecules known for other biological effects in man such as erythropoietin and statins were discovered to also exhibit neuroprotective properties (reviewed in Scolding and Dubois-Dalcq, <xref ref-type="bibr" rid="B117">2008</xref>; Greenberg and Calabresi, <xref ref-type="bibr" rid="B50">2008</xref>). Yet, one would predict that statins, which are inhibitors of cholesterol synthesis, might not help remyelination, taking into account that cholesterol represents 25% of myelin lipids, which in turn accounts for 70% of myelin constituents. Nevertheless, with several drugs at hand, there is reason to believe that healthy axons could be maintained until OPCs arrive in the vicinity of demyelinated fibres, allowing successful recognition of axons and remyelination.</p></sec>
<sec><title>Towards discovery of specific mechanisms of remyelination</title>
<p>During demyelination in MS, it is thought that normal saltatory conduction is rapidly disturbed due to the loss of clustering of axonal sodium channels at the nodes of Ranvier (reviewed in Waxman, <xref ref-type="bibr" rid="B139">2006</xref>). Yet, as observed in the visual system, partial restoration of current can occur in a continuous manner due to the presence of Nav1.2 channels along otherwise undamaged demyelinated axons. The paranode and juxtanode which surround the node are structures particularly vulnerable during demyelination (reviewed in Zawadzka and Franklin, <xref ref-type="bibr" rid="B151">2007</xref>). The paranode, containing paranodin (Caspr) and the glial form of neurofascin (Nfasc155), is indeed dismantled in MS lesions, allowing Kv1.2 channels to diffuse to the node (Howell <italic>et al</italic>., <xref ref-type="bibr" rid="B54">2006</xref>). This results in a diffuse distribution of Nav1.2 channels, paranodin and Kv1.2 channels on intact demyelinated axons (Coman <italic>et al</italic>., <xref ref-type="bibr" rid="B28">2006</xref>; Howell <italic>et al</italic>., <xref ref-type="bibr" rid="B54">2006</xref>).</p>
<p>To begin understanding the process of remyelination, it seems appropriate to consider what has been learned from developmental myelination in rodents. A mouse postnatal transcriptome performed on oligodendrocytes and their precursors acutely isolated during the first postnatal month has revealed two waves of gene expression patterns during CNS myelination (Cahoy <italic>et al</italic>., <xref ref-type="bibr" rid="B22">2008</xref>). The first wave of myelin gene up-regulation, concomitant with down-regulation of cytoskeleton maintenance-related genes, leads to ensheathment of nerve fibres. The second wave of up-regulation of intercellular junction genes may be linked to the assembly of the nodes of Ranvier.</p>
<p>How Ranvier nodes and paranodes form during rodent CNS development is not fully understood but apparently requires two steps (Kaplan <italic>et al</italic>., <xref ref-type="bibr" rid="B57">2001</xref>; Dupree <italic>et al</italic>., <xref ref-type="bibr" rid="B36">2005</xref>; Schafer <italic>et al</italic>., <xref ref-type="bibr" rid="B113">2006</xref>). A complete, functional nodal region depends on each myelin loop maintaining a septate-like junction with the axon, while Kv1.2 channels are kept at bay in the juxtanodes. A first event in node formation is the induction of axonal Nav1.2 channel clusters, possibly by an as yet uncharacterized soluble factor made by oligodendrocytes (Kaplan <italic>et al</italic>., <xref ref-type="bibr" rid="B58">1997</xref>, <xref ref-type="bibr" rid="B57">2001</xref>). This process defines domains where oligodendrocytes position themselves along the axon to synthesize myelin internodes. Myelin excludes axonal Nav1.2 channels along the internode and promotes clustering of newly emerging Nav1.6 channels at the node while specific axon–glia interactions result in paranode/juxtanode formation. In the case of axon branching, collaterals dictate the position of the nodes of Ranvier. Since collaterals are branching before OPCs migrate towards axons, the position of branching points determines where the nodes of Ranvier will assemble. Thus, the putative oligodendroglial clustering factor can only regulate the distribution of nodes between two collaterals, therefore controlling the number (<italic>n</italic>) and the length (<italic>L</italic>) of the internode. The latter is calculated by the simple equation: <italic>L</italic> = <italic>Dc</italic>/<italic>n</italic>, where <italic>Dc</italic> is the distance between two branch points (Lubetzki and Zalc, <xref ref-type="bibr" rid="B78">2001</xref>).</p>
<p>Our knowledge of internodal axonal signals is also derived from developmental myelination studies in rodents. The adhesion molecule L1 positively regulates CNS and PNS myelination whereas Neuregulin 1 (Nrg1) type III is a major regulator of PNS myelination (Barbin <italic>et al</italic>., <xref ref-type="bibr" rid="B14">2004</xref>; Coman <italic>et al</italic>., <xref ref-type="bibr" rid="B29">2005</xref>; Nave and Salzer, <xref ref-type="bibr" rid="B94">2006</xref>). Although Nrg1 is also expressed on CNS axons, its role in CNS myelination is not clear. Induction of Fyn kinase in OPCs by axons triggers oligodendrocyte process extension which is an essential event preceding myelin wrapping (Klein <italic>et al</italic>., <xref ref-type="bibr" rid="B63">2002</xref>). Nrg1 and Laminin 2 on axons may strengthen axon recognition by OPC processes bearing their respective ErbB and alpha 6 beta1 integrin receptors. Laminin2 has a second receptor on OPCs called dystroglycan which regulates myelin membrane synthesis and the terminal stages of myelination (Colognato <italic>et al</italic>., <xref ref-type="bibr" rid="B27">2007</xref>).</p>
<p>During the period preceding myelination in juvenile rats, unmyelinated axons of the corpus callosum release glutamate by exocytosis in response to electrical stimulation and groups of vesicles are detected at the axon contact sites with OPC processes (Kukley <italic>et al</italic>., <xref ref-type="bibr" rid="B69">2007</xref>). Also, in optic nerve, small clusters of axonal vesicles are seen at ‘arbitrary’ sites of contact with OPCs, suggesting that axonal glutamate release mediates the recorded axo-glial currents at a premyelinating stage (ibidem). The concept emerging from these studies is that glutamate release by axons helps OPCs to find axons through an activity-dependent process, reinforcing the importance of electrical activity in OPC development and myelination (Barres and Raff, <xref ref-type="bibr" rid="B16">1993</xref>; Demerens <italic>et al</italic>., <xref ref-type="bibr" rid="B33">1996</xref>; Stevens <italic>et al</italic>., <xref ref-type="bibr" rid="B129">2002</xref>; Karadottir and Attwell, <xref ref-type="bibr" rid="B59">2007</xref>). Another important mediator liberated by firing axons is ATP which induces astrocytes to synthesize LIF. LIF in turn promotes myelination by cultured oligodendrocytes (Ishibashi <italic>et al</italic>., <xref ref-type="bibr" rid="B56">2006</xref>).</p>
<p>Returning to the subject of remyelination in man, it appears that the first requirement is to reset the nodes by re-assembly of specific molecular complexes with adhesion molecules (Sasaki <italic>et al</italic>., <xref ref-type="bibr" rid="B112">2006</xref>). The scenario for remyelination in MS is proposed as starting with the formation of several nodal-like clusters of Nav channels, often in partially remyelinated lesions as visualized on fibres that are still PLP-negative (Coman <italic>et al</italic>., <xref ref-type="bibr" rid="B28">2006</xref>). In the rodent PNS, Nav channel clustering is promoted by gliomedin at the tips of Schwann cells and its cleavage product released in the node area (Eshed <italic>et al</italic>., <xref ref-type="bibr" rid="B40">2007</xref>; Maertens <italic>et al</italic>., <xref ref-type="bibr" rid="B81">2007</xref>). Gliomedin has been detected in the CNS but it is not yet fully characterized (Manuel Koch, personal communication). As CNS myelin synthesis progresses, Nav1.6 clusters are emerging and associate with the neuronal form of neurofascin (Nfasc186), a signature of node restoration (Howell <italic>et al</italic>., <xref ref-type="bibr" rid="B54">2006</xref>). Consolidation of node organisation may occur at the time when persisting currents with glutamate release sites along demyelinated axons may guide the correct positioning of adult OPCs processes before they enwrap axons to make myelin internodes. Intriguingly, this proposed sequence of repair events in MS is the reverse of the one predicted from the developmental waves of mouse oligodendrocyte gene expression discussed above where myelin internode synthesis starts first (Cahoy <italic>et al</italic>., <xref ref-type="bibr" rid="B22">2008</xref>). If the nodes of Ranvier are recontructed when internode synthesis is not yet occurring or is far from completion, could it result in node/internode abnormalities?</p></sec>
<sec><title>Why is repaired and developmental myelin different?</title>
<p>Is it true that a neuron whose axon is contacted for the second time by an oligodendrocyte is not able to trigger normal myelin sheath synthesis (Wolburg, <xref ref-type="bibr" rid="B142">1981</xref>)? As mentioned above, a thin myelin sheath and increased nodal length are often observed during remyelination in vertebrates. Yet the association of remyelinating cells with naked axons in rodents closely resembles that in normal myelin (reviewed in Franklin and Hinks, <xref ref-type="bibr" rid="B45">1999</xref>). These characteristics are observed whether remyelinating cells are endogenous or exogenous and also in remyelination by Schwann cells. There is no substantial increase in axon diameter during remyelination whereas during development, as the animal grows and matures, the axons increase in length and diameter leading to an increase of myelin internode length and thickness. This suggests that axons may bear or release molecules that increase in density or production proportional to growth to control these parameters.</p>
<p>In developing peripheral nerves, myelin thickness is regulated by Nrg1 Type III isoform with the number of myelin wraps proportional to gene dosage (Michaelov <italic>et al</italic>., <xref ref-type="bibr" rid="B90">2004</xref>). Despite recent data, a role for Nrg1 in CNS myelination is questionable (Taveggia <italic>et al</italic>., <xref ref-type="bibr" rid="B130">2008</xref>). However, it is quite possible that another axonal surface molecule, yet to be discovered, control CNS myelin thickness. A decrease in concentration of this putative axonal molecule in the adult would result in a thinner myelin sheath during remyelination.</p>
<p>Loss of function studies in mutant mice have revealed several other candidate molecules for the control of CNS myelin thickness such as the transmembrane aspartyl protease Bace (Hu <italic>et al</italic>., <xref ref-type="bibr" rid="B55">2006</xref>). Deletion of the chemokine receptor CXCR2 in oligodendrocytes also results in thinner myelin (Padovani-Claudio <italic>et al</italic>., <xref ref-type="bibr" rid="B100">2006</xref>) suggesting the possibility that CXCL1 (released by axons?) may enhance oligodendrocyte wrapping by signalling through the CXCR2 receptor on OPCs. In the case of the axonal adhesion protein Tag1, Tag1 defective adult mice show thinner myelin sheaths as well as increased numbers of nodes of Ranvier compared to controls (E. Chadzopollou and J.L. Thomas, personal communication).</p>
<p>A zebrafish mutant lacking alpha II spectrin shows abnormally long nodes (Voas <italic>et al</italic>., <xref ref-type="bibr" rid="B137">2007</xref>). In wild type zebrafish, alpha II spectrin is normally enriched in nodes and paranodes during development and is essential to stabilize sodium channel clusters and the maturation of the nodes of Ranvier. This channel clustering is controlled by neurons, as wild-type neurons can rescue the mutant. It is presently unclear whether channel clustering at the nodes is also controlled by neurons in mammals and whether neuronal expression of alpha II spectrin is increased at nodes during repair in MS.</p>
<p>The presence of thinner and shorter myelin internodes does not appear to have a strong impact on physiological impulse conduction (Utzschneider <italic>et al</italic>., <xref ref-type="bibr" rid="B133">1994</xref>; Honmou <italic>et al</italic>., <xref ref-type="bibr" rid="B53">1996</xref> among others). However, it is unclear whether this makes myelin more vulnerable to future injury (Smith, <xref ref-type="bibr" rid="B123">2006</xref>). Funch and Faber (<xref ref-type="bibr" rid="B47">1984</xref>), who measured myelin sheath resistance, commented that ‘altering myelin thickness will be expected to have only minimal effects on the axon currents flowing in the axon’, whereas … ‘minor changes in the paranodal junctions may have major consequences’. In that context, nature may have provided the best way to start remyelination by first securing the reconstruction of the nodes/paranodes. This brings us to the next question on how to enhance the endogenous remyelination program.</p></sec>
<sec><title>Remyelination enhancement strategies</title>
<sec><title>Finding new targets</title>
<p>Transcriptome studies are powerful tools to unravel which neural and immune genes are differentially expressed in the course of human myelin repair. These studies are now considerably facilitated by the expansion of MS tissue banks where tissue integrity is optimized, providing access to a range of demyelinated lesions starting to be remyelinated and where remyelination is completed (shadow plaques). Such human studies may be guided by technologies already successfully applied to developmental myelination. A comparative transcriptome analysis from fish to man would consolidate the list of essential, conserved genes involved in signalling myelin repair and help the design of small compounds acting on their signalling pathways. As Olig 1 is a transcription factor essential for rodent remyelination (Arnett <italic>et al</italic>., <xref ref-type="bibr" rid="B8">2004</xref>), ongoing gene profiling studies comparing remyelination in Olig1 deficient mice to wild-type mice is likely to yield interesting data on key regulators of remyelination downstream from Olig1 (S. Fancy, R. Franklin, and D. Rowitch, personal communication).</p>
<p>It would be a milestone if transcriptome data would reveal candidate neural or immune molecules or signalling pathways that could both decrease immune-mediated demyelination and enhance remyelination. For instance, TGF beta 2 is a potent inhibitor of inflammation but can also promote oligodendrocyte differentiation (McKinnon <italic>et al</italic>., <xref ref-type="bibr" rid="B85">1993</xref>), which may be useful when OPCs have arrived in demyelinating plaques. Unfortunately, TGF beta 2 is also nephrotoxic, but if this toxicity could be suppressed, it may down-regulate the immune response and reduce relapses in MS (discussed by Arnett and Viney, <xref ref-type="bibr" rid="B9">2007</xref>). However, TGFbeta 2 may also down-regulate the promyelinating components of inflammation. This hypothetical double-edged sword highlights the importance of transcriptome/proteome studies to identify the exact pathways that favour myelin repair.</p></sec>
<sec><title>Testing pro-remyelinating therapies</title>
<p>To test potential pro-remyelinating therapies, we need suitable and appropriate animal models, and imaging correlates differentiating demyelination and remyelination.</p>
<p>In spite of the fact that only a small proportion of biologics active in mouse EAE have reached the bed side, those that modulate successfully T-cell activation and their traffic to the brain were first identified in EAE models and proved beneficial to relapsing-remitting MS patients (Arnett and Viney, <xref ref-type="bibr" rid="B9">2007</xref>). This is the case of Nataluzimab, an antibody to alpha 4 integrin, which decreases the number of relapses in relapsing-remitting MS. The anti-CD20 B-cell antibody rituximab, now in phase II clinical trials, has a rapid effect on acute disease activity and also reduces the number of clinical relapses. This antibody effect may result from an inhibition of B-cell antigen presentation to T cells as well as the re-emergence of naïve B cells, leading to a reduction in the number of pathological antibodies (Mc Farland, <xref ref-type="bibr" rid="B84">2008</xref>). The possibility that both of these treatments also promote or facilitate remyelination will have to be explored.</p>
<p>In considering translational aspects of pro-remyelinating strategies, a ‘sensible use’ of animal models is a key factor (Arnett and Viney, <xref ref-type="bibr" rid="B9">2007</xref>). Using animal models of progressive complexity would seem appropriate. For candidate drugs for myelin repair, first compounds could be rapidly screened in a demyelination/remyelination fish model. Then rodent chemical demyelination models would be used. Finally, one could use focal EAE models in rodents for testing the selected candidate molecules.</p></sec>
<sec><title>Inhibitors and promoters of remyelination as targets</title>
<p>Promoters of remyelination and antagonists of myelination inhibitors are extremely interesting as therapeutic targets for MS. During developmental myelination, positive and negative regulators control the timing of myelination (Miller and Mi, <xref ref-type="bibr" rid="B91">2007</xref>). In the adult-diseased CNS, some inhibitory immune mediators may contribute to the demise of oligodendrocytes.</p>
<p><italic>Among developmental regulators of myelination</italic>, at least three may inhibit myelin repair. One is PSA-NCAM which is re-expressed on demyelinated axons in MS while axons in remyelinated plaques do not express PSA (Charles <italic>et al</italic>., <xref ref-type="bibr" rid="B25">2002</xref>), which is consistent with the known down-regulation of axonal PSA preceding myelination. PSA re-emergence could also be related to axonal regrowth. In contrast to axonal PSA, PSA on glial precursors promotes rather than inhibits remyelination by stimulating migration (Zhang <italic>et al</italic>., <xref ref-type="bibr" rid="B152">2004</xref>; Glaser <italic>et al</italic>., <xref ref-type="bibr" rid="B48">2007</xref>). Therefore, inhibiting PSA-NCAM expression could be a double-edged sword.</p>
<p>FGF2 is a strong mitogen for postnatal rodent OPCs. This proliferative effect is later over-ridden by positive regulators of oligodendrocyte differentiation and by FGF receptor switching (reviewed by Rogister <italic>et al</italic>., <xref ref-type="bibr" rid="B109">1999</xref>; Fortin <italic>et al</italic>., <xref ref-type="bibr" rid="B44">2005</xref>). Furthermore siRNA to FGFR1, but not FGFR2 or 3, releases this FGF2-induced block of oligodendrocyte differentiation (Zhou <italic>et al</italic>., <xref ref-type="bibr" rid="B156">2006</xref>). In adult mouse CNS demyelinated by corona virus infection or exposed for a long time to cuprizone, FGF2 increases in the lesions, leading to chronic demyelination whereas FGF2-deficient mouse OPCs repopulate the lesions and remyelinate completely (Armstrong <italic>et al</italic>., <xref ref-type="bibr" rid="B7">2002</xref>, <xref ref-type="bibr" rid="B6">2006</xref>). These results show that deletion of FGF creates a permissive environment for endogenous remyelination. Studies of FGF2 expression and its possible correlation with lack of remyelination of demyelinated lesions in MS are awaited.</p>
<p>Lingo-1 is a protein interacting with the Nogo-receptor complex (Nogo is one of the three or four major components of myelin that inhibit neurite regeneration (reviewed in Schwab <italic>et al</italic>., <xref ref-type="bibr" rid="B115">2006</xref>). Lingo-1 is made by oligodendrocytes and neurons, and inhibits oligodendrocyte differentiation and myelination (Mi <italic>et al</italic>., <xref ref-type="bibr" rid="B89">2005</xref>; Lee <italic>et al</italic>., <xref ref-type="bibr" rid="B75">2007</xref>). This inhibition is reversed by treatment with human soluble Lingo-1-Fc which increases Fyn kinase phosphorylation and myelination. When Lingo-1 antibody was delivered intrathecally by osmotic pump in rats with EAE, it enhanced remyelination and axonal integrity in the spinal cord (Mi <italic>et al</italic>., <xref ref-type="bibr" rid="B88">2007</xref>). If Lingo-1 expression was found to be increased in MS demyelinating lesions, a Lingo-1 antagonist would be a candidate to promote endogenous remyelination (Miller and Mi, <xref ref-type="bibr" rid="B91">2007</xref>).</p>
<p><italic>Among immune mediators</italic>, IFN gamma has long been identified as an inhibitor of recovery/repair. It is present in active MS lesions and, when administered to MS patients, it aggravated clinical signs and this was attributed to an increase in immune activation (Panitch <italic>et al</italic>., <xref ref-type="bibr" rid="B101">1987</xref>). In hindsight, this detrimental effect may have also been due partly to oligodendrocyte death and/or stress as both occur in mice overexpressing this cytokine. Such effects can be attenuated by Stat pathway inhibitors such as the ‘suppressor of cytokine signalling’ (Balabanov <italic>et al</italic>., <xref ref-type="bibr" rid="B12">2006</xref>). The effect of IFN gamma at the lesion site—at concentrations close to those observed <italic>in vivo</italic>—was examined in mice by inducing cytokine release during recovery from EAE or cuprizone treatment (Lin <italic>et al</italic>., <xref ref-type="bibr" rid="B77">2006</xref>). In both models, the induction of IFN gamma synthesis strongly inhibited lesion repopulation by OPCs, remyelination and clinical recovery (in the case of EAE). This was correlated with endoplasmic reticulum stress in remyelinating oligodendrocytes, suggesting that inhibitors of such stress responses may help repair in MS.</p>
<p>Lymphotoxin (Lt) beta receptor (LtBr) expressed on microglia in MS could be activated by its ligand Lt alpha/beta made by astrocytes. Such activation might be detrimental and is also observed during demyelination in the cuprizone model. After stopping the cuprizone diet, repeated intraperitoneal injection of a fusion decoy, LtBr-Ig, dramatically enhanced spontaneous remyelination (Plant <italic>et al</italic>., <xref ref-type="bibr" rid="B106">2007</xref>). Therefore, LtBr-Ig may be another candidate antagonist to enhance myelin repair.</p>
<p>Chondroitin sulfate proteoglycans such as NG2 and proteoglycans with glycosaminoglycan (GAG) chains can often accumulate in lesions and be inhibitory to repair (reviewed in Sherman and Back, <xref ref-type="bibr" rid="B120">2008</xref>). OPC proliferation is inhibited by NG2 whose protein backbone can be degraded by metalloproteases MMP-9 which in turn facilitates remyelination (Larsen <italic>et al</italic>., <xref ref-type="bibr" rid="B70">2003</xref>). The GAG hyaluronan is synthesized at the inner surface of cell membranes and composed of repeating units of glucuronic acid and <italic>N</italic>-acetyl glycosamine. It is made by reactive astrocytes, inhibits oligodendrocyte differentiation <italic>in vitro</italic> and accumulates in chronic lesions in MS and EAE (Back <italic>et al</italic>., <xref ref-type="bibr" rid="B11">2005</xref>). These effects can be reversed by hyaluronidase, providing another avenue to enhance repair.</p>
<p><italic>Among pro-myelinating molecules</italic>, the strongest candidate may be LIF which, as mentioned before, enhances oligodendrocyte survival and myelin repair in different experimental models while it also decreases demyelination (Marriott <italic>et al</italic>., <xref ref-type="bibr" rid="B83">2008</xref>). In addition, OPC promigratory factors such as PDGF, EGF and Semaphorin 3F, discussed above, are promising, also in view of the possible use of synthetic peptides stimulating their downstream signalling pathway. Experimental models should be used to determine whether a local vector delivery or placement of a delivery pump nearby a large demyelinated lesion is a feasible and safe approach. Ongoing studies are also exploring the possible effects on neuroprotection and remyelination of progesterone and thyroid hormone (Schumacher <italic>et al</italic>., <xref ref-type="bibr" rid="B114">2007</xref>; M. Schumacher and S. Ghandour, personal communication).</p>
<p>In the long term, it should become possible to combine neuroprotective and remyelination strategies with the most efficient immunomodulators tailored to each type of MS presentation. Most importantly, appraisal of any clinical trial in this field will rely on the ability to detect the status of the demyelinating lesions by imaging.</p></sec>
</sec>
<sec><title>Imaging remyelination</title>
<p>Before embarking on any clinical trial to promote endogenous remyelination, the functional benefits of remyelination need to be solidly established in primates (including man) and good imaging correlates of remyelination should be available. There are many as yet unanswered questions. How many axons need to be remyelinated to restore function in a particular fibre tract and how tightly is remyelination correlated with clinical recovery? Thus an essential milestone before testing pro-remyelinating therapies in man is to image newly demyelinated axons and endogenous remyelination <italic>in vivo</italic> while measuring its effect on functional recovery.</p>
<p>The most frequently used imaging technology in this regard is currently MRI. Conventional T1 hypointense lesions likely indicate irreversible demyelination and axonal loss while T2 hyperintense lesions may reflect inflammation or persisting damage (reviewed in Neema <italic>et al</italic>., <xref ref-type="bibr" rid="B95">2007</xref>). However both measures lack specificity to assess myelin loss and repair. The use of newer technologies such as magnetisation transfer imaging, myelin water imaging, diffusion tensor imaging, and high field MRI strongly enhance the specificity of myelinated white matter imaging (Zivadinov, <xref ref-type="bibr" rid="B157">2007</xref>).</p>
<p>Magnetisation transfer imaging is based on the interaction and exchange of unbound protons in free water with protons bound to macromolecules such as those present in myelin. A decrease of exchange of these protons occurring in injured CNS structures can result in a decreased magnetization transfer ratio (MTR). A reduced MTR likely reflects loss of myelin whereas an MTR increase may indicate remyelination (Deloire-Grassin <italic>et al</italic>., <xref ref-type="bibr" rid="B32">2000</xref>; Barkhof <italic>et al</italic>., <xref ref-type="bibr" rid="B15">2003</xref>; Chen <italic>et al</italic>., <xref ref-type="bibr" rid="B26">2005</xref>). Importantly, the persistent loss of MTR in lesions is linked with disability and disease modifying treatments may cause an increase in MTR measures (Neema <italic>et al</italic>., <xref ref-type="bibr" rid="B95">2007</xref>). Moreover, in optic neuritis, MTR correlates with function as assayed by visual evoked potential latency and optical coherence tomography, a measure of retinal neuroaxonal loss (Trip <italic>et al</italic>., <xref ref-type="bibr" rid="B132">2007</xref>). The measure of myelin water fraction, which probably corresponds to water trapped within the myelin bilayer, has been shown to correlate with MTR measures on MRI of MS lesions and to luxol fast blue staining of myelin on histopathology (Tozer <italic>et al</italic>., <xref ref-type="bibr" rid="B131">2005</xref>; Laule <italic>et al</italic>., <xref ref-type="bibr" rid="B71">2006</xref>).</p>
<p>Diffusion tensor imaging (DTI), a measure of diffusion of water molecules and anisotropy, has provided details of tissue microstructure and has allowed fibre tractography which reveals brain anatomy in the living (Le Bihan <italic>et al</italic>., <xref ref-type="bibr" rid="B74">2001</xref>; reviewed by Nucifora <italic>et al</italic>., <xref ref-type="bibr" rid="B97">2007</xref>). Studies of animal models indicate that a decrease in water axial diffusivity is associated with axonal degeneration, whereas increased radial diffusivity reflects demyelination in corpus callosum (Song <italic>et al</italic>., <xref ref-type="bibr" rid="B124">2002</xref>, <xref ref-type="bibr" rid="B125">2005</xref>). Accordingly radial diffusivity decreases during remyelination, indicating the importance of applications of DTI to measure repair in man. A DTI-fibre tracking study using 7 Tesla field MRI on marmosets has accurately traced damage in the cortico-spinal tract after spinal cord hemisection (Fujiyoshi <italic>et al</italic>., <xref ref-type="bibr" rid="B46">2007</xref>). Experiments are ongoing to improve this technology in order to visualize regenerating fibres, information also of relevance to MS.</p>
<p>Seven Tesla high-field MRI can be combined with a multi-channel detector of increased sensitivity to reveal the heterogeneity of white matter intensity (Li <italic>et al</italic>., <xref ref-type="bibr" rid="B76">2006</xref>) as well as its relation to vasculature (Bagnato <italic>et al</italic>., <xref ref-type="bibr" rid="B13">2007</xref>). This method produced T2-weighted images with increased spatial resolution, revealing differences between fibre tracts and details of the brain cortical substructure (Duyn <italic>et al</italic>., <xref ref-type="bibr" rid="B38">2007</xref>). Such structural aspects revealed by high-field MRI are presently being analysed in MS patients, and this should allow characterization of myelin changes during different phases of the disease (Bagnato <italic>et al</italic>., <xref ref-type="bibr" rid="B13">2007</xref>).</p>
<p>In addition to these major advances in MRI techniques, it would be useful to develop a molecular imaging technique specific for myelin that would quantify CNS remyelination and further validate the MRI approaches. This could be achieved using positron emission tomography (PET). Of great interest is the recent identification of a newly synthesized fluorescent Congo red derivative, 1,4-<italic>bis</italic>-(<italic>p</italic>-aminostyryl)-2-methoxy benzene), also named BMB, that selectively binds to myelin <italic>ex vivo</italic> and <italic>in vivo</italic> (<xref ref-type="fig" rid="F3">Fig. 3</xref>A; Stankoff <italic>et al</italic>., <xref ref-type="bibr" rid="B128">2006</xref>). This compound allowed the detection of dysmyelination in myelin mutants and of demyelinated lesions in EAE. In MS brain samples, levels of BMB staining can differentiate remyelination in shadow plaques from either demyelinated lesions or normal appearing white matter (<xref ref-type="fig" rid="F3">Fig. 3</xref>B), suggesting that this biomarker could be used to quantify myelin loss and repair. BMB was shown to cross the blood brain barrier and, when radiolabelled with carbon-11, imaging of CNS myelin was obtained by PET in non-human primates (<xref ref-type="fig" rid="F3">Fig. 3</xref>C). Interestingly, a similar affinity for CNS myelin was reported for several other Congo red derivatives (Xiang <italic>et al</italic>., <xref ref-type="bibr" rid="B146">2005</xref>; Wu <italic>et al</italic>., <xref ref-type="bibr" rid="B145">2006</xref>). As Congo red derivatives were previously known to be amyloid markers, these findings suggest the existence of a molecular target common to amyloid plaques and CNS myelin. In favour of this proposal is the observation that other amyloid markers, related to thioflavinT, could also stain myelin and be used as a PET radiotracer for myelin (Stankoff <italic>et al</italic>., unpublished data).
<fig id="F3"><label><bold>Fig. 3</bold></label><caption><p>The Congo Red derivative BMB is a myelin marker on brain sections (<bold>A, B</bold>) and is suitable for PET imaging (<bold>C</bold>). (<bold>A</bold>) When injected into mice intraperitoneally (40 mg/g), BMB crosses the blood brain barrier and stains the cerebellar white matter (green fluorescence, arrows). (<bold>B</bold>) When 1 mM of BMB was incubated <italic>in vitro</italic> on MS brains sections a clear fluorescent staining of the normal appearing white matter (NAWM) was obtained. The demyelinated area (‘Dem’ delineated by dotted line in the upper left corner) was visualized as a lack of staining. In the shadow plaque area (‘Rem’ surrounded by arrowheads), BMB staining is of intermediate intensity between that observed in demyelinated plaques (‘Dem’) and normal appearing white matter (NAWM). <bold>(C</bold>) CNS PET imaging using [11C]-BMB (about 100 MBq) injected intravenously in an anaesthetized baboon. This 110 min PET examination was performed using an ECAT HR+ camera. The axial slice from PET imaging was co-registered with a corresponding slice of the brain MRI scan. <italic>Source:</italic> (<bold>A</bold>) and (<bold>B</bold>) are Figs 4A and 5F reproduced with ‘Copyright (2006) National Academy of Sciences, USA’ (Stankoff <italic>et al</italic>., <xref ref-type="bibr" rid="B128">2006</xref>). Scale bar in (<bold>A</bold>) 300 µm, in (<bold>B)</bold> 150 µm and in (<bold>C</bold>) 12 mm.</p></caption><graphic xlink:href="awn076f3"></graphic></fig></p></sec>
<sec sec-type="conclusions"><title>Conclusion</title>
<p>Where do we go from here? Ideally, the best way to promote remyelination and therefore protect demyelinated axons is to promote efficient endogenous remyelination by native cells rather than surgically introducing exogenous cells. As the advantages and risks of transplantation approaches in MS have been reviewed elsewhere (Lubetzki <italic>et al</italic>., <xref ref-type="bibr" rid="B79">2005</xref>; Zujovic <italic>et al</italic>., <xref ref-type="bibr" rid="B158">2007</xref>; Chandran <italic>et al</italic>., <xref ref-type="bibr" rid="B24">2008</xref>; Scolding and Dubois-Dalcq, in press), we have chosen here to discuss spontaneous remyelination in the CNS because expansion of this field of research might bring promyelinating therapies to the bedside. To do this, we must continue to learn more about the normal repair process in all animal models, including fish. We also must be able to consistently visualise remyelination in living mammals and correlate this to functional recovery, otherwise <italic>in vivo</italic> testing of putative remyelination enhancers will be slow and uncertain. Concomitantly, the postulated impact of remyelination on the clinical course of MS should become measurable with increasingly myelin-specific imaging technologies.</p>
<p>We may be able to learn from research into spinal cord injury, where there is great interplay between damaged axons and myelin-forming cells and where stimulation of remyelination plays an important role in functional recovery (Pearse <italic>et al</italic>., <xref ref-type="bibr" rid="B104">2007</xref>). Promoters of neurite outgrowth may also be important in MS as transected and damaged axons cannot be effectively remyelinated. The characterization of the NOGO receptor complex, its interaction with myelin inhibitors (reviewed by Schwab <italic>et al</italic>., <xref ref-type="bibr" rid="B115">2006</xref>) and the demonstration that intracellular cAMP and its downstream targets may promote axonal regeneration (reviewed by Hannila and Filbin, <xref ref-type="bibr" rid="B52">2008</xref>), have led to new clinical approaches in attempting to treat spinal cord injury (Rossignol <italic>et al</italic>., <xref ref-type="bibr" rid="B110">2007</xref>). If patients with spinal cord injury show motor improvement in clinical trials, it might also be of benefit in some MS patients with acute axonal damage.</p>
<p>Bearing in mind that remyelination was only described in the CNS in 1961 (Bunge <italic>et al</italic>., <xref ref-type="bibr" rid="B19">1961</xref>) and in MS in 1965 (Perier and Gregoire, <xref ref-type="bibr" rid="B105">1965</xref>), we have made great progress, but effective clinical promotion of remyelination is still not quite within our reach. However, as discussed here and before (Lubetzki <italic>et al</italic>., <xref ref-type="bibr" rid="B79">2005</xref>), there are a number of promising avenues being explored that might reach the bedside in the next few years provided that research in basic and clinical science keeps its momentum.</p></sec>
</body>
<back>
<ack><title>Acknowledgements</title>
<p>Monique Dubois-Dalcq thanks the National Institute for Neurological Disorders and Stroke (NINDS) at the National Institutes of Health (Bethesda, MD, USA) for its support. Christine Stadelmann is supported by the Medical Faculty of Goettingen (junior research group), the DFG research centre for molecular physiology of the brain (CMPB), and the DFG collaborative research centre 43.</p>
<p>C. Lubetzki, B. Stankoff and B. Zalc are supported by ‘Institut national de la Santé et de la Recherche Médicale (Inserm)’ and by the ‘Association de Recherche sur la Sclérose en Plaques (ARSEP)’. Bruno Stankoff thanks the CEA (Commissariat à l’énergie atomique) and the European Leukodystrophy Foundation for their support. We thank Heinz Arnheiter and Bruce Appel for their advise and reading of the manuscript. We are grateful to our colleagues whose personal communication of unpublished results is quoted in the text. Last but not least Norio Takada and Bruce Appel (Department of Biological Sciences, Vanderbilt University, Tennessee, USA) kindly provided <xref ref-type="fig" rid="F1">Fig. 1</xref>.</p></ack>
<ref-list><title>References</title>
<ref id="B1"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Aguirre</surname><given-names>AA</given-names></name><name><surname>Chittajallu</surname><given-names>R</given-names></name><name><surname>Belachew</surname><given-names>S</given-names></name><name><surname>Gallo</surname><given-names>V</given-names></name></person-group><article-title>NG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in thepostnatal hippocampus</article-title><source>J Cell Biol</source><year>2004</year><volume>165</volume><fpage>575</fpage><lpage>89</lpage></nlm-citation></ref>
<ref id="B2"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Aguirre</surname><given-names>A</given-names></name><name><surname>Dupree</surname><given-names>JL</given-names></name><name><surname>Mangin</surname><given-names>JM</given-names></name><name><surname>Gallo</surname><given-names>V</given-names></name></person-group><article-title>A functional role for EGFR signaling in myelination and remyelination</article-title><source>Nat Neurosci</source><year>2007</year><volume>10</volume><fpage>990</fpage><lpage>1002</lpage></nlm-citation></ref>
<ref id="B3"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Airas</surname><given-names>L</given-names></name><name><surname>Nikula</surname><given-names>T</given-names></name><name><surname>Huang</surname><given-names>YH</given-names></name><name><surname>Lahesmaa</surname><given-names>R</given-names></name><name><surname>Wiendl</surname><given-names>H</given-names></name></person-group><article-title>Postpartum-activation of multiple sclerosis is associated with down-regulation of tolerogenic HLA-G</article-title><source>J Neuroimmunol</source><year>2007</year><volume>187</volume><fpage>205</fpage><lpage>11</lpage></nlm-citation></ref>
<ref id="B4"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Albert</surname><given-names>M</given-names></name><name><surname>Antel</surname><given-names>J</given-names></name><name><surname>Bruck</surname><given-names>W</given-names></name><name><surname>Stadelmann</surname><given-names>C</given-names></name></person-group><article-title>Extensive cortical remyelination in patients with chronic multiple sclerosis</article-title><source>Brain Pathol</source><year>2007</year><volume>17</volume><fpage>129</fpage><lpage>38</lpage></nlm-citation></ref>
<ref id="B5"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Armstrong</surname><given-names>R</given-names></name><name><surname>Friedrich VL</surname><given-names>Jr</given-names></name><name><surname>Holmes</surname><given-names>KV</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>In vitro analysis of the oligodendrocyte lineage in mice during demyelination and remyelination</article-title><source>J Cell Biol</source><year>1990</year><volume>111</volume><fpage>1183</fpage><lpage>95</lpage></nlm-citation></ref>
<ref id="B6"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Armstrong</surname><given-names>RC</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Flint</surname><given-names>NC</given-names></name><name><surname>Vana</surname><given-names>AC</given-names></name><name><surname>Zhou</surname><given-names>YX</given-names></name></person-group><article-title>Endogenous cell repair of chronic demyelination</article-title><source>J Neuropathol Exp Neurol</source><year>2006</year><volume>65</volume><fpage>245</fpage><lpage>56</lpage></nlm-citation></ref>
<ref id="B7"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Armstrong</surname><given-names>RC</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Frost</surname><given-names>EE</given-names></name><name><surname>Borke</surname><given-names>RC</given-names></name><name><surname>Vana</surname><given-names>AC</given-names></name></person-group><article-title>Absence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matter</article-title><source>J Neurosci</source><year>2002</year><volume>22</volume><fpage>8574</fpage><lpage>85</lpage></nlm-citation></ref>
<ref id="B8"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Arnett</surname><given-names>HA</given-names></name><name><surname>Fancy</surname><given-names>SP</given-names></name><name><surname>Alberta</surname><given-names>JA</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Plant</surname><given-names>SR</given-names></name><name><surname>Kaing</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS</article-title><source>Science</source><year>2004</year><volume>306</volume><fpage>2111</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="B9"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Arnett</surname><given-names>HA</given-names></name><name><surname>Viney</surname><given-names>JL</given-names></name></person-group><article-title>Considerations for the sensible use of rodent models of inflammatory disease in predicting efficacy of new biological therapeutics in the clinic</article-title><source>Adv Drug Deliv Rev</source><year>2007</year><volume>59</volume><fpage>1084</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="B10"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Arnett</surname><given-names>HA</given-names></name><name><surname>Wang</surname><given-names>Y</given-names></name><name><surname>Matsushima</surname><given-names>GK</given-names></name><name><surname>Suzuki</surname><given-names>K</given-names></name><name><surname>Ting</surname><given-names>JP</given-names></name></person-group><article-title>Functional genomic analysis of remyelination reveals importance of inflammation in oligodendrocyte regeneration</article-title><source>J Neurosci</source><year>2003</year><volume>23</volume><fpage>9824</fpage><lpage>32</lpage></nlm-citation></ref>
<ref id="B11"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Back</surname><given-names>SA</given-names></name><name><surname>Tuohy</surname><given-names>TM</given-names></name><name><surname>Chen</surname><given-names>H</given-names></name><name><surname>Wallingford</surname><given-names>N</given-names></name><name><surname>Craig</surname><given-names>A</given-names></name><name><surname>Struve</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation</article-title><source>Nat Med</source><year>2005</year><volume>11</volume><fpage>966</fpage><lpage>72</lpage></nlm-citation></ref>
<ref id="B12"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Balabanov</surname><given-names>R</given-names></name><name><surname>Strand</surname><given-names>K</given-names></name><name><surname>Kemper</surname><given-names>A</given-names></name><name><surname>Lee</surname><given-names>JY</given-names></name><name><surname>Popko</surname><given-names>B</given-names></name></person-group><article-title>Suppressor of cytokine signaling 1 expression protects oligodendrocytes from the deleterious effects of interferon-gamma</article-title><source>J Neurosci</source><year>2006</year><volume>26</volume><fpage>5143</fpage><lpage>52</lpage></nlm-citation></ref>
<ref id="B13"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Bagnato</surname><given-names>F</given-names></name><name><surname>Ikonomidou</surname><given-names>VN</given-names></name><name><surname>van Gelderen</surname><given-names>P</given-names></name><name><surname>Yao</surname><given-names>B</given-names></name><name><surname>Ohayon</surname><given-names>J</given-names></name><name><surname>Fulton</surname><given-names>S</given-names></name><etal></etal></person-group><article-title>7 Tesla magnetic resonance imaging of patients with Multiple Sclerosis: initial experience</article-title><source>Multiple Sclerosis</source><year>2007</year><volume>13</volume><supplement>Suppl 2</supplement><fpage>255</fpage></nlm-citation></ref>
<ref id="B14"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Barbin</surname><given-names>G</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Charles</surname><given-names>P</given-names></name><name><surname>Schachner</surname><given-names>M</given-names></name><name><surname>Grumet</surname><given-names>M</given-names></name><name><surname>Zalc</surname><given-names>B</given-names></name><etal></etal></person-group><article-title>Axonal cell adhesion molecule L1 and central nervous system myelination</article-title><source>Neuron Glia Biol</source><year>2004</year><volume>1</volume><fpage>65</fpage><lpage>72</lpage></nlm-citation></ref>
<ref id="B15"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Barkhof</surname><given-names>F</given-names></name><name><surname>Bruck</surname><given-names>W</given-names></name><name><surname>De Groot</surname><given-names>CJ</given-names></name><name><surname>Bergers</surname><given-names>E</given-names></name><name><surname>Hulshof</surname><given-names>S</given-names></name><name><surname>Geurts</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>Remyelinated lesions in multiple sclerosis: magnetic resonance image appearance</article-title><source>Arch Neurol</source><year>2003</year><volume>60</volume><fpage>1073</fpage><lpage>81</lpage></nlm-citation></ref>
<ref id="B16"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Barres</surname><given-names>BA</given-names></name><name><surname>Raff</surname><given-names>MC</given-names></name></person-group><article-title>Proliferation of oligodendrocyte precursor cells depends on electrical activity in axons</article-title><source>Nature</source><year>1993</year><volume>361</volume><fpage>258</fpage><lpage>60</lpage></nlm-citation></ref>
<ref id="B17"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Black</surname><given-names>JA</given-names></name><name><surname>Waxman</surname><given-names>SG</given-names></name><name><surname>Smith</surname><given-names>KJ</given-names></name></person-group><article-title>Remyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of Ranvier</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>1319</fpage><lpage>29</lpage></nlm-citation></ref>
<ref id="B18"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Blakemore</surname><given-names>WF</given-names></name></person-group><article-title>Remyelination of the superior cerebellar peduncle in the mouse following demyelination induced by feeding cuprizone</article-title><source>J Neurol Sci</source><year>1973</year><volume>20</volume><fpage>73</fpage><lpage>83</lpage></nlm-citation></ref>
<ref id="B19"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Bunge</surname><given-names>MB</given-names></name><name><surname>Bunge</surname><given-names>RP</given-names></name><name><surname>Ris</surname><given-names>H</given-names></name></person-group><article-title>Ultrastructural study of remyelination in an experimental lesion in adult cat spinal cord</article-title><source>J Biophys Biochem Cytol</source><year>1961</year><volume>10</volume><fpage>67</fpage><lpage>94</lpage></nlm-citation></ref>
<ref id="B20"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Butzkueven</surname><given-names>H</given-names></name><name><surname>Emery</surname><given-names>B</given-names></name><name><surname>Cipriani</surname><given-names>T</given-names></name><name><surname>Marriott</surname><given-names>MP</given-names></name><name><surname>Kilpatrick</surname><given-names>TJ</given-names></name></person-group><article-title>Endogenous leukemia inhibitory factor production limits autoimmune demyelination and oligodendrocyte loss</article-title><source>Glia</source><year>2006</year><volume>53</volume><fpage>696</fpage><lpage>703</lpage></nlm-citation></ref>
<ref id="B21"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Butzkueven</surname><given-names>H</given-names></name><name><surname>Zhang</surname><given-names>JG</given-names></name><name><surname>Soilu-Hanninen</surname><given-names>M</given-names></name><name><surname>Hochrein</surname><given-names>H</given-names></name><name><surname>Chionh</surname><given-names>F</given-names></name><name><surname>Shipham</surname><given-names>KA</given-names></name><etal></etal></person-group><article-title>LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival</article-title><source>Nat Med</source><year>2002</year><volume>8</volume><fpage>613</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B22"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Cahoy</surname><given-names>JD</given-names></name><name><surname>Emery</surname><given-names>B</given-names></name><name><surname>Kaushal</surname><given-names>A</given-names></name><name><surname>Foo</surname><given-names>LC</given-names></name><name><surname>Zamanian</surname><given-names>JL</given-names></name><name><surname>Christopherson</surname><given-names>KS</given-names></name><etal></etal></person-group><article-title>A transcriptome database for astrocytes, neurons, and oligodendrocytes: a new resource for understanding brain development and function</article-title><source>J Neurosci</source><year>2008</year><volume>28</volume><fpage>264</fpage><lpage>78</lpage></nlm-citation></ref>
<ref id="B23"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Calderon</surname><given-names>TM</given-names></name><name><surname>Eugenin</surname><given-names>EA</given-names></name><name><surname>Lopez</surname><given-names>L</given-names></name><name><surname>Kumar</surname><given-names>SS</given-names></name><name><surname>Hesselgesser</surname><given-names>J</given-names></name><name><surname>Raine</surname><given-names>CS</given-names></name><etal></etal></person-group><article-title>A role for CXCL12 (SDF-1alpha) in the pathogenesis of multiple sclerosis: regulation of CXCL12 expression in astrocytes by soluble myelin basic protein</article-title><source>J Neuroimmunol</source><year>2006</year><volume>177</volume><fpage>27</fpage><lpage>39</lpage></nlm-citation></ref>
<ref id="B24"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Chandran</surname><given-names>S</given-names></name><name><surname>Hunt</surname><given-names>D</given-names></name><name><surname>Joannides</surname><given-names>A</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Compston</surname><given-names>A</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Myelin repair: the role of stem and precursor cells in multiple sclerosis</article-title><source>Philos Trans R Soc Lond B Biol Sci</source><year>2008</year><volume>363</volume><fpage>171</fpage><lpage>83</lpage></nlm-citation></ref>
<ref id="B25"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Charles</surname><given-names>P</given-names></name><name><surname>Reynolds</surname><given-names>R</given-names></name><name><surname>Seilhean</surname><given-names>D</given-names></name><name><surname>Rougon</surname><given-names>G</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Niezgoda</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Reexpression of PSA-NCAM by demyelinated axons: an inhibitor of remyelination in multiple sclerosis?</article-title><source>Brain</source><year>2002</year><volume>125</volume><fpage>1972</fpage><lpage>79</lpage></nlm-citation></ref>
<ref id="B26"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Chen</surname><given-names>JT</given-names></name><name><surname>Collins</surname><given-names>DL</given-names></name><name><surname>Freedman</surname><given-names>MS</given-names></name><name><surname>Atkins</surname><given-names>HL</given-names></name><name><surname>Arnold</surname><given-names>DL</given-names></name></person-group><article-title>Local magnetization transfer ratio signal inhomogeneity is related to subsequent change in MTR in lesions and normal-appearing white-matter of multiple sclerosis patients</article-title><source>Neuroimage</source><year>2005</year><volume>25</volume><fpage>1272</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="B27"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Colognato</surname><given-names>H</given-names></name><name><surname>Galvin</surname><given-names>J</given-names></name><name><surname>Wang</surname><given-names>Z</given-names></name><name><surname>Relucio</surname><given-names>J</given-names></name><name><surname>Nguyen</surname><given-names>T</given-names></name><name><surname>Harrison</surname><given-names>D</given-names></name><etal></etal></person-group><article-title>Identification of dystroglycan as a second laminin receptor in oligodendrocytes, with a role in myelination</article-title><source>Development</source><year>2007</year><volume>134</volume><fpage>1723</fpage><lpage>36</lpage></nlm-citation></ref>
<ref id="B28"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Coman</surname><given-names>I</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Seilhean</surname><given-names>D</given-names></name><name><surname>Reynolds</surname><given-names>R</given-names></name><name><surname>Girault</surname><given-names>JA</given-names></name><name><surname>Zalc</surname><given-names>B</given-names></name><etal></etal></person-group><article-title>Nodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosis</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>3186</fpage><lpage>95</lpage></nlm-citation></ref>
<ref id="B29"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Coman</surname><given-names>I</given-names></name><name><surname>Barbin</surname><given-names>G</given-names></name><name><surname>Charles</surname><given-names>P</given-names></name><name><surname>Zalc</surname><given-names>B</given-names></name><name><surname>Lubetzki</surname><given-names>C</given-names></name></person-group><article-title>Axonal signals in central nervous system myelination, demyelination and remyelination</article-title><source>J Neurol Sci</source><year>2005</year><volume>233</volume><fpage>67</fpage><lpage>71</lpage></nlm-citation></ref>
<ref id="B30"><nlm-citation citation-type="book"><person-group person-group-type="author"><name><surname>Compston</surname><given-names>A</given-names></name><name><surname>Lassmann</surname><given-names>H</given-names></name><name><surname>Smith</surname><given-names>KJ</given-names></name></person-group><person-group person-group-type="editor"><name><surname>Compston</surname><given-names>A</given-names></name><name><surname>Confravreux</surname><given-names>C</given-names></name><name><surname>Lassmann</surname><given-names>H</given-names></name><name><surname>Mc Donald</surname><given-names>I</given-names></name><name><surname>Miller</surname><given-names>D</given-names></name><name><surname>Noseworthy</surname><given-names>J</given-names></name><etal></etal></person-group><article-title>The neurobiology of remyelination</article-title><source>McAlpine's multiple sclerosis</source><year>2006</year><edition>4th</edition><publisher-name>Churchill Livingstone Elsevier</publisher-name><fpage>449</fpage><lpage>90</lpage></nlm-citation></ref>
<ref id="B31"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Delaunay</surname><given-names>D</given-names></name><name><surname>Heydon</surname><given-names>K</given-names></name><name><surname>Cumano</surname><given-names>A</given-names></name><name><surname>Schwab</surname><given-names>MH</given-names></name><name><surname>Thomas</surname><given-names>JL</given-names></name><name><surname>Suter</surname><given-names>U</given-names></name><etal></etal></person-group><article-title>Early neuronal and glial fate restriction of embryonic neural stem cells</article-title><source>J Neurosci</source><year>2008</year><volume>28</volume><fpage>2551</fpage><lpage>62</lpage></nlm-citation></ref>
<ref id="B32"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Deloire-Grassin</surname><given-names>MS</given-names></name><name><surname>Brochet</surname><given-names>B</given-names></name><name><surname>Quesson</surname><given-names>B</given-names></name><name><surname>Delalande</surname><given-names>C</given-names></name><name><surname>Dousset</surname><given-names>V</given-names></name><name><surname>Canioni</surname><given-names>P</given-names></name><etal></etal></person-group><article-title>In vivo evaluation of remyelination in rat brain by magnetization transfer imaging</article-title><source>J Neurol Sci</source><year>2000</year><volume>178</volume><fpage>10</fpage><lpage>16</lpage></nlm-citation></ref>
<ref id="B33"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Demerens</surname><given-names>C</given-names></name><name><surname>Stankoff</surname><given-names>B</given-names></name><name><surname>Logak</surname><given-names>M</given-names></name><name><surname>Anglade</surname><given-names>P</given-names></name><name><surname>Allinquant</surname><given-names>B</given-names></name><name><surname>Couraud</surname><given-names>F</given-names></name><etal></etal></person-group><article-title>Induction of myelination in the central nervous system by electrical activity</article-title><source>Proc Natl Acad Sci USA</source><year>1996</year><volume>93</volume><fpage>9887</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="B34"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Doetsch</surname><given-names>F</given-names></name><name><surname>Petreanu</surname><given-names>L</given-names></name><name><surname>Caille</surname><given-names>I</given-names></name><name><surname>Garcia-Verdugo</surname><given-names>JM</given-names></name><name><surname>Alvarez-Buylla</surname><given-names>A</given-names></name></person-group><article-title>EGF converts transit-amplifying neurogenic precursors in the adult brain into multipotent stem cells</article-title><source>Neuron</source><year>2002</year><volume>36</volume><fpage>1021</fpage><lpage>34</lpage></nlm-citation></ref>
<ref id="B35"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name><name><surname>Ffrench-Constant</surname><given-names>C</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Enhancing central nervous system remyelination in multiple sclerosis</article-title><source>Neuron</source><year>2005</year><volume>48</volume><fpage>9</fpage><lpage>12</lpage></nlm-citation></ref>
<ref id="B36"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dupree</surname><given-names>JL</given-names></name><name><surname>Mason</surname><given-names>JL</given-names></name><name><surname>Marcus</surname><given-names>JR</given-names></name><name><surname>Stull</surname><given-names>M</given-names></name><name><surname>Levinson</surname><given-names>R</given-names></name><name><surname>Matsushima</surname><given-names>GK</given-names></name><etal></etal></person-group><article-title>Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath</article-title><source>Neuron Glia Biol</source><year>2005</year><volume>1</volume><fpage>1</fpage><lpage>14</lpage></nlm-citation></ref>
<ref id="B37"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dutta</surname><given-names>R</given-names></name><name><surname>McDonough</surname><given-names>J</given-names></name><name><surname>Chang</surname><given-names>A</given-names></name><name><surname>Swamy</surname><given-names>L</given-names></name><name><surname>Siu</surname><given-names>A</given-names></name><name><surname>Kidd</surname><given-names>GJ</given-names></name><etal></etal></person-group><article-title>Activation of the ciliary neurotrophic factor (CNTF) signalling pathway in cortical neurons of multiple sclerosis patients</article-title><source>Brain</source><year>2007</year><volume>130</volume><fpage>2566</fpage><lpage>76</lpage></nlm-citation></ref>
<ref id="B38"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Duyn</surname><given-names>JH</given-names></name><name><surname>van Gelderen</surname><given-names>P</given-names></name><name><surname>Li</surname><given-names>TQ</given-names></name><name><surname>de Zwart</surname><given-names>JA</given-names></name><name><surname>Koretsky</surname><given-names>AP</given-names></name><name><surname>Fukunaga</surname><given-names>M</given-names></name></person-group><article-title>High-field MRI of brain cortical substructure based on signal phase</article-title><source>Proc Natl Acad Sci USA</source><year>2007</year><volume>104</volume><fpage>11796</fpage><lpage>801</lpage></nlm-citation></ref>
<ref id="B39"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Dziembowska</surname><given-names>M</given-names></name><name><surname>Tham</surname><given-names>TN</given-names></name><name><surname>Lau</surname><given-names>P</given-names></name><name><surname>Vitry</surname><given-names>S</given-names></name><name><surname>Lazarini</surname><given-names>F</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>A role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursors</article-title><source>Glia</source><year>2005</year><volume>50</volume><fpage>258</fpage><lpage>69</lpage></nlm-citation></ref>
<ref id="B40"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Eshed</surname><given-names>Y</given-names></name><name><surname>Feinberg</surname><given-names>K</given-names></name><name><surname>Carey</surname><given-names>DJ</given-names></name><name><surname>Peles</surname><given-names>E</given-names></name></person-group><article-title>Secreted gliomedin is a perinodal matrix component of peripheral nerves</article-title><source>J Cell Biol</source><year>2007</year><volume>177</volume><fpage>551</fpage><lpage>62</lpage></nlm-citation></ref>
<ref id="B41"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Fancy</surname><given-names>SP</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Increased expression of Nkx2.2 and Olig2 identifies reactive oligodendrocyte progenitor cells responding to demyelination in the adult CNS</article-title><source>Mol Cell Neurosci</source><year>2004</year><volume>27</volume><fpage>247</fpage><lpage>54</lpage></nlm-citation></ref>
<ref id="B42"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Felts</surname><given-names>PA</given-names></name><name><surname>Smith</surname><given-names>KJ</given-names></name></person-group><article-title>Conduction properties of central nerve fibers remyelinated by Schwann cells</article-title><source>Brain Res</source><year>1992</year><volume>574</volume><fpage>178</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="B43"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Foote</surname><given-names>AK</given-names></name><name><surname>Blakemore</surname><given-names>WF</given-names></name></person-group><article-title>Inflammation stimulates remyelination in areas of chronic demyelination</article-title><source>Brain</source><year>2005</year><volume>128</volume><fpage>528</fpage><lpage>39</lpage></nlm-citation></ref>
<ref id="B44"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Fortin</surname><given-names>D</given-names></name><name><surname>Rom</surname><given-names>E</given-names></name><name><surname>Sun</surname><given-names>H</given-names></name><name><surname>Yayon</surname><given-names>A</given-names></name><name><surname>Bansal</surname><given-names>R</given-names></name></person-group><article-title>Distinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineage</article-title><source>J Neurosci</source><year>2005</year><volume>25</volume><fpage>7470</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B45"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Franklin</surname><given-names>RJ</given-names></name><name><surname>Hinks</surname><given-names>GL</given-names></name></person-group><article-title>Understanding CNS remyelination: clues from developmental and regeneration biology</article-title><source>J Neurosci Res</source><year>1999</year><volume>58</volume><fpage>207</fpage><lpage>13</lpage></nlm-citation></ref>
<ref id="B46"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Fujiyoshi</surname><given-names>K</given-names></name><name><surname>Yamada</surname><given-names>M</given-names></name><name><surname>Nakamura</surname><given-names>M</given-names></name><name><surname>Yamane</surname><given-names>J</given-names></name><name><surname>Katoh</surname><given-names>H</given-names></name><name><surname>Kitamura</surname><given-names>K</given-names></name><etal></etal></person-group><article-title>In vivo tracing of neural tracts in the intact and injured spinal cord of marmosets by diffusion tensor tractography</article-title><source>J Neurosci</source><year>2007</year><volume>27</volume><fpage>11991</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="B47"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Funch</surname><given-names>PG</given-names></name><name><surname>Faber</surname><given-names>DS</given-names></name></person-group><article-title>Measurement of myelin sheath resistances: implications for axonal conduction and pathophysiology</article-title><source>Science</source><year>1984</year><volume>225</volume><fpage>538</fpage><lpage>40</lpage></nlm-citation></ref>
<ref id="B48"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Glaser</surname><given-names>T</given-names></name><name><surname>Brose</surname><given-names>C</given-names></name><name><surname>Franceschini</surname><given-names>I</given-names></name><name><surname>Hamann</surname><given-names>K</given-names></name><name><surname>Smorodchenko</surname><given-names>A</given-names></name><name><surname>Zipp</surname><given-names>F</given-names></name><etal></etal></person-group><article-title>Neural cell adhesion molecule polysialylation enhances the sensitivity of embryonic stem cell-derived neural precursors to migration guidance cues</article-title><source>Stem Cells</source><year>2007</year><volume>25</volume><fpage>3016</fpage><lpage>25</lpage></nlm-citation></ref>
<ref id="B49"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Gold</surname><given-names>R</given-names></name><name><surname>Linington</surname><given-names>C</given-names></name><name><surname>Lassmann</surname><given-names>H</given-names></name></person-group><article-title>Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>1953</fpage><lpage>71</lpage></nlm-citation></ref>
<ref id="B50"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Greenberg</surname><given-names>BM</given-names></name><name><surname>Calabresi</surname><given-names>PA</given-names></name></person-group><article-title>Future research directions in multiple sclerosis therapies</article-title><source>Semin Neurol</source><year>2008</year><volume>28</volume><fpage>121</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B51"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Hall</surname><given-names>SM</given-names></name></person-group><article-title>The effect of injections of lysophosphatidyl choline into white matter of the adult mouse spinal cord</article-title><source>J Cell Sci</source><year>1972</year><volume>10</volume><fpage>535</fpage><lpage>46</lpage></nlm-citation></ref>
<ref id="B52"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Hannila</surname><given-names>SS</given-names></name><name><surname>Filbin</surname><given-names>MT</given-names></name></person-group><article-title>The role of cyclic AMP signaling in promoting axonal regeneration after spinal cord injury</article-title><source>Exp Neurol</source><year>2008</year><volume>299</volume><fpage>321</fpage><lpage>32</lpage></nlm-citation></ref>
<ref id="B53"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Honmou</surname><given-names>O</given-names></name><name><surname>Felts</surname><given-names>PA</given-names></name><name><surname>Waxman</surname><given-names>SG</given-names></name><name><surname>Kocsis</surname><given-names>JD</given-names></name></person-group><article-title>Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells</article-title><source>J Neurosci</source><year>1996</year><volume>16</volume><fpage>3199</fpage><lpage>208</lpage></nlm-citation></ref>
<ref id="B54"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Howell</surname><given-names>OW</given-names></name><name><surname>Palser</surname><given-names>A</given-names></name><name><surname>Polito</surname><given-names>A</given-names></name><name><surname>Melrose</surname><given-names>S</given-names></name><name><surname>Zonta</surname><given-names>B</given-names></name><name><surname>Scheiermann</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Disruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosis</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>3173</fpage><lpage>85</lpage></nlm-citation></ref>
<ref id="B55"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Hu</surname><given-names>X</given-names></name><name><surname>Hicks</surname><given-names>CW</given-names></name><name><surname>He</surname><given-names>W</given-names></name><name><surname>Wong</surname><given-names>P</given-names></name><name><surname>Macklin</surname><given-names>WB</given-names></name><name><surname>Trapp</surname><given-names>BD</given-names></name><etal></etal></person-group><article-title>Bace1 modulates myelination in the central and peripheral nervous system</article-title><source>Nat Neurosci</source><year>2006</year><volume>9</volume><fpage>1520</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="B56"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Ishibashi</surname><given-names>T</given-names></name><name><surname>Dakin</surname><given-names>KA</given-names></name><name><surname>Stevens</surname><given-names>B</given-names></name><name><surname>Lee</surname><given-names>PR</given-names></name><name><surname>Kozlov</surname><given-names>SV</given-names></name><name><surname>Stewart</surname><given-names>CL</given-names></name><etal></etal></person-group><article-title>Astrocytes promote myelination in response to electrical impulses</article-title><source>Neuron</source><year>2006</year><volume>49</volume><fpage>823</fpage><lpage>32</lpage></nlm-citation></ref>
<ref id="B57"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kaplan</surname><given-names>MR</given-names></name><name><surname>Cho</surname><given-names>MH</given-names></name><name><surname>Ullian</surname><given-names>EM</given-names></name><name><surname>Isom</surname><given-names>LL</given-names></name><name><surname>Levinson</surname><given-names>SR</given-names></name><name><surname>Barres</surname><given-names>BA</given-names></name></person-group><article-title>Differential control of clustering of the sodium channels Na(v)1.2 and Na(v)1.6 at developing CNS nodes of Ranvier</article-title><source>Neuron</source><year>2001</year><volume>30</volume><fpage>105</fpage><lpage>19</lpage></nlm-citation></ref>
<ref id="B58"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kaplan</surname><given-names>MR</given-names></name><name><surname>Meyer-Franke</surname><given-names>A</given-names></name><name><surname>Lambert</surname><given-names>S</given-names></name><name><surname>Bennett</surname><given-names>V</given-names></name><name><surname>Duncan</surname><given-names>ID</given-names></name><name><surname>Levinson</surname><given-names>SR</given-names></name><name><surname>Barres</surname><given-names>BA</given-names></name></person-group><article-title>Induction of sodium channel clustering by oligodendrocytes</article-title><source>Nature</source><year>1997</year><volume>386</volume><fpage>724</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="B59"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Karadottir</surname><given-names>R</given-names></name><name><surname>Attwell</surname><given-names>D</given-names></name></person-group><article-title>Neurotransmitter receptors in the life and death of oligodendrocytes</article-title><source>Neuroscience</source><year>2007</year><volume>145</volume><fpage>1426</fpage><lpage>38</lpage></nlm-citation></ref>
<ref id="B60"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kazakova</surname><given-names>N</given-names></name><name><surname>Li</surname><given-names>H</given-names></name><name><surname>Mora</surname><given-names>A</given-names></name><name><surname>Jessen</surname><given-names>KR</given-names></name><name><surname>Mirsky</surname><given-names>R</given-names></name><name><surname>Richardson</surname><given-names>WD</given-names></name><etal></etal></person-group><article-title>A screen for mutations in zebrafish that affect myelin gene expression in Schwann cells and oligodendrocytes</article-title><source>Dev Biol</source><year>2006</year><volume>297</volume><fpage>1</fpage><lpage>13</lpage></nlm-citation></ref>
<ref id="B61"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kerschensteiner</surname><given-names>M</given-names></name><name><surname>Stadelmann</surname><given-names>C</given-names></name><name><surname>Buddeberg</surname><given-names>BS</given-names></name><name><surname>Merkler</surname><given-names>D</given-names></name><name><surname>Bareyre</surname><given-names>FM</given-names></name><name><surname>Anthony</surname><given-names>DC</given-names></name><etal></etal></person-group><article-title>Targeting experimental autoimmune encephalomyelitis lesions to a predetermined axonal tract system allows for refined behavioral testing in an animal model of multiple sclerosis</article-title><source>Am J Pathol</source><year>2004</year><volume>164</volume><fpage>1455</fpage><lpage>69</lpage></nlm-citation></ref>
<ref id="B62"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kirby</surname><given-names>BB</given-names></name><name><surname>Takada</surname><given-names>N</given-names></name><name><surname>Latimer</surname><given-names>AJ</given-names></name><name><surname>Shin</surname><given-names>J</given-names></name><name><surname>Carney</surname><given-names>TJ</given-names></name><name><surname>Kelsh</surname><given-names>RN</given-names></name><etal></etal></person-group><article-title>In vivo time-lapse imaging shows dynamic oligodendrocyte progenitor behavior during zebrafish development</article-title><source>Nat Neurosci</source><year>2006</year><volume>9</volume><fpage>1506</fpage><lpage>11</lpage></nlm-citation></ref>
<ref id="B63"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Klein</surname><given-names>C</given-names></name><name><surname>Kramer</surname><given-names>EM</given-names></name><name><surname>Cardine</surname><given-names>AM</given-names></name><name><surname>Schraven</surname><given-names>B</given-names></name><name><surname>Brandt</surname><given-names>R</given-names></name><name><surname>Trotter</surname><given-names>J</given-names></name></person-group><article-title>Process outgrowth of oligodendrocytes is promoted by interaction of fyn kinase with the cytoskeletal protein tau</article-title><source>J Neurosci</source><year>2002</year><volume>22</volume><fpage>698</fpage><lpage>707</lpage></nlm-citation></ref>
<ref id="B64"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kohwi</surname><given-names>M</given-names></name><name><surname>Petryniak</surname><given-names>MA</given-names></name><name><surname>Long</surname><given-names>JE</given-names></name><name><surname>Ekker</surname><given-names>M</given-names></name><name><surname>Obata</surname><given-names>K</given-names></name><name><surname>Yanagawa</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>A subpopulation of olfactory bulb GABAergic interneurons is derived from Emx1- and Dlx5/6-expressing progenitors</article-title><source>J Neurosci</source><year>2007</year><volume>27</volume><fpage>6878</fpage><lpage>91</lpage></nlm-citation></ref>
<ref id="B65"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kotter</surname><given-names>MR</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>van Rooijen</surname><given-names>N</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Macrophage-depletion induced impairment of experimental CNS remyelination is associated with a reduced oligodendrocyte progenitor cell response and altered growth factor expression</article-title><source>Neurobiol Dis</source><year>2005</year><volume>18</volume><fpage>166</fpage><lpage>75</lpage></nlm-citation></ref>
<ref id="B66"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kovacs</surname><given-names>GG</given-names></name><name><surname>Laszlo</surname><given-names>L</given-names></name><name><surname>Kovacs</surname><given-names>J</given-names></name><name><surname>Jensen</surname><given-names>PH</given-names></name><name><surname>Lindersson</surname><given-names>E</given-names></name><name><surname>Botond</surname><given-names>G</given-names></name><etal></etal></person-group><article-title>Natively unfolded tubulin polymerization promoting protein TPPP/p25 is a common marker of alpha-synucleinopathies</article-title><source>Neurobiol Dis</source><year>2004</year><volume>17</volume><fpage>155</fpage><lpage>62</lpage></nlm-citation></ref>
<ref id="B67"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kristensson</surname><given-names>K</given-names></name><name><surname>Holmes</surname><given-names>KV</given-names></name><name><surname>Duchala</surname><given-names>CS</given-names></name><name><surname>Zeller</surname><given-names>NK</given-names></name><name><surname>Lazzarini</surname><given-names>RA</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>Increased levels of myelin basic protein transcripts in virus-induced demyelination</article-title><source>Nature</source><year>1986</year><volume>322</volume><fpage>544</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B68"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Krumbholz</surname><given-names>M</given-names></name><name><surname>Theil</surname><given-names>D</given-names></name><name><surname>Cepok</surname><given-names>S</given-names></name><name><surname>Hemmer</surname><given-names>B</given-names></name><name><surname>Kivisakk</surname><given-names>P</given-names></name><name><surname>Ransohoff</surname><given-names>RM</given-names></name><etal></etal></person-group><article-title>Chemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitment</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>200</fpage><lpage>11</lpage></nlm-citation></ref>
<ref id="B69"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Kukley</surname><given-names>M</given-names></name><name><surname>Capetillo-Zarate</surname><given-names>E</given-names></name><name><surname>Dietrich</surname><given-names>D</given-names></name></person-group><article-title>Vesicular glutamate release from axons in white matter</article-title><source>Nat Neurosci</source><year>2007</year><volume>10</volume><fpage>311</fpage><lpage>20</lpage></nlm-citation></ref>
<ref id="B70"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Larsen</surname><given-names>PH</given-names></name><name><surname>Wells</surname><given-names>JE</given-names></name><name><surname>Stallcup</surname><given-names>WB</given-names></name><name><surname>Opdenakker</surname><given-names>G</given-names></name><name><surname>Yong</surname><given-names>VW</given-names></name></person-group><article-title>Matrix metalloproteinase-9 facilitates remyelination in part by processing the inhibitory NG2 proteoglycan</article-title><source>J Neurosci</source><year>2003</year><volume>23</volume><fpage>11127</fpage><lpage>35</lpage></nlm-citation></ref>
<ref id="B71"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Laule</surname><given-names>C</given-names></name><name><surname>Leung</surname><given-names>E</given-names></name><name><surname>Lis</surname><given-names>DK</given-names></name><name><surname>Traboulsee</surname><given-names>AL</given-names></name><name><surname>Paty</surname><given-names>DW</given-names></name><name><surname>MacKay</surname><given-names>AL</given-names></name><etal></etal></person-group><article-title>Myelin water imaging in multiple sclerosis: quantitative correlations with histopathology</article-title><source>Mult Scler</source><year>2006</year><volume>12</volume><fpage>747</fpage><lpage>53</lpage></nlm-citation></ref>
<ref id="B72"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lavdas</surname><given-names>AA</given-names></name><name><surname>Franceschini</surname><given-names>I</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name><name><surname>Matsas</surname><given-names>R</given-names></name></person-group><article-title>Schwann cells genetically engineered to express PSA show enhanced migratory potential without impairment of their myelinating ability in vitro</article-title><source>Glia</source><year>2006</year><volume>53</volume><fpage>868</fpage><lpage>78</lpage></nlm-citation></ref>
<ref id="B73"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lazarini</surname><given-names>F</given-names></name><name><surname>Tham</surname><given-names>TN</given-names></name><name><surname>Casanova</surname><given-names>P</given-names></name><name><surname>Arenzana-Seisdedos</surname><given-names>F</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>Role of the alpha-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous system</article-title><source>Glia</source><year>2003</year><volume>42</volume><fpage>139</fpage><lpage>48</lpage></nlm-citation></ref>
<ref id="B74"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Le Bihan</surname><given-names>D</given-names></name><name><surname>Mangin</surname><given-names>JF</given-names></name><name><surname>Poupon</surname><given-names>C</given-names></name><name><surname>Clark</surname><given-names>CA</given-names></name><name><surname>Pappata</surname><given-names>S</given-names></name><name><surname>Molko</surname><given-names>N</given-names></name><etal></etal></person-group><article-title>Diffusion tensor imaging: concepts and applications</article-title><source>J Magn Reson Imaging</source><year>2001</year><volume>13</volume><fpage>534</fpage><lpage>46</lpage></nlm-citation></ref>
<ref id="B75"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lee</surname><given-names>X</given-names></name><name><surname>Yang</surname><given-names>Z</given-names></name><name><surname>Shao</surname><given-names>Z</given-names></name><name><surname>Rosenberg</surname><given-names>SS</given-names></name><name><surname>Levesque</surname><given-names>M</given-names></name><name><surname>Pepinsky</surname><given-names>RB</given-names></name><etal></etal></person-group><article-title>NGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelination</article-title><source>J Neurosci</source><year>2007</year><volume>27</volume><fpage>220</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="B76"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Li</surname><given-names>TQ</given-names></name><name><surname>van Gelderen</surname><given-names>P</given-names></name><name><surname>Merkle</surname><given-names>H</given-names></name><name><surname>Talagala</surname><given-names>L</given-names></name><name><surname>Koretsky</surname><given-names>AP</given-names></name><name><surname>Duyn</surname><given-names>J</given-names></name></person-group><article-title>Extensive heterogeneity in white matter intensity in high-resolution T2*-weighted MRI of the human brain at 7.0 T</article-title><source>Neuroimage</source><year>2006</year><volume>32</volume><fpage>1032</fpage><lpage>40</lpage></nlm-citation></ref>
<ref id="B77"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lin</surname><given-names>W</given-names></name><name><surname>Kemper</surname><given-names>A</given-names></name><name><surname>Dupree</surname><given-names>JL</given-names></name><name><surname>Harding</surname><given-names>HP</given-names></name><name><surname>Ron</surname><given-names>D</given-names></name><name><surname>Popko</surname><given-names>B</given-names></name></person-group><article-title>Interferon-gamma inhibits central nervous system remyelination through a process modulated by endoplasmic reticulum stress</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>1306</fpage><lpage>18</lpage></nlm-citation></ref>
<ref id="B78"><nlm-citation citation-type="book"><person-group person-group-type="author"><name><surname>Lubetzki</surname><given-names>C</given-names></name><name><surname>Zalc</surname><given-names>B</given-names></name></person-group><person-group person-group-type="editor"><name><surname>Filippi</surname><given-names>M</given-names></name><name><surname>Arnold</surname><given-names>DL</given-names></name></person-group><article-title>Axonal signals and central nervous system myelination</article-title><source>Magnetic resonance spectroscopy in multiple sclerosis</source><year>2001</year><publisher-loc>Heidelberg, New York, London</publisher-loc><publisher-name>Springer Verlag</publisher-name><fpage>5</fpage><lpage>14</lpage></nlm-citation></ref>
<ref id="B79"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Lubetzki</surname><given-names>C</given-names></name><name><surname>Williams</surname><given-names>A</given-names></name><name><surname>Stankoff</surname><given-names>B</given-names></name></person-group><article-title>Promoting repair in multiple sclerosis: problems and prospects</article-title><source>Curr Opin Neurol</source><year>2005</year><volume>18</volume><fpage>237</fpage><lpage>44</lpage></nlm-citation></ref>
<ref id="B80"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Ludwin</surname><given-names>SK</given-names></name></person-group><article-title>Central nervous system demyelination and remyelination in the mouse: an ultrastructural study of cuprizone toxicity</article-title><source>Lab Invest</source><year>1978</year><volume>39</volume><fpage>597</fpage><lpage>612</lpage></nlm-citation></ref>
<ref id="B81"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Maertens</surname><given-names>B</given-names></name><name><surname>Hopkins</surname><given-names>D</given-names></name><name><surname>Franzke</surname><given-names>CW</given-names></name><name><surname>Keene</surname><given-names>DR</given-names></name><name><surname>Bruckner-Tuderman</surname><given-names>L</given-names></name><name><surname>Greenspan</surname><given-names>DS</given-names></name><etal></etal></person-group><article-title>Cleavage and oligomerization of gliomedin, a transmembrane collagen required for node of ranvier formation</article-title><source>J Biol Chem</source><year>2007</year><volume>282</volume><fpage>10647</fpage><lpage>59</lpage></nlm-citation></ref>
<ref id="B82"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Magliozzi</surname><given-names>R</given-names></name><name><surname>Howell</surname><given-names>O</given-names></name><name><surname>Vora</surname><given-names>A</given-names></name><name><surname>Serafini</surname><given-names>B</given-names></name><name><surname>Nicholas</surname><given-names>R</given-names></name><name><surname>Puopolo</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology</article-title><source>Brain</source><year>2007</year><volume>130</volume><fpage>1089</fpage><lpage>104</lpage></nlm-citation></ref>
<ref id="B83"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Marriott</surname><given-names>MP</given-names></name><name><surname>Emery</surname><given-names>B</given-names></name><name><surname>Cate</surname><given-names>HS</given-names></name><name><surname>Binder</surname><given-names>MD</given-names></name><name><surname>Kemper</surname><given-names>D</given-names></name><name><surname>Wu</surname><given-names>Q</given-names></name><etal></etal></person-group><article-title>Leukemia inhibitory factor signaling modulates both central nervous system demyelination and myelin repair</article-title><source>Glia</source><year>2008</year><volume>56</volume><fpage>686</fpage><lpage>98</lpage></nlm-citation></ref>
<ref id="B84"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Mc Farland</surname><given-names>HF</given-names></name></person-group><article-title>The B cell∼Old player, New position on the team</article-title><source>New Engl J Med</source><year>2008</year><volume>358</volume><fpage>664</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="B85"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>McKinnon</surname><given-names>RD</given-names></name><name><surname>Piras</surname><given-names>G</given-names></name><name><surname>Ida JA</surname><given-names>Jr</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>A role for TGF-beta in oligodendrocyte differentiation</article-title><source>J Cell Biol</source><year>1993</year><volume>121</volume><fpage>1397</fpage><lpage>407</lpage></nlm-citation></ref>
<ref id="B86"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Menn</surname><given-names>B</given-names></name><name><surname>Garcia-Verdugo</surname><given-names>JM</given-names></name><name><surname>Yaschine</surname><given-names>C</given-names></name><name><surname>Gonzalez-Perez</surname><given-names>O</given-names></name><name><surname>Rowitch</surname><given-names>D</given-names></name><name><surname>Alvarez-Buylla</surname><given-names>A</given-names></name></person-group><article-title>Origin of oligodendrocytes in the subventricular zone of the adult brain</article-title><source>J Neurosci</source><year>2006</year><volume>26</volume><fpage>7907</fpage><lpage>18</lpage></nlm-citation></ref>
<ref id="B87"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Merkler</surname><given-names>D</given-names></name><name><surname>Ernsting</surname><given-names>T</given-names></name><name><surname>Kerschensteiner</surname><given-names>M</given-names></name><name><surname>Bruck</surname><given-names>W</given-names></name><name><surname>Stadelmann</surname><given-names>C</given-names></name></person-group><article-title>A new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelination</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>1972</fpage><lpage>83</lpage></nlm-citation></ref>
<ref id="B88"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Mi</surname><given-names>S</given-names></name><name><surname>Hu</surname><given-names>B</given-names></name><name><surname>Hahm</surname><given-names>K</given-names></name><name><surname>Luo</surname><given-names>Y</given-names></name><name><surname>Kam Hui</surname><given-names>ES</given-names></name><name><surname>Yuan</surname><given-names>Q</given-names></name><etal></etal></person-group><article-title>LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis</article-title><source>Nat Med</source><year>2007</year><volume>13</volume><fpage>1228</fpage><lpage>33</lpage></nlm-citation></ref>
<ref id="B89"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Mi</surname><given-names>S</given-names></name><name><surname>Miller</surname><given-names>RH</given-names></name><name><surname>Lee</surname><given-names>X</given-names></name><name><surname>Scott</surname><given-names>ML</given-names></name><name><surname>Shulag-Morskaya</surname><given-names>S</given-names></name><name><surname>Shao</surname><given-names>Z</given-names></name><etal></etal></person-group><article-title>LINGO-1 negatively regulates myelination by oligodendrocytes</article-title><source>Nat Neurosci</source><year>2005</year><volume>8</volume><fpage>745</fpage><lpage>51</lpage></nlm-citation></ref>
<ref id="B90"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Michailov</surname><given-names>GV</given-names></name><name><surname>Sereda</surname><given-names>MW</given-names></name><name><surname>Brinkmann</surname><given-names>BG</given-names></name><name><surname>Fischer</surname><given-names>TM</given-names></name><name><surname>Haug</surname><given-names>B</given-names></name><name><surname>Birchmeier</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Axonal neuregulin-1 regulates myelin sheath thickness</article-title><source>Science</source><year>2004</year><volume>304</volume><fpage>700</fpage><lpage>3</lpage></nlm-citation></ref>
<ref id="B91"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Miller</surname><given-names>RH</given-names></name><name><surname>Mi</surname><given-names>S</given-names></name></person-group><article-title>Dissecting demyelination</article-title><source>Nat Neurosci</source><year>2007</year><volume>10</volume><fpage>1351</fpage><lpage>4</lpage></nlm-citation></ref>
<ref id="B92"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Murray</surname><given-names>M</given-names></name></person-group><article-title>Regeneration of retinal axons into the goldfish optic tectum</article-title><source>J Comp Neurol</source><year>1976</year><volume>168</volume><fpage>175</fpage><lpage>95</lpage></nlm-citation></ref>
<ref id="B93"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Nait-Oumesmar</surname><given-names>B</given-names></name><name><surname>Picard-Riera</surname><given-names>N</given-names></name><name><surname>Kerninon</surname><given-names>C</given-names></name><name><surname>Decker</surname><given-names>L</given-names></name><name><surname>Seilhean</surname><given-names>D</given-names></name><name><surname>Hoglinger</surname><given-names>GU</given-names></name><etal></etal></person-group><article-title>Activation of the subventricular zone in multiple sclerosis: evidence for early glial progenitors</article-title><source>Proc Natl Acad Sci USA</source><year>2007</year><volume>104</volume><fpage>4694</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B94"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Nave</surname><given-names>KA</given-names></name><name><surname>Salzer</surname><given-names>JL</given-names></name></person-group><article-title>Axonal regulation of myelination by neuregulin 1</article-title><source>Curr Opin Neurobiol</source><year>2006</year><volume>16</volume><fpage>492</fpage><lpage>500</lpage></nlm-citation></ref>
<ref id="B95"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Neema</surname><given-names>M</given-names></name><name><surname>Stankiewicz</surname><given-names>J</given-names></name><name><surname>Arora</surname><given-names>A</given-names></name><name><surname>Guss</surname><given-names>ZD</given-names></name><name><surname>Bakshi</surname><given-names>R</given-names></name></person-group><article-title>MRI in multiple sclerosis: what's inside the toolbox?</article-title><source>Neurotherapeutics</source><year>2007</year><volume>4</volume><fpage>602</fpage><lpage>17</lpage></nlm-citation></ref>
<ref id="B96"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Nona</surname><given-names>SN</given-names></name><name><surname>Thomlinson</surname><given-names>AM</given-names></name><name><surname>Bartlett</surname><given-names>CA</given-names></name><name><surname>Scholes</surname><given-names>J</given-names></name></person-group><article-title>Schwann cells in the regenerating fish optic nerve: evidence that CNS axons, not the glia, determine when myelin formation begins</article-title><source>J Neurocytol</source><year>2000</year><volume>29</volume><fpage>285</fpage><lpage>300</lpage></nlm-citation></ref>
<ref id="B97"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Nucifora</surname><given-names>PG</given-names></name><name><surname>Verma</surname><given-names>R</given-names></name><name><surname>Lee</surname><given-names>SK</given-names></name><name><surname>Melhem</surname><given-names>ER</given-names></name></person-group><article-title>Diffusion-tensor MR imaging and tractography: exploring brain microstructure and connectivity</article-title><source>Radiology</source><year>2007</year><volume>245</volume><fpage>367</fpage><lpage>84</lpage></nlm-citation></ref>
<ref id="B98"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Nunes</surname><given-names>MC</given-names></name><name><surname>Roy</surname><given-names>NS</given-names></name><name><surname>Keyoung</surname><given-names>HM</given-names></name><name><surname>Goodman</surname><given-names>RR</given-names></name><name><surname>McKhann</surname><given-names>G</given-names><suffix>II</suffix></name><name><surname>Jiang</surname><given-names>L</given-names></name><etal></etal></person-group><article-title>Identification and isolation of multipotential neural progenitor cells from the subcortical white matter of the adult human brain</article-title><source>Nat Med</source><year>2003</year><volume>9</volume><fpage>439</fpage><lpage>47</lpage></nlm-citation></ref>
<ref id="B99"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Omari</surname><given-names>KM</given-names></name><name><surname>John</surname><given-names>GR</given-names></name><name><surname>Sealfon</surname><given-names>SC</given-names></name><name><surname>Raine</surname><given-names>CS</given-names></name></person-group><article-title>CXC chemokine receptors on human oligodendrocytes: implications for multiple sclerosis</article-title><source>Brain</source><year>2005</year><volume>128</volume><fpage>1003</fpage><lpage>15</lpage></nlm-citation></ref>
<ref id="B100"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Padovani-Claudio</surname><given-names>DA</given-names></name><name><surname>Liu</surname><given-names>L</given-names></name><name><surname>Ransohoff</surname><given-names>RM</given-names></name><name><surname>Miller</surname><given-names>RH</given-names></name></person-group><article-title>Alterations in the oligodendrocyte lineage, myelin, and white matter in adult mice lacking the chemokine receptor CXCR2</article-title><source>Glia</source><year>2006</year><volume>54</volume><fpage>471</fpage><lpage>83</lpage></nlm-citation></ref>
<ref id="B101"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Panitch</surname><given-names>HS</given-names></name><name><surname>Hirsch</surname><given-names>RL</given-names></name><name><surname>Haley</surname><given-names>AS</given-names></name><name><surname>Johnson</surname><given-names>KP</given-names></name></person-group><article-title>Exacerbations of multiple sclerosis in patients treated with gamma interferon</article-title><source>Lancet</source><year>1987</year><volume>1</volume><fpage>893</fpage><lpage>5</lpage></nlm-citation></ref>
<ref id="B102"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Patani</surname><given-names>R</given-names></name><name><surname>Balaratnam</surname><given-names>M</given-names></name><name><surname>Vora</surname><given-names>A</given-names></name><name><surname>Reynolds</surname><given-names>R</given-names></name></person-group><article-title>Remyelination can be extensive in multiple sclerosis despite a long disease course</article-title><source>Neuropathol Appl Neurobiol</source><year>2007</year><volume>33</volume><fpage>277</fpage><lpage>87</lpage></nlm-citation></ref>
<ref id="B103"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Patrikios</surname><given-names>P</given-names></name><name><surname>Stadelmann</surname><given-names>C</given-names></name><name><surname>Kutzelnigg</surname><given-names>A</given-names></name><name><surname>Rauschka</surname><given-names>H</given-names></name><name><surname>Schmidbauer</surname><given-names>M</given-names></name><name><surname>Laursen</surname><given-names>H</given-names></name><etal></etal></person-group><article-title>Remyelination is extensive in a subset of multiple sclerosis patients</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>3165</fpage><lpage>72</lpage></nlm-citation></ref>
<ref id="B104"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Pearse</surname><given-names>DD</given-names></name><name><surname>Sanchez</surname><given-names>AR</given-names></name><name><surname>Pereira</surname><given-names>FC</given-names></name><name><surname>Andrade</surname><given-names>CM</given-names></name><name><surname>Puzis</surname><given-names>R</given-names></name><name><surname>Pressman</surname><given-names>Y</given-names></name><etal></etal></person-group><article-title>Transplantation of Schwann cells and/or olfactory ensheathing glia into the contused spinal cord: survival, migration, axon association, and functional recovery</article-title><source>Glia</source><year>2007</year><volume>55</volume><fpage>976</fpage><lpage>1000</lpage></nlm-citation></ref>
<ref id="B105"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Perier</surname><given-names>O</given-names></name><name><surname>Gregoire</surname><given-names>A</given-names></name></person-group><article-title>Electron microscopic features of multiple sclerosis lesions</article-title><source>Brain</source><year>1965</year><volume>88</volume><fpage>937</fpage><lpage>52</lpage></nlm-citation></ref>
<ref id="B106"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Plant</surname><given-names>SR</given-names></name><name><surname>Iocca</surname><given-names>HA</given-names></name><name><surname>Wang</surname><given-names>Y</given-names></name><name><surname>Thrash</surname><given-names>JC</given-names></name><name><surname>O’Connor</surname><given-names>BP</given-names></name><name><surname>Arnett</surname><given-names>HA</given-names></name><etal></etal></person-group><article-title>Lymphotoxin beta receptor (Lt betaR): dual roles in demyelination and remyelination and successful therapeutic intervention using Lt betaR-Ig protein</article-title><source>J Neurosci</source><year>2007</year><volume>27</volume><fpage>7429</fpage><lpage>37</lpage></nlm-citation></ref>
<ref id="B107"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Pogoda</surname><given-names>HM</given-names></name><name><surname>Sternheim</surname><given-names>N</given-names></name><name><surname>Lyons</surname><given-names>DA</given-names></name><name><surname>Diamond</surname><given-names>B</given-names></name><name><surname>Hawkins</surname><given-names>TA</given-names></name><name><surname>Woods</surname><given-names>IG</given-names></name><etal></etal></person-group><article-title>A genetic screen identifies genes essential for development of myelinated axons in zebrafish</article-title><source>Dev Biol</source><year>2006</year><volume>298</volume><fpage>118</fpage><lpage>31</lpage></nlm-citation></ref>
<ref id="B108"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Rodriguez</surname><given-names>M</given-names></name></person-group><article-title>Effectors of demyelination and remyelination in the CNS: implications for multiple sclerosis</article-title><source>Brain Pathol</source><year>2007</year><volume>17</volume><fpage>219</fpage><lpage>29</lpage></nlm-citation></ref>
<ref id="B109"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Rogister</surname><given-names>B</given-names></name><name><surname>Ben-Hur</surname><given-names>T</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><article-title>From neural stem cells to myelinating oligodendrocytes</article-title><source>Mol Cell Neurosci</source><year>1999</year><volume>14</volume><fpage>287</fpage><lpage>300</lpage></nlm-citation></ref>
<ref id="B110"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Rossignol</surname><given-names>S</given-names></name><name><surname>Schwab</surname><given-names>M</given-names></name><name><surname>Schwartz</surname><given-names>M</given-names></name><name><surname>Fehlings</surname><given-names>MG</given-names></name></person-group><article-title>Spinal cord injury: time to move?</article-title><source>J Neurosci</source><year>2007</year><volume>27</volume><fpage>11782</fpage><lpage>92</lpage></nlm-citation></ref>
<ref id="B111"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sarchielli</surname><given-names>P</given-names></name><name><surname>Zaffaroni</surname><given-names>M</given-names></name><name><surname>Floridi</surname><given-names>A</given-names></name><name><surname>Greco</surname><given-names>L</given-names></name><name><surname>Candeliere</surname><given-names>A</given-names></name><name><surname>Mattioni</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins</article-title><source>Mult Scler</source><year>2007</year><volume>13</volume><fpage>313</fpage><lpage>31</lpage></nlm-citation></ref>
<ref id="B112"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sasaki</surname><given-names>M</given-names></name><name><surname>Black</surname><given-names>JA</given-names></name><name><surname>Lankford</surname><given-names>KL</given-names></name><name><surname>Tokuno</surname><given-names>HA</given-names></name><name><surname>Waxman</surname><given-names>SG</given-names></name><name><surname>Kocsis</surname><given-names>JD</given-names></name></person-group><article-title>Molecular reconstruction of nodes of Ranvier after remyelination by transplanted olfactory ensheathing cells in the demyelinated spinal cord</article-title><source>J Neurosci</source><year>2006</year><volume>26</volume><fpage>1803</fpage><lpage>12</lpage></nlm-citation></ref>
<ref id="B113"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Schafer</surname><given-names>DP</given-names></name><name><surname>Custer</surname><given-names>AW</given-names></name><name><surname>Shrager</surname><given-names>P</given-names></name><name><surname>Rasband</surname><given-names>MN</given-names></name></person-group><article-title>Early events in node of Ranvier formation during myelination and remyelination in the PNS</article-title><source>Neuron Glia Biol</source><year>2006</year><volume>2</volume><fpage>69</fpage><lpage>79</lpage></nlm-citation></ref>
<ref id="B114"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Schumacher</surname><given-names>M</given-names></name><name><surname>Guennon</surname><given-names>R</given-names></name><name><surname>Stein</surname><given-names>DG</given-names></name><name><surname>De Nicola</surname><given-names>EF</given-names></name></person-group><article-title>Progesterone: therapeutic opportunities for neuroprotection and myelin repair</article-title><source>Pharmacol Ther</source><year>2007</year><volume>116</volume><fpage>77</fpage><lpage>106</lpage></nlm-citation></ref>
<ref id="B115"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Schwab</surname><given-names>JM</given-names></name><name><surname>Tuli</surname><given-names>SK</given-names></name><name><surname>Failli</surname><given-names>V</given-names></name></person-group><article-title>The Nogo receptor complex: confining molecules to molecular mechanisms</article-title><source>Trends Mol Med</source><year>2006</year><volume>12</volume><fpage>293</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B116"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Schweitzer</surname><given-names>J</given-names></name><name><surname>Becker</surname><given-names>T</given-names></name><name><surname>Becker</surname><given-names>CG</given-names></name><name><surname>Schachner</surname><given-names>M</given-names></name></person-group><article-title>Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish</article-title><source>Glia</source><year>2003</year><volume>41</volume><fpage>301</fpage><lpage>17</lpage></nlm-citation></ref>
<ref id="B117"><nlm-citation citation-type="book"><person-group person-group-type="author"><name><surname>Scolding</surname><given-names>N</given-names></name><name><surname>Dubois-Dalcq</surname><given-names>M</given-names></name></person-group><person-group person-group-type="editor"><name><surname>Raine</surname><given-names>CS</given-names></name><name><surname>McFarland</surname><given-names>H</given-names></name><name><surname>Hohlfeld</surname><given-names>R</given-names></name></person-group><article-title>Moving toward remyelinating and neuroprotective therapies in multiple Sclerosis</article-title><source>Multiple Sclerosis, A Comprehensive Text</source><year>2008</year><publisher-name>Elsevier B.V</publisher-name><comment>in press</comment></nlm-citation></ref>
<ref id="B118"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Seifert</surname><given-names>T</given-names></name><name><surname>Bauer</surname><given-names>J</given-names></name><name><surname>Weissert</surname><given-names>R</given-names></name><name><surname>Fazekas</surname><given-names>F</given-names></name><name><surname>Storch</surname><given-names>MK</given-names></name></person-group><article-title>Notch1 and its ligand Jagged1 are present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelination</article-title><source>Acta Neuropathol</source><year>2007</year><volume>113</volume><fpage>195</fpage><lpage>203</lpage></nlm-citation></ref>
<ref id="B119"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Setzu</surname><given-names>A</given-names></name><name><surname>Lathia</surname><given-names>JD</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Wells</surname><given-names>K</given-names></name><name><surname>Rao</surname><given-names>MS</given-names></name><name><surname>Ffrench-Constant</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Inflammation stimulates myelination by transplanted oligodendrocyte precursor cells</article-title><source>Glia</source><year>2006</year><volume>54</volume><fpage>297</fpage><lpage>303</lpage></nlm-citation></ref>
<ref id="B120"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sherman</surname><given-names>LS</given-names></name><name><surname>Back</surname><given-names>SA</given-names></name></person-group><article-title>A ‘GAG’ reflex prevents repair of the damaged CNS</article-title><source>Trends Neurosci</source><year>2008</year><volume>31</volume><fpage>44</fpage><lpage>52</lpage></nlm-citation></ref>
<ref id="B121"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sim</surname><given-names>FJ</given-names></name><name><surname>Lang</surname><given-names>JK</given-names></name><name><surname>Waldau</surname><given-names>B</given-names></name><name><surname>Roy</surname><given-names>NS</given-names></name><name><surname>Schwartz</surname><given-names>TE</given-names></name><name><surname>Pilcher</surname><given-names>WH</given-names></name><etal></etal></person-group><article-title>Complementary patterns of gene expression by human oligodendrocyte progenitors and their environment predict determinants of progenitor maintenance and differentiation</article-title><source>Ann Neurol</source><year>2006</year><volume>59</volume><fpage>763</fpage><lpage>79</lpage></nlm-citation></ref>
<ref id="B122"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Sim</surname><given-names>FJ</given-names></name><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Penderis</surname><given-names>J</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>The age-related decrease in CNS remyelination efficiency is attributable to an impairment of both oligodendrocyte progenitor recruitment and differentiation</article-title><source>J Neurosci</source><year>2002</year><volume>22</volume><fpage>2451</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B123"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Smith</surname><given-names>KJ</given-names></name></person-group><article-title>Axonal protection in multiple sclerosis – a particular need during remyelination?</article-title><source>Brain</source><year>2006</year><volume>129</volume><fpage>3147</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B124"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Song</surname><given-names>SK</given-names></name><name><surname>Sun</surname><given-names>SW</given-names></name><name><surname>Ramsbottom</surname><given-names>MJ</given-names></name><name><surname>Chang</surname><given-names>C</given-names></name><name><surname>Russell</surname><given-names>J</given-names></name><name><surname>Cross</surname><given-names>AH</given-names></name></person-group><article-title>Dysmyelination revealed through MRI as increased radial (but unchanged axial) diffusion of water</article-title><source>Neuroimage</source><year>2002</year><volume>17</volume><fpage>1429</fpage><lpage>36</lpage></nlm-citation></ref>
<ref id="B125"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Song</surname><given-names>SK</given-names></name><name><surname>Yoshino</surname><given-names>J</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Lin</surname><given-names>SJ</given-names></name><name><surname>Sun</surname><given-names>SW</given-names></name><name><surname>Cross</surname><given-names>AH</given-names></name><etal></etal></person-group><article-title>Demyelination increases radial diffusivity in corpus callosum of mouse brain</article-title><source>Neuroimage</source><year>2005</year><volume>26</volume><fpage>132</fpage><lpage>40</lpage></nlm-citation></ref>
<ref id="B126"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Spassky</surname><given-names>N</given-names></name><name><surname>de Castro</surname><given-names>F</given-names></name><name><surname>Le Bras</surname><given-names>B</given-names></name><name><surname>Heydon</surname><given-names>K</given-names></name><name><surname>Queraud-LeSaux</surname><given-names>F</given-names></name><name><surname>Bloch-Gallego</surname><given-names>E</given-names></name><etal></etal></person-group><article-title>Directional guidance of oligodendroglial migration by class 3 semaphorins and netrin-1</article-title><source>J Neurosci</source><year>2002</year><volume>22</volume><fpage>5992</fpage><lpage>6004</lpage></nlm-citation></ref>
<ref id="B127"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Stankoff</surname><given-names>B</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Noel</surname><given-names>F</given-names></name><name><surname>Wattilliaux</surname><given-names>A</given-names></name><name><surname>Zalc</surname><given-names>B</given-names></name><name><surname>Lubetzki</surname><given-names>C</given-names></name></person-group><article-title>Ciliary neurotrophic factor (CNTF) enhances myelin formation: a novel role for CNTF and CNTF-related molecules</article-title><source>J Neurosci</source><year>2002</year><volume>22</volume><fpage>9221</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B128"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Stankoff</surname><given-names>B</given-names></name><name><surname>Wang</surname><given-names>Y</given-names></name><name><surname>Bottlaender</surname><given-names>M</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Dolle</surname><given-names>F</given-names></name><name><surname>Wu</surname><given-names>C</given-names></name><etal></etal></person-group><article-title>Imaging of CNS myelin by positron-emission tomography</article-title><source>Proc Natl Acad Sci USA</source><year>2006</year><volume>103</volume><fpage>9304</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B129"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Stevens</surname><given-names>B</given-names></name><name><surname>Porta</surname><given-names>S</given-names></name><name><surname>Haak</surname><given-names>LL</given-names></name><name><surname>Gallo</surname><given-names>V</given-names></name><name><surname>Fields</surname><given-names>RD</given-names></name></person-group><article-title>Adenosine: a neuron-glial transmitter promoting myelination in the CNS in response to action potentials</article-title><source>Neuron</source><year>2002</year><volume>36</volume><fpage>855</fpage><lpage>68</lpage></nlm-citation></ref>
<ref id="B130"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Taveggia</surname><given-names>C</given-names></name><name><surname>Thaker</surname><given-names>P</given-names></name><name><surname>Petrylak</surname><given-names>A</given-names></name><name><surname>Caporaso</surname><given-names>GL</given-names></name><name><surname>Toews</surname><given-names>A</given-names></name><name><surname>Falls</surname><given-names>DL</given-names></name><name><surname>Einheber</surname><given-names>S</given-names></name><name><surname>Salzer</surname><given-names>JL</given-names></name></person-group><article-title>Type III neuregulin-1 promotes oligodendrocyte myelination</article-title><source>Glia</source><year>2008</year><volume>56</volume><fpage>284</fpage><lpage>93</lpage></nlm-citation></ref>
<ref id="B131"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Tozer</surname><given-names>DJ</given-names></name><name><surname>Davies</surname><given-names>GR</given-names></name><name><surname>Altmann</surname><given-names>DR</given-names></name><name><surname>Miller</surname><given-names>DH</given-names></name><name><surname>Tofts</surname><given-names>PS</given-names></name></person-group><article-title>Correlation of apparent myelin measures obtained in multiple sclerosis patients and controls from magnetization transfer and multicompartmental T2 analysis</article-title><source>Magn Reson Med</source><year>2005</year><volume>53</volume><fpage>1415</fpage><lpage>22</lpage></nlm-citation></ref>
<ref id="B132"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Trip</surname><given-names>SA</given-names></name><name><surname>Schlottmann</surname><given-names>PG</given-names></name><name><surname>Jones</surname><given-names>SJ</given-names></name><name><surname>Li</surname><given-names>WY</given-names></name><name><surname>Garway-Heath</surname><given-names>DF</given-names></name><name><surname>Thompson</surname><given-names>AJ</given-names></name><etal></etal></person-group><article-title>Optic nerve magnetization transfer imaging and measures of axonal loss and demyelination in optic neuritis</article-title><source>Mult Scler</source><year>2007</year><volume>13</volume><fpage>875</fpage><lpage>9</lpage></nlm-citation></ref>
<ref id="B133"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Utzschneider</surname><given-names>DA</given-names></name><name><surname>Archer</surname><given-names>DR</given-names></name><name><surname>Kocsis</surname><given-names>JD</given-names></name><name><surname>Waxman</surname><given-names>SG</given-names></name><name><surname>Duncan</surname><given-names>ID</given-names></name></person-group><article-title>Transplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient rat</article-title><source>Proc Natl Acad Sci USA</source><year>1994</year><volume>91</volume><fpage>53</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B134"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Vana</surname><given-names>AC</given-names></name><name><surname>Flint</surname><given-names>NC</given-names></name><name><surname>Harwood</surname><given-names>NE</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Fruttiger</surname><given-names>M</given-names></name><name><surname>Armstrong</surname><given-names>RC</given-names></name></person-group><article-title>Platelet-derived growth factor promotes repair of chronically demyelinated white matter</article-title><source>J Neuropathol Exp Neurol</source><year>2007</year><volume>66</volume><fpage>975</fpage><lpage>88</lpage></nlm-citation></ref>
<ref id="B135"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Vana</surname><given-names>AC</given-names></name><name><surname>Lucchinetti</surname><given-names>CF</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Armstrong</surname><given-names>RC</given-names></name></person-group><article-title>Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS</article-title><source>Glia</source><year>2007</year><volume>55</volume><fpage>687</fpage><lpage>97</lpage></nlm-citation></ref>
<ref id="B136"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Vanderlocht</surname><given-names>J</given-names></name><name><surname>Hellings</surname><given-names>N</given-names></name><name><surname>Hendriks</surname><given-names>JJ</given-names></name><name><surname>Vandenabeele</surname><given-names>F</given-names></name><name><surname>Moreels</surname><given-names>M</given-names></name><name><surname>Buntinx</surname><given-names>M</given-names></name><etal></etal></person-group><article-title>Leukemia inhibitory factor is produced by myelin-reactive T cells from multiple sclerosis patients and protects against tumor necrosis factor-alpha-induced oligodendrocyte apoptosis</article-title><source>J Neurosci Res</source><year>2006</year><volume>83</volume><fpage>763</fpage><lpage>74</lpage></nlm-citation></ref>
<ref id="B137"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Voas</surname><given-names>MG</given-names></name><name><surname>Lyons</surname><given-names>DA</given-names></name><name><surname>Naylor</surname><given-names>SG</given-names></name><name><surname>Arana</surname><given-names>N</given-names></name><name><surname>Rasband</surname><given-names>MN</given-names></name><name><surname>Talbot</surname><given-names>WS</given-names></name></person-group><article-title>alphaII-spectrin is essential for assembly of the nodes of Ranvier in myelinated axons</article-title><source>Curr Biol</source><year>2007</year><volume>17</volume><fpage>562</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="B138"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Wakamatsu</surname><given-names>Y</given-names></name><name><surname>Pristyazhnyuk</surname><given-names>S</given-names></name><name><surname>Kinoshita</surname><given-names>M</given-names></name><name><surname>Tanaka</surname><given-names>M</given-names></name><name><surname>Ozato</surname><given-names>K</given-names></name></person-group><article-title>The see-through medaka: a fish model that is transparent throughout life</article-title><source>Proc Natl Acad Sci USA</source><year>2001</year><volume>98</volume><fpage>10046</fpage><lpage>50</lpage></nlm-citation></ref>
<ref id="B139"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Waxman</surname><given-names>SG</given-names></name></person-group><article-title>Axonal conduction and injury in multiple sclerosis: the role of sodium channels</article-title><source>Nat Rev Neurosci</source><year>2006</year><volume>7</volume><fpage>932</fpage><lpage>41</lpage></nlm-citation></ref>
<ref id="B140"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Williams</surname><given-names>A</given-names></name><name><surname>Piaton</surname><given-names>G</given-names></name><name><surname>Aigrot</surname><given-names>MS</given-names></name><name><surname>Belhadi</surname><given-names>A</given-names></name><name><surname>Theaudin</surname><given-names>M</given-names></name><name><surname>Petermann</surname><given-names>F</given-names></name><etal></etal></person-group><article-title>Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?</article-title><source>Brain</source><year>2007</year><volume>130</volume><fpage>2554</fpage><lpage>65</lpage></nlm-citation></ref>
<ref id="B141"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Windrem</surname><given-names>MS</given-names></name><name><surname>Nunes</surname><given-names>MC</given-names></name><name><surname>Rashbaum</surname><given-names>WK</given-names></name><name><surname>Schwartz</surname><given-names>TH</given-names></name><name><surname>Goodman</surname><given-names>RA</given-names></name><name><surname>McKhann G</surname><given-names>2nd</given-names></name><etal></etal></person-group><article-title>Fetal and adult human oligodendrocyte progenitor cell isolates myelinate the congenitally dysmyelinated brain</article-title><source>Nat Med</source><year>2004</year><volume>10</volume><fpage>93</fpage><lpage>7</lpage></nlm-citation></ref>
<ref id="B142"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Wolburg</surname><given-names>H</given-names></name></person-group><article-title>Myelination and remyelination in the regenerating visual system of the goldfish</article-title><source>Exp Brain Res</source><year>1981</year><volume>43</volume><fpage>199</fpage><lpage>206</lpage></nlm-citation></ref>
<ref id="B143"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Woodruff</surname><given-names>RH</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Demyelination and remyelination of the caudal cerebellar peduncle of adult rats following stereotaxic injections of lysolecithin, ethidium bromide, and complement/anti-galactocerebroside: a comparative study</article-title><source>Glia</source><year>1999</year><volume>25</volume><fpage>216</fpage><lpage>28</lpage></nlm-citation></ref>
<ref id="B144"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Woods</surname><given-names>IG</given-names></name><name><surname>Lyons</surname><given-names>DA</given-names></name><name><surname>Voas</surname><given-names>MG</given-names></name><name><surname>Pogoda</surname><given-names>HM</given-names></name><name><surname>Talbot</surname><given-names>WS</given-names></name></person-group><article-title>nsf is essential for organization of myelinated axons in zebrafish</article-title><source>Curr Biol</source><year>2006</year><volume>16</volume><fpage>636</fpage><lpage>48</lpage></nlm-citation></ref>
<ref id="B145"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Wu</surname><given-names>C</given-names></name><name><surname>Tian</surname><given-names>D</given-names></name><name><surname>Feng</surname><given-names>Y</given-names></name><name><surname>Polak</surname><given-names>P</given-names></name><name><surname>Wei</surname><given-names>J</given-names></name><name><surname>Sharp</surname><given-names>A</given-names></name><etal></etal></person-group><article-title>A novel fluorescent probe that is brain permeable and selectively binds to myelin</article-title><source>J Histochem Cytochem</source><year>2006</year><volume>54</volume><fpage>997</fpage><lpage>1004</lpage></nlm-citation></ref>
<ref id="B146"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Xiang</surname><given-names>Z</given-names></name><name><surname>Nesterov</surname><given-names>EE</given-names></name><name><surname>Skoch</surname><given-names>J</given-names></name><name><surname>Lin</surname><given-names>T</given-names></name><name><surname>Hyman</surname><given-names>BT</given-names></name><name><surname>Swager</surname><given-names>TM</given-names></name><etal></etal></person-group><article-title>Detection of myelination using a novel histological probe</article-title><source>J Histochem Cytochem</source><year>2005</year><volume>53</volume><fpage>1511</fpage><lpage>6</lpage></nlm-citation></ref>
<ref id="B147"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zalc</surname><given-names>B</given-names></name></person-group><article-title>The acquisition of myelin: a success story.</article-title><source>Novartis Found Symp</source><year>2006</year><volume>276</volume><fpage>15</fpage><lpage>21</lpage><comment>discussion 21–5, 54–7, 275–81</comment></nlm-citation></ref>
<ref id="B148"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zalc</surname><given-names>B</given-names></name><name><surname>Colman</surname><given-names>DR</given-names></name></person-group><article-title>Origin of vertebrate success</article-title><source>Science</source><year>2000</year><volume>288</volume><fpage>271</fpage><lpage>2</lpage></nlm-citation></ref>
<ref id="B149"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zalc</surname><given-names>B</given-names></name><name><surname>Goujet</surname><given-names>D</given-names></name><name><surname>Colman</surname><given-names>DR</given-names></name></person-group><article-title>The origin of the myelination program in vertebrates</article-title><source>Current Biol</source><year>2008</year><comment>in press</comment></nlm-citation></ref>
<ref id="B150"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zapata</surname><given-names>A</given-names></name><name><surname>Diez</surname><given-names>B</given-names></name><name><surname>Cejalvo</surname><given-names>T</given-names></name><name><surname>Gutierrez-de Frias</surname><given-names>C</given-names></name><name><surname>Cortes</surname><given-names>A</given-names></name></person-group><article-title>Ontogeny of the immune system of fish</article-title><source>Fish Shellfish Immunol</source><year>2006</year><volume>20</volume><fpage>126</fpage><lpage>36</lpage></nlm-citation></ref>
<ref id="B151"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zawadzka</surname><given-names>M</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Myelin regeneration in demyelinating disorders: new developments in biology and clinical pathology</article-title><source>Curr Opin Neurol</source><year>2007</year><volume>20</volume><fpage>294</fpage><lpage>8</lpage></nlm-citation></ref>
<ref id="B152"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>H</given-names></name><name><surname>Vutskits</surname><given-names>L</given-names></name><name><surname>Calaora</surname><given-names>V</given-names></name><name><surname>Durbec</surname><given-names>P</given-names></name><name><surname>Kiss</surname><given-names>JZ</given-names></name></person-group><article-title>A role for the polysialic acid-neural cell adhesion molecule in PDGF-induced chemotaxis of oligodendrocyte precursor cells</article-title><source>J Cell Sci</source><year>2004</year><volume>117</volume><fpage>93</fpage><lpage>103</lpage></nlm-citation></ref>
<ref id="B153"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhang</surname><given-names>Y</given-names></name><name><surname>Taveggia</surname><given-names>C</given-names></name><name><surname>Melendez-Vasquez</surname><given-names>C</given-names></name><name><surname>Einheber</surname><given-names>S</given-names></name><name><surname>Raine</surname><given-names>CS</given-names></name><name><surname>Salzer</surname><given-names>JL</given-names></name><etal></etal></person-group><article-title>Interleukin-11 potentiates oligodendrocyte survival and maturation, and myelin formation</article-title><source>J Neurosci</source><year>2006</year><volume>26</volume><fpage>12174</fpage><lpage>85</lpage></nlm-citation></ref>
<ref id="B154"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Fancy</surname><given-names>SP</given-names></name><name><surname>Kotter</surname><given-names>MR</given-names></name><name><surname>Li</surname><given-names>WW</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Mechanisms of CNS remyelination – the key to therapeutic advances</article-title><source>J Neurol Sci</source><year>2005</year><volume>233</volume><fpage>87</fpage><lpage>91</lpage></nlm-citation></ref>
<ref id="B155"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhao</surname><given-names>C</given-names></name><name><surname>Zawadzka</surname><given-names>M</given-names></name><name><surname>Roulois</surname><given-names>AJ</given-names></name><name><surname>Bruce</surname><given-names>CC</given-names></name><name><surname>Franklin</surname><given-names>RJ</given-names></name></person-group><article-title>Promoting remyelination in multiple sclerosis by endogenous adult neural stem/precursor cells: defining cellular targets</article-title><source>J Neurol Sci</source><year>2008</year><volume>265</volume><fpage>12</fpage><lpage>16</lpage></nlm-citation></ref>
<ref id="B156"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zhou</surname><given-names>YX</given-names></name><name><surname>Flint</surname><given-names>NC</given-names></name><name><surname>Murtie</surname><given-names>JC</given-names></name><name><surname>Le</surname><given-names>TQ</given-names></name><name><surname>Armstrong</surname><given-names>RC</given-names></name></person-group><article-title>Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation</article-title><source>Glia</source><year>2006</year><volume>54</volume><fpage>578</fpage><lpage>90</lpage></nlm-citation></ref>
<ref id="B157"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zivadinov</surname><given-names>R</given-names></name></person-group><article-title>Can imaging techniques measure neuroprotection and remyelination in multiple sclerosis?</article-title><source>Neurology</source><year>2007</year><volume>68</volume><fpage>S72</fpage><lpage>82</lpage><comment>discussion S91–6</comment></nlm-citation></ref>
<ref id="B158"><nlm-citation citation-type="journal"><person-group person-group-type="author"><name><surname>Zujovic</surname><given-names>V</given-names></name><name><surname>Bachelin</surname><given-names>C</given-names></name><name><surname>Baron-Van Evercooren</surname><given-names>A</given-names></name></person-group><article-title>Remyelination of the central nervous system: a valuable contribution from the periphery</article-title><source>Neuroscientist</source><year>2007</year><volume>13</volume><fpage>383</fpage><lpage>91</lpage></nlm-citation></ref></ref-list>
<glossary>
<def-list><title><bold>Abbreviations:</bold></title>
<def-item><term id="G1">AMPA</term><def><p>amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid</p></def></def-item>
<def-item><term id="G2">BDNF</term><def><p>brain-derived neurotrophic factor</p></def></def-item>
<def-item><term id="G3">BMB</term><def><p>1,4-bis (p-aminostyryl)-2-methoxy benzene)</p></def></def-item>
<def-item><term id="G4">CNS</term><def><p>central nervous system</p></def></def-item>
<def-item><term id="G5">CNTF</term><def><p>ciliary neurotrophic factor</p></def></def-item>
<def-item><term id="G6">CXCL</term><def><p>alpha chemokines</p></def></def-item>
<def-item><term id="G7">CXCLR</term><def><p>alpha chemokine receptor</p></def></def-item>
<def-item><term id="G8">DTI</term><def><p>diffusion tensor imaging</p></def></def-item>
<def-item><term id="G9">EAE</term><def><p>experimental autoimmune encephalitis</p></def></def-item>
<def-item><term id="G10">EB</term><def><p>ethidium bromide</p></def></def-item>
<def-item><term id="G11">EGF</term><def><p>epidermal growth factor</p></def></def-item>
<def-item><term id="G12">FGF-R</term><def><p>fibroblast growth factor receptor</p></def></def-item>
<def-item><term id="G13">GAG</term><def><p>glycosaminoglycan</p></def></def-item>
<def-item><term id="G14">IFN</term><def><p>interferon</p></def></def-item>
<def-item><term id="G15">LIF</term><def><p>leukemia inhibitory factor</p></def></def-item>
<def-item><term id="G16">LtBr</term><def><p>lymphotoxin beta receptor</p></def></def-item>
<def-item><term id="G17">MRI</term><def><p>magnetic resonance imaging</p></def></def-item>
<def-item><term id="G18">MS</term><def><p>multiple sclerosis</p></def></def-item>
<def-item><term id="G19">MTR</term><def><p>magnetisation transfer ratio</p></def></def-item>
<def-item><term id="G20">Nfasc</term><def><p>neurofascin</p></def></def-item>
<def-item><term id="G21">NMDA</term><def><p>N-methyl-D-aspartate</p></def></def-item>
<def-item><term id="G22">Nrg 1</term><def><p>neuregulin 1</p></def></def-item>
<def-item><term id="G23">OPC</term><def><p>oligodendrocyte precursor cells</p></def></def-item>
<def-item><term id="G24">PDGF A</term><def><p>platelet-derived growth factor A</p></def></def-item>
<def-item><term id="G25">PDGF-R</term><def><p>PDGF receptor</p></def></def-item>
<def-item><term id="G26">PET</term><def><p>positron emission tomography</p></def></def-item>
<def-item><term id="G27">PNS</term><def><p>peripheral nervous system</p></def></def-item>
<def-item><term id="G28">PSA-NCAM</term><def><p>polysialylated neural adhesion molecule</p></def></def-item>
<def-item><term id="G29">Sema</term><def><p>semaphorin</p></def></def-item>
<def-item><term id="G30">SVZ</term><def><p>subventricular zone</p></def></def-item>
<def-item><term id="G31">TGFbeta</term><def><p>transforming growth factor beta</p></def></def-item>
</def-list>
</glossary>
</back>
</article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases</title></titleInfo><name type="personal" displayLabel="corresp"><namePart type="given">Monique</namePart><namePart type="family">Dubois-Dalcq</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><affiliation>E-mail: mdalcq@pasteur.fr</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Anna</namePart><namePart type="family">Williams</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Stadelmann</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bruno</namePart><namePart type="family">Stankoff</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bernard</namePart><namePart type="family">Zalc</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Catherine</namePart><namePart type="family">Lubetzki</namePart><affiliation>National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, Inserm, U711, 75013 Paris, Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-L5L7X3NF-P">review-article</genre><originInfo><publisher>Oxford University Press</publisher><dateIssued encoding="w3cdtf">2008-07</dateIssued><dateCreated encoding="w3cdtf">2008-03-26</dateCreated><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><abstract>In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.</abstract><subject><genre>keywords</genre><topic>multiple sclerosis</topic><topic>nodes of Ranvier</topic><topic>enhancing repair</topic><topic>animal models</topic><topic>transparent fish</topic></subject><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><topic>Review Article</topic></subject><identifier type="ISSN">0006-8950</identifier><identifier type="eISSN">1460-2156</identifier><identifier type="PublisherID">brainj</identifier><identifier type="PublisherID-hwp">brain</identifier><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>131</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>1686</start><end>1700</end></extent></part></relatedItem><relatedItem type="references" displayLabel="B1"><titleInfo><title>NG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in thepostnatal hippocampus</title></titleInfo><name type="personal"><namePart type="given">AA</namePart><namePart type="family">Aguirre</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Chittajallu</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Belachew</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Gallo</namePart></name><genre>journal</genre><note>AguirreAAChittajalluRBelachewSGalloVNG2-expressing cells in the subventricular zone are type C-like cells and contribute to interneuron generation in thepostnatal hippocampusJ Cell Biol200416557589</note><relatedItem type="host"><titleInfo><title>J Cell Biol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>165</number></detail><extent unit="pages"><start>575</start><end>89</end><list>575-89</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B2"><titleInfo><title>A functional role for EGFR signaling in myelination and remyelination</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Aguirre</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Dupree</namePart></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Mangin</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Gallo</namePart></name><genre>journal</genre><note>AguirreADupreeJLManginJMGalloVA functional role for EGFR signaling in myelination and remyelinationNat Neurosci2007109901002</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>990</start><end>1002</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B3"><titleInfo><title>Postpartum-activation of multiple sclerosis is associated with down-regulation of tolerogenic HLA-G</title></titleInfo><name type="personal"><namePart type="given">L</namePart><namePart type="family">Airas</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nikula</namePart></name><name type="personal"><namePart type="given">YH</namePart><namePart type="family">Huang</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Lahesmaa</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Wiendl</namePart></name><genre>journal</genre><note>AirasLNikulaTHuangYHLahesmaaRWiendlHPostpartum-activation of multiple sclerosis is associated with down-regulation of tolerogenic HLA-GJ Neuroimmunol200718720511</note><relatedItem type="host"><titleInfo><title>J Neuroimmunol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>187</number></detail><extent unit="pages"><start>205</start><end>11</end><list>205-11</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B4"><titleInfo><title>Extensive cortical remyelination in patients with chronic multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Albert</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Antel</namePart></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Bruck</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Stadelmann</namePart></name><genre>journal</genre><note>AlbertMAntelJBruckWStadelmannCExtensive cortical remyelination in patients with chronic multiple sclerosisBrain Pathol20071712938</note><relatedItem type="host"><titleInfo><title>Brain Pathol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>129</start><end>38</end><list>129-38</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B5"><titleInfo><title>In vitro analysis of the oligodendrocyte lineage in mice during demyelination and remyelination</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Armstrong</namePart></name><name type="personal"><namePart type="given">Jr</namePart><namePart type="family">Friedrich VL</namePart></name><name type="personal"><namePart type="given">KV</namePart><namePart type="family">Holmes</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>ArmstrongRFriedrich VLJrHolmesKVDubois-DalcqMIn vitro analysis of the oligodendrocyte lineage in mice during demyelination and remyelinationJ Cell Biol1990111118395</note><relatedItem type="host"><titleInfo><title>J Cell Biol</title></titleInfo><part><date>1990</date><detail type="volume"><caption>vol.</caption><number>111</number></detail><extent unit="pages"><start>1183</start><end>95</end><list>1183-95</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B6"><titleInfo><title>Endogenous cell repair of chronic demyelination</title></titleInfo><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Armstrong</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">NC</namePart><namePart type="family">Flint</namePart></name><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Vana</namePart></name><name type="personal"><namePart type="given">YX</namePart><namePart type="family">Zhou</namePart></name><genre>journal</genre><note>ArmstrongRCLeTQFlintNCVanaACZhouYXEndogenous cell repair of chronic demyelinationJ Neuropathol Exp Neurol20066524556</note><relatedItem type="host"><titleInfo><title>J Neuropathol Exp Neurol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>65</number></detail><extent unit="pages"><start>245</start><end>56</end><list>245-56</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B7"><titleInfo><title>Absence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matter</title></titleInfo><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Armstrong</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">EE</namePart><namePart type="family">Frost</namePart></name><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Borke</namePart></name><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Vana</namePart></name><genre>journal</genre><note>ArmstrongRCLeTQFrostEEBorkeRCVanaACAbsence of fibroblast growth factor 2 promotes oligodendroglial repopulation of demyelinated white matterJ Neurosci200222857485</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>8574</start><end>85</end><list>8574-85</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B8"><titleInfo><title>bHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNS</title></titleInfo><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Arnett</namePart></name><name type="personal"><namePart type="given">SP</namePart><namePart type="family">Fancy</namePart></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Alberta</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">SR</namePart><namePart type="family">Plant</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Kaing</namePart></name><genre>journal</genre><note>ArnettHAFancySPAlbertaJAZhaoCPlantSRKaingSbHLH transcription factor Olig1 is required to repair demyelinated lesions in the CNSScience200430621115</note><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>306</number></detail><extent unit="pages"><start>2111</start><end>5</end><list>2111-5</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B9"><titleInfo><title>Considerations for the sensible use of rodent models of inflammatory disease in predicting efficacy of new biological therapeutics in the clinic</title></titleInfo><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Arnett</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Viney</namePart></name><genre>journal</genre><note>ArnettHAVineyJLConsiderations for the sensible use of rodent models of inflammatory disease in predicting efficacy of new biological therapeutics in the clinicAdv Drug Deliv Rev200759108492</note><relatedItem type="host"><titleInfo><title>Adv Drug Deliv Rev</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>59</number></detail><extent unit="pages"><start>1084</start><end>92</end><list>1084-92</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B10"><titleInfo><title>Functional genomic analysis of remyelination reveals importance of inflammation in oligodendrocyte regeneration</title></titleInfo><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Arnett</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wang</namePart></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Matsushima</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Suzuki</namePart></name><name type="personal"><namePart type="given">JP</namePart><namePart type="family">Ting</namePart></name><genre>journal</genre><note>ArnettHAWangYMatsushimaGKSuzukiKTingJPFunctional genomic analysis of remyelination reveals importance of inflammation in oligodendrocyte regenerationJ Neurosci200323982432</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><extent unit="pages"><start>9824</start><end>32</end><list>9824-32</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B11"><titleInfo><title>Hyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturation</title></titleInfo><name type="personal"><namePart type="given">SA</namePart><namePart type="family">Back</namePart></name><name type="personal"><namePart type="given">TM</namePart><namePart type="family">Tuohy</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Chen</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Wallingford</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Craig</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Struve</namePart></name><genre>journal</genre><note>BackSATuohyTMChenHWallingfordNCraigAStruveJHyaluronan accumulates in demyelinated lesions and inhibits oligodendrocyte progenitor maturationNat Med20051196672</note><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>11</number></detail><extent unit="pages"><start>966</start><end>72</end><list>966-72</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B12"><titleInfo><title>Suppressor of cytokine signaling 1 expression protects oligodendrocytes from the deleterious effects of interferon-gamma</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Balabanov</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Strand</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Kemper</namePart></name><name type="personal"><namePart type="given">JY</namePart><namePart type="family">Lee</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Popko</namePart></name><genre>journal</genre><note>BalabanovRStrandKKemperALeeJYPopkoBSuppressor of cytokine signaling 1 expression protects oligodendrocytes from the deleterious effects of interferon-gammaJ Neurosci200626514352</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><extent unit="pages"><start>5143</start><end>52</end><list>5143-52</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B13"><titleInfo><title>7 Tesla magnetic resonance imaging of patients with Multiple Sclerosis: initial experience</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Bagnato</namePart></name><name type="personal"><namePart type="given">VN</namePart><namePart type="family">Ikonomidou</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">van Gelderen</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Yao</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Ohayon</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Fulton</namePart></name><genre>journal</genre><note>BagnatoFIkonomidouVNvan GelderenPYaoBOhayonJFultonS7 Tesla magnetic resonance imaging of patients with Multiple Sclerosis: initial experienceMultiple Sclerosis200713Suppl 2255</note><relatedItem type="host"><titleInfo><title>Multiple Sclerosis</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>255</start></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B14"><titleInfo><title>Axonal cell adhesion molecule L1 and central nervous system myelination</title></titleInfo><name type="personal"><namePart type="given">G</namePart><namePart type="family">Barbin</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Charles</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schachner</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Grumet</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><genre>journal</genre><note>BarbinGAigrotMSCharlesPSchachnerMGrumetMZalcBAxonal cell adhesion molecule L1 and central nervous system myelinationNeuron Glia Biol200416572</note><relatedItem type="host"><titleInfo><title>Neuron Glia Biol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><extent unit="pages"><start>65</start><end>72</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B15"><titleInfo><title>Remyelinated lesions in multiple sclerosis: magnetic resonance image appearance</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Barkhof</namePart></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Bruck</namePart></name><name type="personal"><namePart type="given">CJ</namePart><namePart type="family">De Groot</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Bergers</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Hulshof</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Geurts</namePart></name><genre>journal</genre><note>BarkhofFBruckWDe GrootCJBergersEHulshofSGeurtsJRemyelinated lesions in multiple sclerosis: magnetic resonance image appearanceArch Neurol200360107381</note><relatedItem type="host"><titleInfo><title>Arch Neurol</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>60</number></detail><extent unit="pages"><start>1073</start><end>81</end><list>1073-81</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B16"><titleInfo><title>Proliferation of oligodendrocyte precursor cells depends on electrical activity in axons</title></titleInfo><name type="personal"><namePart type="given">BA</namePart><namePart type="family">Barres</namePart></name><name type="personal"><namePart type="given">MC</namePart><namePart type="family">Raff</namePart></name><genre>journal</genre><note>BarresBARaffMCProliferation of oligodendrocyte precursor cells depends on electrical activity in axonsNature199336125860</note><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>361</number></detail><extent unit="pages"><start>258</start><end>60</end><list>258-60</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B17"><titleInfo><title>Remyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of Ranvier</title></titleInfo><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Black</namePart></name><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Waxman</namePart></name><name type="personal"><namePart type="given">KJ</namePart><namePart type="family">Smith</namePart></name><genre>journal</genre><note>BlackJAWaxmanSGSmithKJRemyelination of dorsal column axons by endogenous Schwann cells restores the normal pattern of Nav1.6 and Kv1.2 at nodes of RanvierBrain2006129131929</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>1319</start><end>29</end><list>1319-29</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B18"><titleInfo><title>Remyelination of the superior cerebellar peduncle in the mouse following demyelination induced by feeding cuprizone</title></titleInfo><name type="personal"><namePart type="given">WF</namePart><namePart type="family">Blakemore</namePart></name><genre>journal</genre><note>BlakemoreWFRemyelination of the superior cerebellar peduncle in the mouse following demyelination induced by feeding cuprizoneJ Neurol Sci1973207383</note><relatedItem type="host"><titleInfo><title>J Neurol Sci</title></titleInfo><part><date>1973</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>73</start><end>83</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B19"><titleInfo><title>Ultrastructural study of remyelination in an experimental lesion in adult cat spinal cord</title></titleInfo><name type="personal"><namePart type="given">MB</namePart><namePart type="family">Bunge</namePart></name><name type="personal"><namePart type="given">RP</namePart><namePart type="family">Bunge</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Ris</namePart></name><genre>journal</genre><note>BungeMBBungeRPRisHUltrastructural study of remyelination in an experimental lesion in adult cat spinal cordJ Biophys Biochem Cytol1961106794</note><relatedItem type="host"><titleInfo><title>J Biophys Biochem Cytol</title></titleInfo><part><date>1961</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>67</start><end>94</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B20"><titleInfo><title>Endogenous leukemia inhibitory factor production limits autoimmune demyelination and oligodendrocyte loss</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Butzkueven</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Emery</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Cipriani</namePart></name><name type="personal"><namePart type="given">MP</namePart><namePart type="family">Marriott</namePart></name><name type="personal"><namePart type="given">TJ</namePart><namePart type="family">Kilpatrick</namePart></name><genre>journal</genre><note>ButzkuevenHEmeryBCiprianiTMarriottMPKilpatrickTJEndogenous leukemia inhibitory factor production limits autoimmune demyelination and oligodendrocyte lossGlia200653696703</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><extent unit="pages"><start>696</start><end>703</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B21"><titleInfo><title>LIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survival</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Butzkueven</namePart></name><name type="personal"><namePart type="given">JG</namePart><namePart type="family">Zhang</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Soilu-Hanninen</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Hochrein</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Chionh</namePart></name><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Shipham</namePart></name><genre>journal</genre><note>ButzkuevenHZhangJGSoilu-HanninenMHochreinHChionhFShiphamKALIF receptor signaling limits immune-mediated demyelination by enhancing oligodendrocyte survivalNat Med200286139</note><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>613</start><end>9</end><list>613-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B22"><titleInfo><title>A transcriptome database for astrocytes, neurons, and oligodendrocytes: a new resource for understanding brain development and function</title></titleInfo><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Cahoy</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Emery</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Kaushal</namePart></name><name type="personal"><namePart type="given">LC</namePart><namePart type="family">Foo</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Zamanian</namePart></name><name type="personal"><namePart type="given">KS</namePart><namePart type="family">Christopherson</namePart></name><genre>journal</genre><note>CahoyJDEmeryBKaushalAFooLCZamanianJLChristophersonKSA transcriptome database for astrocytes, neurons, and oligodendrocytes: a new resource for understanding brain development and functionJ Neurosci20082826478</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><extent unit="pages"><start>264</start><end>78</end><list>264-78</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B23"><titleInfo><title>A role for CXCL12 (SDF-1alpha) in the pathogenesis of multiple sclerosis: regulation of CXCL12 expression in astrocytes by soluble myelin basic protein</title></titleInfo><name type="personal"><namePart type="given">TM</namePart><namePart type="family">Calderon</namePart></name><name type="personal"><namePart type="given">EA</namePart><namePart type="family">Eugenin</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Lopez</namePart></name><name type="personal"><namePart type="given">SS</namePart><namePart type="family">Kumar</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Hesselgesser</namePart></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Raine</namePart></name><genre>journal</genre><note>CalderonTMEugeninEALopezLKumarSSHesselgesserJRaineCSA role for CXCL12 (SDF-1alpha) in the pathogenesis of multiple sclerosis: regulation of CXCL12 expression in astrocytes by soluble myelin basic proteinJ Neuroimmunol20061772739</note><relatedItem type="host"><titleInfo><title>J Neuroimmunol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>177</number></detail><extent unit="pages"><start>27</start><end>39</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B24"><titleInfo><title>Myelin repair: the role of stem and precursor cells in multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Chandran</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Hunt</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Joannides</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Compston</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>ChandranSHuntDJoannidesAZhaoCCompstonAFranklinRJMyelin repair: the role of stem and precursor cells in multiple sclerosisPhilos Trans R Soc Lond B Biol Sci200836317183</note><relatedItem type="host"><titleInfo><title>Philos Trans R Soc Lond B Biol Sci</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>363</number></detail><extent unit="pages"><start>171</start><end>83</end><list>171-83</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B25"><titleInfo><title>Reexpression of PSA-NCAM by demyelinated axons: an inhibitor of remyelination in multiple sclerosis?</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Charles</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Reynolds</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Seilhean</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Rougon</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Niezgoda</namePart></name><genre>journal</genre><note>CharlesPReynoldsRSeilheanDRougonGAigrotMSNiezgodaAReexpression of PSA-NCAM by demyelinated axons: an inhibitor of remyelination in multiple sclerosis?Brain2002125197279</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>125</number></detail><extent unit="pages"><start>1972</start><end>79</end><list>1972-79</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B26"><titleInfo><title>Local magnetization transfer ratio signal inhomogeneity is related to subsequent change in MTR in lesions and normal-appearing white-matter of multiple sclerosis patients</title></titleInfo><name type="personal"><namePart type="given">JT</namePart><namePart type="family">Chen</namePart></name><name type="personal"><namePart type="given">DL</namePart><namePart type="family">Collins</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Freedman</namePart></name><name type="personal"><namePart type="given">HL</namePart><namePart type="family">Atkins</namePart></name><name type="personal"><namePart type="given">DL</namePart><namePart type="family">Arnold</namePart></name><genre>journal</genre><note>ChenJTCollinsDLFreedmanMSAtkinsHLArnoldDLLocal magnetization transfer ratio signal inhomogeneity is related to subsequent change in MTR in lesions and normal-appearing white-matter of multiple sclerosis patientsNeuroimage20052512728</note><relatedItem type="host"><titleInfo><title>Neuroimage</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>1272</start><end>8</end><list>1272-8</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B27"><titleInfo><title>Identification of dystroglycan as a second laminin receptor in oligodendrocytes, with a role in myelination</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Colognato</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Galvin</namePart></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Wang</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Relucio</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Nguyen</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Harrison</namePart></name><genre>journal</genre><note>ColognatoHGalvinJWangZRelucioJNguyenTHarrisonDIdentification of dystroglycan as a second laminin receptor in oligodendrocytes, with a role in myelinationDevelopment2007134172336</note><relatedItem type="host"><titleInfo><title>Development</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>134</number></detail><extent unit="pages"><start>1723</start><end>36</end><list>1723-36</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B28"><titleInfo><title>Nodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">I</namePart><namePart type="family">Coman</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Seilhean</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Reynolds</namePart></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Girault</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><genre>journal</genre><note>ComanIAigrotMSSeilheanDReynoldsRGiraultJAZalcBNodal, paranodal and juxtaparanodal axonal proteins during demyelination and remyelination in multiple sclerosisBrain2006129318695</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>3186</start><end>95</end><list>3186-95</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B29"><titleInfo><title>Axonal signals in central nervous system myelination, demyelination and remyelination</title></titleInfo><name type="personal"><namePart type="given">I</namePart><namePart type="family">Coman</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Barbin</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Charles</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Lubetzki</namePart></name><genre>journal</genre><note>ComanIBarbinGCharlesPZalcBLubetzkiCAxonal signals in central nervous system myelination, demyelination and remyelinationJ Neurol Sci20052336771</note><relatedItem type="host"><titleInfo><title>J Neurol Sci</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>233</number></detail><extent unit="pages"><start>67</start><end>71</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B30"><titleInfo><title>The neurobiology of remyelination</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Compston</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Lassmann</namePart></name><name type="personal"><namePart type="given">KJ</namePart><namePart type="family">Smith</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Compston</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Confravreux</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Lassmann</namePart></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Mc Donald</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Miller</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Noseworthy</namePart></name><genre>book</genre><note>CompstonALassmannHSmithKJCompstonAConfravreuxCLassmannHMc DonaldIMillerDNoseworthyJThe neurobiology of remyelinationMcAlpine's multiple sclerosis20064thChurchill Livingstone Elsevier44990</note><relatedItem type="host"><titleInfo><title>McAlpine's multiple sclerosis</title></titleInfo><originInfo><publisher>Churchill Livingstone Elsevier. </publisher><edition>4th</edition></originInfo><part><date>2006</date><extent unit="pages"><start>449</start><end>90</end><list>449-90</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B31"><titleInfo><title>Early neuronal and glial fate restriction of embryonic neural stem cells</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Delaunay</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Heydon</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Cumano</namePart></name><name type="personal"><namePart type="given">MH</namePart><namePart type="family">Schwab</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Thomas</namePart></name><name type="personal"><namePart type="given">U</namePart><namePart type="family">Suter</namePart></name><genre>journal</genre><note>DelaunayDHeydonKCumanoASchwabMHThomasJLSuterUEarly neuronal and glial fate restriction of embryonic neural stem cellsJ Neurosci200828255162</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><extent unit="pages"><start>2551</start><end>62</end><list>2551-62</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B32"><titleInfo><title>In vivo evaluation of remyelination in rat brain by magnetization transfer imaging</title></titleInfo><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Deloire-Grassin</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Brochet</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Quesson</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Delalande</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Dousset</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Canioni</namePart></name><genre>journal</genre><note>Deloire-GrassinMSBrochetBQuessonBDelalandeCDoussetVCanioniPIn vivo evaluation of remyelination in rat brain by magnetization transfer imagingJ Neurol Sci20001781016</note><relatedItem type="host"><titleInfo><title>J Neurol Sci</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>178</number></detail><extent unit="pages"><start>10</start><end>16</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B33"><titleInfo><title>Induction of myelination in the central nervous system by electrical activity</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Demerens</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stankoff</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Logak</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Anglade</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Allinquant</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Couraud</namePart></name><genre>journal</genre><note>DemerensCStankoffBLogakMAngladePAllinquantBCouraudFInduction of myelination in the central nervous system by electrical activityProc Natl Acad Sci USA199693988792</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>93</number></detail><extent unit="pages"><start>9887</start><end>92</end><list>9887-92</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B34"><titleInfo><title>EGF converts transit-amplifying neurogenic precursors in the adult brain into multipotent stem cells</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Doetsch</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Petreanu</namePart></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Caille</namePart></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Garcia-Verdugo</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Alvarez-Buylla</namePart></name><genre>journal</genre><note>DoetschFPetreanuLCailleIGarcia-VerdugoJMAlvarez-BuyllaAEGF converts transit-amplifying neurogenic precursors in the adult brain into multipotent stem cellsNeuron200236102134</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>36</number></detail><extent unit="pages"><start>1021</start><end>34</end><list>1021-34</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B35"><titleInfo><title>Enhancing central nervous system remyelination in multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Ffrench-Constant</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>Dubois-DalcqMFfrench-ConstantCFranklinRJEnhancing central nervous system remyelination in multiple sclerosisNeuron200548912</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>48</number></detail><extent unit="pages"><start>9</start><end>12</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B36"><titleInfo><title>Oligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheath</title></titleInfo><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Dupree</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Mason</namePart></name><name type="personal"><namePart type="given">JR</namePart><namePart type="family">Marcus</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Stull</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Levinson</namePart></name><name type="personal"><namePart type="given">GK</namePart><namePart type="family">Matsushima</namePart></name><genre>journal</genre><note>DupreeJLMasonJLMarcusJRStullMLevinsonRMatsushimaGKOligodendrocytes assist in the maintenance of sodium channel clusters independent of the myelin sheathNeuron Glia Biol20051114</note><relatedItem type="host"><titleInfo><title>Neuron Glia Biol</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><extent unit="pages"><start>1</start><end>14</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B37"><titleInfo><title>Activation of the ciliary neurotrophic factor (CNTF) signalling pathway in cortical neurons of multiple sclerosis patients</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Dutta</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">McDonough</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Chang</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Swamy</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Siu</namePart></name><name type="personal"><namePart type="given">GJ</namePart><namePart type="family">Kidd</namePart></name><genre>journal</genre><note>DuttaRMcDonoughJChangASwamyLSiuAKiddGJActivation of the ciliary neurotrophic factor (CNTF) signalling pathway in cortical neurons of multiple sclerosis patientsBrain2007130256676</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>130</number></detail><extent unit="pages"><start>2566</start><end>76</end><list>2566-76</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B38"><titleInfo><title>High-field MRI of brain cortical substructure based on signal phase</title></titleInfo><name type="personal"><namePart type="given">JH</namePart><namePart type="family">Duyn</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">van Gelderen</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Li</namePart></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">de Zwart</namePart></name><name type="personal"><namePart type="given">AP</namePart><namePart type="family">Koretsky</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Fukunaga</namePart></name><genre>journal</genre><note>DuynJHvan GelderenPLiTQde ZwartJAKoretskyAPFukunagaMHigh-field MRI of brain cortical substructure based on signal phaseProc Natl Acad Sci USA200710411796801</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>104</number></detail><extent unit="pages"><start>11796</start><end>801</end><list>11796-801</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B39"><titleInfo><title>A role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursors</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dziembowska</namePart></name><name type="personal"><namePart type="given">TN</namePart><namePart type="family">Tham</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Lau</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Vitry</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Lazarini</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>DziembowskaMThamTNLauPVitrySLazariniFDubois-DalcqMA role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursorsGlia20055025869</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>50</number></detail><extent unit="pages"><start>258</start><end>69</end><list>258-69</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B40"><titleInfo><title>Secreted gliomedin is a perinodal matrix component of peripheral nerves</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Eshed</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Feinberg</namePart></name><name type="personal"><namePart type="given">DJ</namePart><namePart type="family">Carey</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Peles</namePart></name><genre>journal</genre><note>EshedYFeinbergKCareyDJPelesESecreted gliomedin is a perinodal matrix component of peripheral nervesJ Cell Biol200717755162</note><relatedItem type="host"><titleInfo><title>J Cell Biol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>177</number></detail><extent unit="pages"><start>551</start><end>62</end><list>551-62</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B41"><titleInfo><title>Increased expression of Nkx2.2 and Olig2 identifies reactive oligodendrocyte progenitor cells responding to demyelination in the adult CNS</title></titleInfo><name type="personal"><namePart type="given">SP</namePart><namePart type="family">Fancy</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>FancySPZhaoCFranklinRJIncreased expression of Nkx2.2 and Olig2 identifies reactive oligodendrocyte progenitor cells responding to demyelination in the adult CNSMol Cell Neurosci20042724754</note><relatedItem type="host"><titleInfo><title>Mol Cell Neurosci</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>247</start><end>54</end><list>247-54</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B42"><titleInfo><title>Conduction properties of central nerve fibers remyelinated by Schwann cells</title></titleInfo><name type="personal"><namePart type="given">PA</namePart><namePart type="family">Felts</namePart></name><name type="personal"><namePart type="given">KJ</namePart><namePart type="family">Smith</namePart></name><genre>journal</genre><note>FeltsPASmithKJConduction properties of central nerve fibers remyelinated by Schwann cellsBrain Res199257417892</note><relatedItem type="host"><titleInfo><title>Brain Res</title></titleInfo><part><date>1992</date><detail type="volume"><caption>vol.</caption><number>574</number></detail><extent unit="pages"><start>178</start><end>92</end><list>178-92</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B43"><titleInfo><title>Inflammation stimulates remyelination in areas of chronic demyelination</title></titleInfo><name type="personal"><namePart type="given">AK</namePart><namePart type="family">Foote</namePart></name><name type="personal"><namePart type="given">WF</namePart><namePart type="family">Blakemore</namePart></name><genre>journal</genre><note>FooteAKBlakemoreWFInflammation stimulates remyelination in areas of chronic demyelinationBrain200512852839</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>128</number></detail><extent unit="pages"><start>528</start><end>39</end><list>528-39</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B44"><titleInfo><title>Distinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineage</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Fortin</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Rom</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Sun</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Yayon</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Bansal</namePart></name><genre>journal</genre><note>FortinDRomESunHYayonABansalRDistinct fibroblast growth factor (FGF)/FGF receptor signaling pairs initiate diverse cellular responses in the oligodendrocyte lineageJ Neurosci20052574709</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>7470</start><end>9</end><list>7470-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B45"><titleInfo><title>Understanding CNS remyelination: clues from developmental and regeneration biology</title></titleInfo><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><name type="personal"><namePart type="given">GL</namePart><namePart type="family">Hinks</namePart></name><genre>journal</genre><note>FranklinRJHinksGLUnderstanding CNS remyelination: clues from developmental and regeneration biologyJ Neurosci Res19995820713</note><relatedItem type="host"><titleInfo><title>J Neurosci Res</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>58</number></detail><extent unit="pages"><start>207</start><end>13</end><list>207-13</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B46"><titleInfo><title>In vivo tracing of neural tracts in the intact and injured spinal cord of marmosets by diffusion tensor tractography</title></titleInfo><name type="personal"><namePart type="given">K</namePart><namePart type="family">Fujiyoshi</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Yamada</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Nakamura</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Yamane</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Katoh</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Kitamura</namePart></name><genre>journal</genre><note>FujiyoshiKYamadaMNakamuraMYamaneJKatohHKitamuraKIn vivo tracing of neural tracts in the intact and injured spinal cord of marmosets by diffusion tensor tractographyJ Neurosci200727119918</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>11991</start><end>8</end><list>11991-8</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B47"><titleInfo><title>Measurement of myelin sheath resistances: implications for axonal conduction and pathophysiology</title></titleInfo><name type="personal"><namePart type="given">PG</namePart><namePart type="family">Funch</namePart></name><name type="personal"><namePart type="given">DS</namePart><namePart type="family">Faber</namePart></name><genre>journal</genre><note>FunchPGFaberDSMeasurement of myelin sheath resistances: implications for axonal conduction and pathophysiologyScience198422553840</note><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>1984</date><detail type="volume"><caption>vol.</caption><number>225</number></detail><extent unit="pages"><start>538</start><end>40</end><list>538-40</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B48"><titleInfo><title>Neural cell adhesion molecule polysialylation enhances the sensitivity of embryonic stem cell-derived neural precursors to migration guidance cues</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Glaser</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Brose</namePart></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Franceschini</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Hamann</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Smorodchenko</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Zipp</namePart></name><genre>journal</genre><note>GlaserTBroseCFranceschiniIHamannKSmorodchenkoAZippFNeural cell adhesion molecule polysialylation enhances the sensitivity of embryonic stem cell-derived neural precursors to migration guidance cuesStem Cells200725301625</note><relatedItem type="host"><titleInfo><title>Stem Cells</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>3016</start><end>25</end><list>3016-25</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B49"><titleInfo><title>Understanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis research</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Gold</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Linington</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Lassmann</namePart></name><genre>journal</genre><note>GoldRLiningtonCLassmannHUnderstanding pathogenesis and therapy of multiple sclerosis via animal models: 70 years of merits and culprits in experimental autoimmune encephalomyelitis researchBrain2006129195371</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>1953</start><end>71</end><list>1953-71</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B50"><titleInfo><title>Future research directions in multiple sclerosis therapies</title></titleInfo><name type="personal"><namePart type="given">BM</namePart><namePart type="family">Greenberg</namePart></name><name type="personal"><namePart type="given">PA</namePart><namePart type="family">Calabresi</namePart></name><genre>journal</genre><note>GreenbergBMCalabresiPAFuture research directions in multiple sclerosis therapiesSemin Neurol2008281217</note><relatedItem type="host"><titleInfo><title>Semin Neurol</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><extent unit="pages"><start>121</start><end>7</end><list>121-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B51"><titleInfo><title>The effect of injections of lysophosphatidyl choline into white matter of the adult mouse spinal cord</title></titleInfo><name type="personal"><namePart type="given">SM</namePart><namePart type="family">Hall</namePart></name><genre>journal</genre><note>HallSMThe effect of injections of lysophosphatidyl choline into white matter of the adult mouse spinal cordJ Cell Sci19721053546</note><relatedItem type="host"><titleInfo><title>J Cell Sci</title></titleInfo><part><date>1972</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>535</start><end>46</end><list>535-46</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B52"><titleInfo><title>The role of cyclic AMP signaling in promoting axonal regeneration after spinal cord injury</title></titleInfo><name type="personal"><namePart type="given">SS</namePart><namePart type="family">Hannila</namePart></name><name type="personal"><namePart type="given">MT</namePart><namePart type="family">Filbin</namePart></name><genre>journal</genre><note>HannilaSSFilbinMTThe role of cyclic AMP signaling in promoting axonal regeneration after spinal cord injuryExp Neurol200829932132</note><relatedItem type="host"><titleInfo><title>Exp Neurol</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>299</number></detail><extent unit="pages"><start>321</start><end>32</end><list>321-32</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B53"><titleInfo><title>Restoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cells</title></titleInfo><name type="personal"><namePart type="given">O</namePart><namePart type="family">Honmou</namePart></name><name type="personal"><namePart type="given">PA</namePart><namePart type="family">Felts</namePart></name><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Waxman</namePart></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Kocsis</namePart></name><genre>journal</genre><note>HonmouOFeltsPAWaxmanSGKocsisJDRestoration of normal conduction properties in demyelinated spinal cord axons in the adult rat by transplantation of exogenous Schwann cellsJ Neurosci1996163199208</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>3199</start><end>208</end><list>3199-208</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B54"><titleInfo><title>Disruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">OW</namePart><namePart type="family">Howell</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Palser</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Polito</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Melrose</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zonta</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Scheiermann</namePart></name><genre>journal</genre><note>HowellOWPalserAPolitoAMelroseSZontaBScheiermannCDisruption of neurofascin localization reveals early changes preceding demyelination and remyelination in multiple sclerosisBrain2006129317385</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>3173</start><end>85</end><list>3173-85</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B55"><titleInfo><title>Bace1 modulates myelination in the central and peripheral nervous system</title></titleInfo><name type="personal"><namePart type="given">X</namePart><namePart type="family">Hu</namePart></name><name type="personal"><namePart type="given">CW</namePart><namePart type="family">Hicks</namePart></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">He</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Wong</namePart></name><name type="personal"><namePart type="given">WB</namePart><namePart type="family">Macklin</namePart></name><name type="personal"><namePart type="given">BD</namePart><namePart type="family">Trapp</namePart></name><genre>journal</genre><note>HuXHicksCWHeWWongPMacklinWBTrappBDBace1 modulates myelination in the central and peripheral nervous systemNat Neurosci2006915205</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1520</start><end>5</end><list>1520-5</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B56"><titleInfo><title>Astrocytes promote myelination in response to electrical impulses</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Ishibashi</namePart></name><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Dakin</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stevens</namePart></name><name type="personal"><namePart type="given">PR</namePart><namePart type="family">Lee</namePart></name><name type="personal"><namePart type="given">SV</namePart><namePart type="family">Kozlov</namePart></name><name type="personal"><namePart type="given">CL</namePart><namePart type="family">Stewart</namePart></name><genre>journal</genre><note>IshibashiTDakinKAStevensBLeePRKozlovSVStewartCLAstrocytes promote myelination in response to electrical impulsesNeuron20064982332</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>49</number></detail><extent unit="pages"><start>823</start><end>32</end><list>823-32</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B57"><titleInfo><title>Differential control of clustering of the sodium channels Na(v)1.2 and Na(v)1.6 at developing CNS nodes of Ranvier</title></titleInfo><name type="personal"><namePart type="given">MR</namePart><namePart type="family">Kaplan</namePart></name><name type="personal"><namePart type="given">MH</namePart><namePart type="family">Cho</namePart></name><name type="personal"><namePart type="given">EM</namePart><namePart type="family">Ullian</namePart></name><name type="personal"><namePart type="given">LL</namePart><namePart type="family">Isom</namePart></name><name type="personal"><namePart type="given">SR</namePart><namePart type="family">Levinson</namePart></name><name type="personal"><namePart type="given">BA</namePart><namePart type="family">Barres</namePart></name><genre>journal</genre><note>KaplanMRChoMHUllianEMIsomLLLevinsonSRBarresBADifferential control of clustering of the sodium channels Na(v)1.2 and Na(v)1.6 at developing CNS nodes of RanvierNeuron20013010519</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>30</number></detail><extent unit="pages"><start>105</start><end>19</end><list>105-19</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B58"><titleInfo><title>Induction of sodium channel clustering by oligodendrocytes</title></titleInfo><name type="personal"><namePart type="given">MR</namePart><namePart type="family">Kaplan</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Meyer-Franke</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Lambert</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Bennett</namePart></name><name type="personal"><namePart type="given">ID</namePart><namePart type="family">Duncan</namePart></name><name type="personal"><namePart type="given">SR</namePart><namePart type="family">Levinson</namePart></name><name type="personal"><namePart type="given">BA</namePart><namePart type="family">Barres</namePart></name><genre>journal</genre><note>KaplanMRMeyer-FrankeALambertSBennettVDuncanIDLevinsonSRBarresBAInduction of sodium channel clustering by oligodendrocytesNature19973867248</note><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>386</number></detail><extent unit="pages"><start>724</start><end>8</end><list>724-8</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B59"><titleInfo><title>Neurotransmitter receptors in the life and death of oligodendrocytes</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Karadottir</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Attwell</namePart></name><genre>journal</genre><note>KaradottirRAttwellDNeurotransmitter receptors in the life and death of oligodendrocytesNeuroscience2007145142638</note><relatedItem type="host"><titleInfo><title>Neuroscience</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>145</number></detail><extent unit="pages"><start>1426</start><end>38</end><list>1426-38</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B60"><titleInfo><title>A screen for mutations in zebrafish that affect myelin gene expression in Schwann cells and oligodendrocytes</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Kazakova</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Li</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Mora</namePart></name><name type="personal"><namePart type="given">KR</namePart><namePart type="family">Jessen</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Mirsky</namePart></name><name type="personal"><namePart type="given">WD</namePart><namePart type="family">Richardson</namePart></name><genre>journal</genre><note>KazakovaNLiHMoraAJessenKRMirskyRRichardsonWDA screen for mutations in zebrafish that affect myelin gene expression in Schwann cells and oligodendrocytesDev Biol2006297113</note><relatedItem type="host"><titleInfo><title>Dev Biol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>297</number></detail><extent unit="pages"><start>1</start><end>13</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B61"><titleInfo><title>Targeting experimental autoimmune encephalomyelitis lesions to a predetermined axonal tract system allows for refined behavioral testing in an animal model of multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kerschensteiner</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Stadelmann</namePart></name><name type="personal"><namePart type="given">BS</namePart><namePart type="family">Buddeberg</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Merkler</namePart></name><name type="personal"><namePart type="given">FM</namePart><namePart type="family">Bareyre</namePart></name><name type="personal"><namePart type="given">DC</namePart><namePart type="family">Anthony</namePart></name><genre>journal</genre><note>KerschensteinerMStadelmannCBuddebergBSMerklerDBareyreFMAnthonyDCTargeting experimental autoimmune encephalomyelitis lesions to a predetermined axonal tract system allows for refined behavioral testing in an animal model of multiple sclerosisAm J Pathol2004164145569</note><relatedItem type="host"><titleInfo><title>Am J Pathol</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>164</number></detail><extent unit="pages"><start>1455</start><end>69</end><list>1455-69</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B62"><titleInfo><title>In vivo time-lapse imaging shows dynamic oligodendrocyte progenitor behavior during zebrafish development</title></titleInfo><name type="personal"><namePart type="given">BB</namePart><namePart type="family">Kirby</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Takada</namePart></name><name type="personal"><namePart type="given">AJ</namePart><namePart type="family">Latimer</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Shin</namePart></name><name type="personal"><namePart type="given">TJ</namePart><namePart type="family">Carney</namePart></name><name type="personal"><namePart type="given">RN</namePart><namePart type="family">Kelsh</namePart></name><genre>journal</genre><note>KirbyBBTakadaNLatimerAJShinJCarneyTJKelshRNIn vivo time-lapse imaging shows dynamic oligodendrocyte progenitor behavior during zebrafish developmentNat Neurosci20069150611</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>1506</start><end>11</end><list>1506-11</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B63"><titleInfo><title>Process outgrowth of oligodendrocytes is promoted by interaction of fyn kinase with the cytoskeletal protein tau</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Klein</namePart></name><name type="personal"><namePart type="given">EM</namePart><namePart type="family">Kramer</namePart></name><name type="personal"><namePart type="given">AM</namePart><namePart type="family">Cardine</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Schraven</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Brandt</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Trotter</namePart></name><genre>journal</genre><note>KleinCKramerEMCardineAMSchravenBBrandtRTrotterJProcess outgrowth of oligodendrocytes is promoted by interaction of fyn kinase with the cytoskeletal protein tauJ Neurosci200222698707</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>698</start><end>707</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B64"><titleInfo><title>A subpopulation of olfactory bulb GABAergic interneurons is derived from Emx1- and Dlx5/6-expressing progenitors</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kohwi</namePart></name><name type="personal"><namePart type="given">MA</namePart><namePart type="family">Petryniak</namePart></name><name type="personal"><namePart type="given">JE</namePart><namePart type="family">Long</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Ekker</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Obata</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Yanagawa</namePart></name><genre>journal</genre><note>KohwiMPetryniakMALongJEEkkerMObataKYanagawaYA subpopulation of olfactory bulb GABAergic interneurons is derived from Emx1- and Dlx5/6-expressing progenitorsJ Neurosci200727687891</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>6878</start><end>91</end><list>6878-91</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B65"><titleInfo><title>Macrophage-depletion induced impairment of experimental CNS remyelination is associated with a reduced oligodendrocyte progenitor cell response and altered growth factor expression</title></titleInfo><name type="personal"><namePart type="given">MR</namePart><namePart type="family">Kotter</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">van Rooijen</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>KotterMRZhaoCvan RooijenNFranklinRJMacrophage-depletion induced impairment of experimental CNS remyelination is associated with a reduced oligodendrocyte progenitor cell response and altered growth factor expressionNeurobiol Dis20051816675</note><relatedItem type="host"><titleInfo><title>Neurobiol Dis</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><extent unit="pages"><start>166</start><end>75</end><list>166-75</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B66"><titleInfo><title>Natively unfolded tubulin polymerization promoting protein TPPP/p25 is a common marker of alpha-synucleinopathies</title></titleInfo><name type="personal"><namePart type="given">GG</namePart><namePart type="family">Kovacs</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Laszlo</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Kovacs</namePart></name><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Jensen</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Lindersson</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Botond</namePart></name><genre>journal</genre><note>KovacsGGLaszloLKovacsJJensenPHLinderssonEBotondGNatively unfolded tubulin polymerization promoting protein TPPP/p25 is a common marker of alpha-synucleinopathiesNeurobiol Dis20041715562</note><relatedItem type="host"><titleInfo><title>Neurobiol Dis</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>155</start><end>62</end><list>155-62</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B67"><titleInfo><title>Increased levels of myelin basic protein transcripts in virus-induced demyelination</title></titleInfo><name type="personal"><namePart type="given">K</namePart><namePart type="family">Kristensson</namePart></name><name type="personal"><namePart type="given">KV</namePart><namePart type="family">Holmes</namePart></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Duchala</namePart></name><name type="personal"><namePart type="given">NK</namePart><namePart type="family">Zeller</namePart></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Lazzarini</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>KristenssonKHolmesKVDuchalaCSZellerNKLazzariniRADubois-DalcqMIncreased levels of myelin basic protein transcripts in virus-induced demyelinationNature19863225447</note><relatedItem type="host"><titleInfo><title>Nature</title></titleInfo><part><date>1986</date><detail type="volume"><caption>vol.</caption><number>322</number></detail><extent unit="pages"><start>544</start><end>7</end><list>544-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B68"><titleInfo><title>Chemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitment</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Krumbholz</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Theil</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Cepok</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Hemmer</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Kivisakk</namePart></name><name type="personal"><namePart type="given">RM</namePart><namePart type="family">Ransohoff</namePart></name><genre>journal</genre><note>KrumbholzMTheilDCepokSHemmerBKivisakkPRansohoffRMChemokines in multiple sclerosis: CXCL12 and CXCL13 up-regulation is differentially linked to CNS immune cell recruitmentBrain200612920011</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>200</start><end>11</end><list>200-11</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B69"><titleInfo><title>Vesicular glutamate release from axons in white matter</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kukley</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Capetillo-Zarate</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Dietrich</namePart></name><genre>journal</genre><note>KukleyMCapetillo-ZarateEDietrichDVesicular glutamate release from axons in white matterNat Neurosci20071031120</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>311</start><end>20</end><list>311-20</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B70"><titleInfo><title>Matrix metalloproteinase-9 facilitates remyelination in part by processing the inhibitory NG2 proteoglycan</title></titleInfo><name type="personal"><namePart type="given">PH</namePart><namePart type="family">Larsen</namePart></name><name type="personal"><namePart type="given">JE</namePart><namePart type="family">Wells</namePart></name><name type="personal"><namePart type="given">WB</namePart><namePart type="family">Stallcup</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Opdenakker</namePart></name><name type="personal"><namePart type="given">VW</namePart><namePart type="family">Yong</namePart></name><genre>journal</genre><note>LarsenPHWellsJEStallcupWBOpdenakkerGYongVWMatrix metalloproteinase-9 facilitates remyelination in part by processing the inhibitory NG2 proteoglycanJ Neurosci2003231112735</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>23</number></detail><extent unit="pages"><start>11127</start><end>35</end><list>11127-35</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B71"><titleInfo><title>Myelin water imaging in multiple sclerosis: quantitative correlations with histopathology</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Laule</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Leung</namePart></name><name type="personal"><namePart type="given">DK</namePart><namePart type="family">Lis</namePart></name><name type="personal"><namePart type="given">AL</namePart><namePart type="family">Traboulsee</namePart></name><name type="personal"><namePart type="given">DW</namePart><namePart type="family">Paty</namePart></name><name type="personal"><namePart type="given">AL</namePart><namePart type="family">MacKay</namePart></name><genre>journal</genre><note>LauleCLeungELisDKTraboulseeALPatyDWMacKayALMyelin water imaging in multiple sclerosis: quantitative correlations with histopathologyMult Scler20061274753</note><relatedItem type="host"><titleInfo><title>Mult Scler</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><extent unit="pages"><start>747</start><end>53</end><list>747-53</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B72"><titleInfo><title>Schwann cells genetically engineered to express PSA show enhanced migratory potential without impairment of their myelinating ability in vitro</title></titleInfo><name type="personal"><namePart type="given">AA</namePart><namePart type="family">Lavdas</namePart></name><name type="personal"><namePart type="given">I</namePart><namePart type="family">Franceschini</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Matsas</namePart></name><genre>journal</genre><note>LavdasAAFranceschiniIDubois-DalcqMMatsasRSchwann cells genetically engineered to express PSA show enhanced migratory potential without impairment of their myelinating ability in vitroGlia20065386878</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><extent unit="pages"><start>868</start><end>78</end><list>868-78</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B73"><titleInfo><title>Role of the alpha-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous system</title></titleInfo><name type="personal"><namePart type="given">F</namePart><namePart type="family">Lazarini</namePart></name><name type="personal"><namePart type="given">TN</namePart><namePart type="family">Tham</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Casanova</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Arenzana-Seisdedos</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>LazariniFThamTNCasanovaPArenzana-SeisdedosFDubois-DalcqMRole of the alpha-chemokine stromal cell-derived factor (SDF-1) in the developing and mature central nervous systemGlia20034213948</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><extent unit="pages"><start>139</start><end>48</end><list>139-48</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B74"><titleInfo><title>Diffusion tensor imaging: concepts and applications</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Le Bihan</namePart></name><name type="personal"><namePart type="given">JF</namePart><namePart type="family">Mangin</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Poupon</namePart></name><name type="personal"><namePart type="given">CA</namePart><namePart type="family">Clark</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Pappata</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Molko</namePart></name><genre>journal</genre><note>Le BihanDManginJFPouponCClarkCAPappataSMolkoNDiffusion tensor imaging: concepts and applicationsJ Magn Reson Imaging20011353446</note><relatedItem type="host"><titleInfo><title>J Magn Reson Imaging</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>534</start><end>46</end><list>534-46</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B75"><titleInfo><title>NGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelination</title></titleInfo><name type="personal"><namePart type="given">X</namePart><namePart type="family">Lee</namePart></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Yang</namePart></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Shao</namePart></name><name type="personal"><namePart type="given">SS</namePart><namePart type="family">Rosenberg</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Levesque</namePart></name><name type="personal"><namePart type="given">RB</namePart><namePart type="family">Pepinsky</namePart></name><genre>journal</genre><note>LeeXYangZShaoZRosenbergSSLevesqueMPepinskyRBNGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelinationJ Neurosci2007272205</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>220</start><end>5</end><list>220-5</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B76"><titleInfo><title>Extensive heterogeneity in white matter intensity in high-resolution T2*-weighted MRI of the human brain at 7.0 T</title></titleInfo><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Li</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">van Gelderen</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Merkle</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Talagala</namePart></name><name type="personal"><namePart type="given">AP</namePart><namePart type="family">Koretsky</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Duyn</namePart></name><genre>journal</genre><note>LiTQvan GelderenPMerkleHTalagalaLKoretskyAPDuynJExtensive heterogeneity in white matter intensity in high-resolution T2*-weighted MRI of the human brain at 7.0 TNeuroimage200632103240</note><relatedItem type="host"><titleInfo><title>Neuroimage</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>32</number></detail><extent unit="pages"><start>1032</start><end>40</end><list>1032-40</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B77"><titleInfo><title>Interferon-gamma inhibits central nervous system remyelination through a process modulated by endoplasmic reticulum stress</title></titleInfo><name type="personal"><namePart type="given">W</namePart><namePart type="family">Lin</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Kemper</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Dupree</namePart></name><name type="personal"><namePart type="given">HP</namePart><namePart type="family">Harding</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Ron</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Popko</namePart></name><genre>journal</genre><note>LinWKemperADupreeJLHardingHPRonDPopkoBInterferon-gamma inhibits central nervous system remyelination through a process modulated by endoplasmic reticulum stressBrain2006129130618</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>1306</start><end>18</end><list>1306-18</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B78"><titleInfo><title>Axonal signals and central nervous system myelination</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Lubetzki</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Filippi</namePart></name><name type="personal"><namePart type="given">DL</namePart><namePart type="family">Arnold</namePart></name><genre>book</genre><note>LubetzkiCZalcBFilippiMArnoldDLAxonal signals and central nervous system myelinationMagnetic resonance spectroscopy in multiple sclerosis2001Heidelberg, New York, LondonSpringer Verlag514</note><relatedItem type="host"><titleInfo><title>Magnetic resonance spectroscopy in multiple sclerosis</title></titleInfo><originInfo><publisher>Springer Verlag. </publisher><place><placeTerm type="text">Heidelberg, New York, London</placeTerm></place></originInfo><part><date>2001</date><extent unit="pages"><start>5</start><end>14</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B79"><titleInfo><title>Promoting repair in multiple sclerosis: problems and prospects</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Lubetzki</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Williams</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stankoff</namePart></name><genre>journal</genre><note>LubetzkiCWilliamsAStankoffBPromoting repair in multiple sclerosis: problems and prospectsCurr Opin Neurol20051823744</note><relatedItem type="host"><titleInfo><title>Curr Opin Neurol</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><extent unit="pages"><start>237</start><end>44</end><list>237-44</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B80"><titleInfo><title>Central nervous system demyelination and remyelination in the mouse: an ultrastructural study of cuprizone toxicity</title></titleInfo><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Ludwin</namePart></name><genre>journal</genre><note>LudwinSKCentral nervous system demyelination and remyelination in the mouse: an ultrastructural study of cuprizone toxicityLab Invest197839597612</note><relatedItem type="host"><titleInfo><title>Lab Invest</title></titleInfo><part><date>1978</date><detail type="volume"><caption>vol.</caption><number>39</number></detail><extent unit="pages"><start>597</start><end>612</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B81"><titleInfo><title>Cleavage and oligomerization of gliomedin, a transmembrane collagen required for node of ranvier formation</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Maertens</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Hopkins</namePart></name><name type="personal"><namePart type="given">CW</namePart><namePart type="family">Franzke</namePart></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Keene</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Bruckner-Tuderman</namePart></name><name type="personal"><namePart type="given">DS</namePart><namePart type="family">Greenspan</namePart></name><genre>journal</genre><note>MaertensBHopkinsDFranzkeCWKeeneDRBruckner-TudermanLGreenspanDSCleavage and oligomerization of gliomedin, a transmembrane collagen required for node of ranvier formationJ Biol Chem20072821064759</note><relatedItem type="host"><titleInfo><title>J Biol Chem</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>282</number></detail><extent unit="pages"><start>10647</start><end>59</end><list>10647-59</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B82"><titleInfo><title>Meningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathology</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Magliozzi</namePart></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Howell</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Vora</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Serafini</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Nicholas</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Puopolo</namePart></name><genre>journal</genre><note>MagliozziRHowellOVoraASerafiniBNicholasRPuopoloMMeningeal B-cell follicles in secondary progressive multiple sclerosis associate with early onset of disease and severe cortical pathologyBrain20071301089104</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>130</number></detail><extent unit="pages"><start>1089</start><end>104</end><list>1089-104</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B83"><titleInfo><title>Leukemia inhibitory factor signaling modulates both central nervous system demyelination and myelin repair</title></titleInfo><name type="personal"><namePart type="given">MP</namePart><namePart type="family">Marriott</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Emery</namePart></name><name type="personal"><namePart type="given">HS</namePart><namePart type="family">Cate</namePart></name><name type="personal"><namePart type="given">MD</namePart><namePart type="family">Binder</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Kemper</namePart></name><name type="personal"><namePart type="given">Q</namePart><namePart type="family">Wu</namePart></name><genre>journal</genre><note>MarriottMPEmeryBCateHSBinderMDKemperDWuQLeukemia inhibitory factor signaling modulates both central nervous system demyelination and myelin repairGlia20085668698</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>56</number></detail><extent unit="pages"><start>686</start><end>98</end><list>686-98</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B84"><titleInfo><title>The B cell∼Old player, New position on the team</title></titleInfo><name type="personal"><namePart type="given">HF</namePart><namePart type="family">Mc Farland</namePart></name><genre>journal</genre><note>Mc FarlandHFThe B cell∼Old player, New position on the teamNew Engl J Med20083586645</note><relatedItem type="host"><titleInfo><title>New Engl J Med</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>358</number></detail><extent unit="pages"><start>664</start><end>5</end><list>664-5</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B85"><titleInfo><title>A role for TGF-beta in oligodendrocyte differentiation</title></titleInfo><name type="personal"><namePart type="given">RD</namePart><namePart type="family">McKinnon</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Piras</namePart></name><name type="personal"><namePart type="given">Jr</namePart><namePart type="family">Ida JA</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>McKinnonRDPirasGIda JAJrDubois-DalcqMA role for TGF-beta in oligodendrocyte differentiationJ Cell Biol19931211397407</note><relatedItem type="host"><titleInfo><title>J Cell Biol</title></titleInfo><part><date>1993</date><detail type="volume"><caption>vol.</caption><number>121</number></detail><extent unit="pages"><start>1397</start><end>407</end><list>1397-407</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B86"><titleInfo><title>Origin of oligodendrocytes in the subventricular zone of the adult brain</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Menn</namePart></name><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Garcia-Verdugo</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Yaschine</namePart></name><name type="personal"><namePart type="given">O</namePart><namePart type="family">Gonzalez-Perez</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Rowitch</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Alvarez-Buylla</namePart></name><genre>journal</genre><note>MennBGarcia-VerdugoJMYaschineCGonzalez-PerezORowitchDAlvarez-BuyllaAOrigin of oligodendrocytes in the subventricular zone of the adult brainJ Neurosci200626790718</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><extent unit="pages"><start>7907</start><end>18</end><list>7907-18</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B87"><titleInfo><title>A new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelination</title></titleInfo><name type="personal"><namePart type="given">D</namePart><namePart type="family">Merkler</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Ernsting</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kerschensteiner</namePart></name><name type="personal"><namePart type="given">W</namePart><namePart type="family">Bruck</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Stadelmann</namePart></name><genre>journal</genre><note>MerklerDErnstingTKerschensteinerMBruckWStadelmannCA new focal EAE model of cortical demyelination: multiple sclerosis-like lesions with rapid resolution of inflammation and extensive remyelinationBrain2006129197283</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>1972</start><end>83</end><list>1972-83</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B88"><titleInfo><title>LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Mi</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Hu</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Hahm</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Luo</namePart></name><name type="personal"><namePart type="given">ES</namePart><namePart type="family">Kam Hui</namePart></name><name type="personal"><namePart type="given">Q</namePart><namePart type="family">Yuan</namePart></name><genre>journal</genre><note>MiSHuBHahmKLuoYKam HuiESYuanQLINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitisNat Med200713122833</note><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>1228</start><end>33</end><list>1228-33</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B89"><titleInfo><title>LINGO-1 negatively regulates myelination by oligodendrocytes</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Mi</namePart></name><name type="personal"><namePart type="given">RH</namePart><namePart type="family">Miller</namePart></name><name type="personal"><namePart type="given">X</namePart><namePart type="family">Lee</namePart></name><name type="personal"><namePart type="given">ML</namePart><namePart type="family">Scott</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Shulag-Morskaya</namePart></name><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Shao</namePart></name><genre>journal</genre><note>MiSMillerRHLeeXScottMLShulag-MorskayaSShaoZLINGO-1 negatively regulates myelination by oligodendrocytesNat Neurosci2005874551</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>8</number></detail><extent unit="pages"><start>745</start><end>51</end><list>745-51</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B90"><titleInfo><title>Axonal neuregulin-1 regulates myelin sheath thickness</title></titleInfo><name type="personal"><namePart type="given">GV</namePart><namePart type="family">Michailov</namePart></name><name type="personal"><namePart type="given">MW</namePart><namePart type="family">Sereda</namePart></name><name type="personal"><namePart type="given">BG</namePart><namePart type="family">Brinkmann</namePart></name><name type="personal"><namePart type="given">TM</namePart><namePart type="family">Fischer</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Haug</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Birchmeier</namePart></name><genre>journal</genre><note>MichailovGVSeredaMWBrinkmannBGFischerTMHaugBBirchmeierCAxonal neuregulin-1 regulates myelin sheath thicknessScience20043047003</note><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>304</number></detail><extent unit="pages"><start>700</start><end>3</end><list>700-3</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B91"><titleInfo><title>Dissecting demyelination</title></titleInfo><name type="personal"><namePart type="given">RH</namePart><namePart type="family">Miller</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Mi</namePart></name><genre>journal</genre><note>MillerRHMiSDissecting demyelinationNat Neurosci20071013514</note><relatedItem type="host"><titleInfo><title>Nat Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>1351</start><end>4</end><list>1351-4</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B92"><titleInfo><title>Regeneration of retinal axons into the goldfish optic tectum</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Murray</namePart></name><genre>journal</genre><note>MurrayMRegeneration of retinal axons into the goldfish optic tectumJ Comp Neurol197616817595</note><relatedItem type="host"><titleInfo><title>J Comp Neurol</title></titleInfo><part><date>1976</date><detail type="volume"><caption>vol.</caption><number>168</number></detail><extent unit="pages"><start>175</start><end>95</end><list>175-95</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B93"><titleInfo><title>Activation of the subventricular zone in multiple sclerosis: evidence for early glial progenitors</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Nait-Oumesmar</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Picard-Riera</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Kerninon</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Decker</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Seilhean</namePart></name><name type="personal"><namePart type="given">GU</namePart><namePart type="family">Hoglinger</namePart></name><genre>journal</genre><note>Nait-OumesmarBPicard-RieraNKerninonCDeckerLSeilheanDHoglingerGUActivation of the subventricular zone in multiple sclerosis: evidence for early glial progenitorsProc Natl Acad Sci USA200710446949</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>104</number></detail><extent unit="pages"><start>4694</start><end>9</end><list>4694-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B94"><titleInfo><title>Axonal regulation of myelination by neuregulin 1</title></titleInfo><name type="personal"><namePart type="given">KA</namePart><namePart type="family">Nave</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Salzer</namePart></name><genre>journal</genre><note>NaveKASalzerJLAxonal regulation of myelination by neuregulin 1Curr Opin Neurobiol200616492500</note><relatedItem type="host"><titleInfo><title>Curr Opin Neurobiol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>492</start><end>500</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B95"><titleInfo><title>MRI in multiple sclerosis: what's inside the toolbox?</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Neema</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Stankiewicz</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Arora</namePart></name><name type="personal"><namePart type="given">ZD</namePart><namePart type="family">Guss</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Bakshi</namePart></name><genre>journal</genre><note>NeemaMStankiewiczJAroraAGussZDBakshiRMRI in multiple sclerosis: what's inside the toolbox?Neurotherapeutics2007460217</note><relatedItem type="host"><titleInfo><title>Neurotherapeutics</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>4</number></detail><extent unit="pages"><start>602</start><end>17</end><list>602-17</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B96"><titleInfo><title>Schwann cells in the regenerating fish optic nerve: evidence that CNS axons, not the glia, determine when myelin formation begins</title></titleInfo><name type="personal"><namePart type="given">SN</namePart><namePart type="family">Nona</namePart></name><name type="personal"><namePart type="given">AM</namePart><namePart type="family">Thomlinson</namePart></name><name type="personal"><namePart type="given">CA</namePart><namePart type="family">Bartlett</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Scholes</namePart></name><genre>journal</genre><note>NonaSNThomlinsonAMBartlettCAScholesJSchwann cells in the regenerating fish optic nerve: evidence that CNS axons, not the glia, determine when myelin formation beginsJ Neurocytol200029285300</note><relatedItem type="host"><titleInfo><title>J Neurocytol</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>29</number></detail><extent unit="pages"><start>285</start><end>300</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B97"><titleInfo><title>Diffusion-tensor MR imaging and tractography: exploring brain microstructure and connectivity</title></titleInfo><name type="personal"><namePart type="given">PG</namePart><namePart type="family">Nucifora</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Verma</namePart></name><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Lee</namePart></name><name type="personal"><namePart type="given">ER</namePart><namePart type="family">Melhem</namePart></name><genre>journal</genre><note>NuciforaPGVermaRLeeSKMelhemERDiffusion-tensor MR imaging and tractography: exploring brain microstructure and connectivityRadiology200724536784</note><relatedItem type="host"><titleInfo><title>Radiology</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>245</number></detail><extent unit="pages"><start>367</start><end>84</end><list>367-84</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B98"><titleInfo><title>Identification and isolation of multipotential neural progenitor cells from the subcortical white matter of the adult human brain</title></titleInfo><name type="personal"><namePart type="given">MC</namePart><namePart type="family">Nunes</namePart></name><name type="personal"><namePart type="given">NS</namePart><namePart type="family">Roy</namePart></name><name type="personal"><namePart type="given">HM</namePart><namePart type="family">Keyoung</namePart></name><name type="personal"><namePart type="given">RR</namePart><namePart type="family">Goodman</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">McKhann II</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Jiang</namePart></name><genre>journal</genre><note>NunesMCRoyNSKeyoungHMGoodmanRRMcKhannGIIJiangLIdentification and isolation of multipotential neural progenitor cells from the subcortical white matter of the adult human brainNat Med2003943947</note><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>9</number></detail><extent unit="pages"><start>439</start><end>47</end><list>439-47</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B99"><titleInfo><title>CXC chemokine receptors on human oligodendrocytes: implications for multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">KM</namePart><namePart type="family">Omari</namePart></name><name type="personal"><namePart type="given">GR</namePart><namePart type="family">John</namePart></name><name type="personal"><namePart type="given">SC</namePart><namePart type="family">Sealfon</namePart></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Raine</namePart></name><genre>journal</genre><note>OmariKMJohnGRSealfonSCRaineCSCXC chemokine receptors on human oligodendrocytes: implications for multiple sclerosisBrain2005128100315</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>128</number></detail><extent unit="pages"><start>1003</start><end>15</end><list>1003-15</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B100"><titleInfo><title>Alterations in the oligodendrocyte lineage, myelin, and white matter in adult mice lacking the chemokine receptor CXCR2</title></titleInfo><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Padovani-Claudio</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Liu</namePart></name><name type="personal"><namePart type="given">RM</namePart><namePart type="family">Ransohoff</namePart></name><name type="personal"><namePart type="given">RH</namePart><namePart type="family">Miller</namePart></name><genre>journal</genre><note>Padovani-ClaudioDALiuLRansohoffRMMillerRHAlterations in the oligodendrocyte lineage, myelin, and white matter in adult mice lacking the chemokine receptor CXCR2Glia20065447183</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><extent unit="pages"><start>471</start><end>83</end><list>471-83</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B101"><titleInfo><title>Exacerbations of multiple sclerosis in patients treated with gamma interferon</title></titleInfo><name type="personal"><namePart type="given">HS</namePart><namePart type="family">Panitch</namePart></name><name type="personal"><namePart type="given">RL</namePart><namePart type="family">Hirsch</namePart></name><name type="personal"><namePart type="given">AS</namePart><namePart type="family">Haley</namePart></name><name type="personal"><namePart type="given">KP</namePart><namePart type="family">Johnson</namePart></name><genre>journal</genre><note>PanitchHSHirschRLHaleyASJohnsonKPExacerbations of multiple sclerosis in patients treated with gamma interferonLancet198718935</note><relatedItem type="host"><titleInfo><title>Lancet</title></titleInfo><part><date>1987</date><detail type="volume"><caption>vol.</caption><number>1</number></detail><extent unit="pages"><start>893</start><end>5</end><list>893-5</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B102"><titleInfo><title>Remyelination can be extensive in multiple sclerosis despite a long disease course</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Patani</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Balaratnam</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Vora</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Reynolds</namePart></name><genre>journal</genre><note>PataniRBalaratnamMVoraAReynoldsRRemyelination can be extensive in multiple sclerosis despite a long disease courseNeuropathol Appl Neurobiol20073327787</note><relatedItem type="host"><titleInfo><title>Neuropathol Appl Neurobiol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>33</number></detail><extent unit="pages"><start>277</start><end>87</end><list>277-87</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B103"><titleInfo><title>Remyelination is extensive in a subset of multiple sclerosis patients</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Patrikios</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Stadelmann</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Kutzelnigg</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Rauschka</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schmidbauer</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">Laursen</namePart></name><genre>journal</genre><note>PatrikiosPStadelmannCKutzelniggARauschkaHSchmidbauerMLaursenHRemyelination is extensive in a subset of multiple sclerosis patientsBrain2006129316572</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>3165</start><end>72</end><list>3165-72</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B104"><titleInfo><title>Transplantation of Schwann cells and/or olfactory ensheathing glia into the contused spinal cord: survival, migration, axon association, and functional recovery</title></titleInfo><name type="personal"><namePart type="given">DD</namePart><namePart type="family">Pearse</namePart></name><name type="personal"><namePart type="given">AR</namePart><namePart type="family">Sanchez</namePart></name><name type="personal"><namePart type="given">FC</namePart><namePart type="family">Pereira</namePart></name><name type="personal"><namePart type="given">CM</namePart><namePart type="family">Andrade</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Puzis</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Pressman</namePart></name><genre>journal</genre><note>PearseDDSanchezARPereiraFCAndradeCMPuzisRPressmanYTransplantation of Schwann cells and/or olfactory ensheathing glia into the contused spinal cord: survival, migration, axon association, and functional recoveryGlia2007559761000</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>976</start><end>1000</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B105"><titleInfo><title>Electron microscopic features of multiple sclerosis lesions</title></titleInfo><name type="personal"><namePart type="given">O</namePart><namePart type="family">Perier</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Gregoire</namePart></name><genre>journal</genre><note>PerierOGregoireAElectron microscopic features of multiple sclerosis lesionsBrain19658893752</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>1965</date><detail type="volume"><caption>vol.</caption><number>88</number></detail><extent unit="pages"><start>937</start><end>52</end><list>937-52</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B106"><titleInfo><title>Lymphotoxin beta receptor (Lt betaR): dual roles in demyelination and remyelination and successful therapeutic intervention using Lt betaR-Ig protein</title></titleInfo><name type="personal"><namePart type="given">SR</namePart><namePart type="family">Plant</namePart></name><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Iocca</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wang</namePart></name><name type="personal"><namePart type="given">JC</namePart><namePart type="family">Thrash</namePart></name><name type="personal"><namePart type="given">BP</namePart><namePart type="family">O’Connor</namePart></name><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Arnett</namePart></name><genre>journal</genre><note>PlantSRIoccaHAWangYThrashJCO’ConnorBPArnettHALymphotoxin beta receptor (Lt betaR): dual roles in demyelination and remyelination and successful therapeutic intervention using Lt betaR-Ig proteinJ Neurosci200727742937</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>7429</start><end>37</end><list>7429-37</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B107"><titleInfo><title>A genetic screen identifies genes essential for development of myelinated axons in zebrafish</title></titleInfo><name type="personal"><namePart type="given">HM</namePart><namePart type="family">Pogoda</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Sternheim</namePart></name><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Lyons</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Diamond</namePart></name><name type="personal"><namePart type="given">TA</namePart><namePart type="family">Hawkins</namePart></name><name type="personal"><namePart type="given">IG</namePart><namePart type="family">Woods</namePart></name><genre>journal</genre><note>PogodaHMSternheimNLyonsDADiamondBHawkinsTAWoodsIGA genetic screen identifies genes essential for development of myelinated axons in zebrafishDev Biol200629811831</note><relatedItem type="host"><titleInfo><title>Dev Biol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>298</number></detail><extent unit="pages"><start>118</start><end>31</end><list>118-31</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B108"><titleInfo><title>Effectors of demyelination and remyelination in the CNS: implications for multiple sclerosis</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Rodriguez</namePart></name><genre>journal</genre><note>RodriguezMEffectors of demyelination and remyelination in the CNS: implications for multiple sclerosisBrain Pathol20071721929</note><relatedItem type="host"><titleInfo><title>Brain Pathol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>219</start><end>29</end><list>219-29</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B109"><titleInfo><title>From neural stem cells to myelinating oligodendrocytes</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Rogister</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Ben-Hur</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><genre>journal</genre><note>RogisterBBen-HurTDubois-DalcqMFrom neural stem cells to myelinating oligodendrocytesMol Cell Neurosci199914287300</note><relatedItem type="host"><titleInfo><title>Mol Cell Neurosci</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>14</number></detail><extent unit="pages"><start>287</start><end>300</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B110"><titleInfo><title>Spinal cord injury: time to move?</title></titleInfo><name type="personal"><namePart type="given">S</namePart><namePart type="family">Rossignol</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schwab</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schwartz</namePart></name><name type="personal"><namePart type="given">MG</namePart><namePart type="family">Fehlings</namePart></name><genre>journal</genre><note>RossignolSSchwabMSchwartzMFehlingsMGSpinal cord injury: time to move?J Neurosci2007271178292</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>27</number></detail><extent unit="pages"><start>11782</start><end>92</end><list>11782-92</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B111"><titleInfo><title>Production of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulins</title></titleInfo><name type="personal"><namePart type="given">P</namePart><namePart type="family">Sarchielli</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Zaffaroni</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Floridi</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Greco</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Candeliere</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Mattioni</namePart></name><genre>journal</genre><note>SarchielliPZaffaroniMFloridiAGrecoLCandeliereAMattioniAProduction of brain-derived neurotrophic factor by mononuclear cells of patients with multiple sclerosis treated with glatiramer acetate, interferon-beta 1a, and high doses of immunoglobulinsMult Scler20071331331</note><relatedItem type="host"><titleInfo><title>Mult Scler</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>313</start><end>31</end><list>313-31</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B112"><titleInfo><title>Molecular reconstruction of nodes of Ranvier after remyelination by transplanted olfactory ensheathing cells in the demyelinated spinal cord</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Sasaki</namePart></name><name type="personal"><namePart type="given">JA</namePart><namePart type="family">Black</namePart></name><name type="personal"><namePart type="given">KL</namePart><namePart type="family">Lankford</namePart></name><name type="personal"><namePart type="given">HA</namePart><namePart type="family">Tokuno</namePart></name><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Waxman</namePart></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Kocsis</namePart></name><genre>journal</genre><note>SasakiMBlackJALankfordKLTokunoHAWaxmanSGKocsisJDMolecular reconstruction of nodes of Ranvier after remyelination by transplanted olfactory ensheathing cells in the demyelinated spinal cordJ Neurosci200626180312</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><extent unit="pages"><start>1803</start><end>12</end><list>1803-12</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B113"><titleInfo><title>Early events in node of Ranvier formation during myelination and remyelination in the PNS</title></titleInfo><name type="personal"><namePart type="given">DP</namePart><namePart type="family">Schafer</namePart></name><name type="personal"><namePart type="given">AW</namePart><namePart type="family">Custer</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Shrager</namePart></name><name type="personal"><namePart type="given">MN</namePart><namePart type="family">Rasband</namePart></name><genre>journal</genre><note>SchaferDPCusterAWShragerPRasbandMNEarly events in node of Ranvier formation during myelination and remyelination in the PNSNeuron Glia Biol200626979</note><relatedItem type="host"><titleInfo><title>Neuron Glia Biol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>2</number></detail><extent unit="pages"><start>69</start><end>79</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B114"><titleInfo><title>Progesterone: therapeutic opportunities for neuroprotection and myelin repair</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schumacher</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Guennon</namePart></name><name type="personal"><namePart type="given">DG</namePart><namePart type="family">Stein</namePart></name><name type="personal"><namePart type="given">EF</namePart><namePart type="family">De Nicola</namePart></name><genre>journal</genre><note>SchumacherMGuennonRSteinDGDe NicolaEFProgesterone: therapeutic opportunities for neuroprotection and myelin repairPharmacol Ther200711677106</note><relatedItem type="host"><titleInfo><title>Pharmacol Ther</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>116</number></detail><extent unit="pages"><start>77</start><end>106</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B115"><titleInfo><title>The Nogo receptor complex: confining molecules to molecular mechanisms</title></titleInfo><name type="personal"><namePart type="given">JM</namePart><namePart type="family">Schwab</namePart></name><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Tuli</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Failli</namePart></name><genre>journal</genre><note>SchwabJMTuliSKFailliVThe Nogo receptor complex: confining molecules to molecular mechanismsTrends Mol Med2006122937</note><relatedItem type="host"><titleInfo><title>Trends Mol Med</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>12</number></detail><extent unit="pages"><start>293</start><end>7</end><list>293-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B116"><titleInfo><title>Expression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafish</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Schweitzer</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Becker</namePart></name><name type="personal"><namePart type="given">CG</namePart><namePart type="family">Becker</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Schachner</namePart></name><genre>journal</genre><note>SchweitzerJBeckerTBeckerCGSchachnerMExpression of protein zero is increased in lesioned axon pathways in the central nervous system of adult zebrafishGlia20034130117</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>41</number></detail><extent unit="pages"><start>301</start><end>17</end><list>301-17</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B117"><titleInfo><title>Moving toward remyelinating and neuroprotective therapies in multiple Sclerosis</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Scolding</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Dubois-Dalcq</namePart></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Raine</namePart></name><name type="personal"><namePart type="given">H</namePart><namePart type="family">McFarland</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Hohlfeld</namePart></name><genre>book</genre><note>in press</note><note>ScoldingNDubois-DalcqMRaineCSMcFarlandHHohlfeldRMoving toward remyelinating and neuroprotective therapies in multiple SclerosisMultiple Sclerosis, A Comprehensive Text2008Elsevier B.Vin press</note><relatedItem type="host"><titleInfo><title>Multiple Sclerosis, A Comprehensive Text</title></titleInfo><originInfo><publisher>Elsevier B.V. </publisher></originInfo><part><date>2008</date></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B118"><titleInfo><title>Notch1 and its ligand Jagged1 are present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelination</title></titleInfo><name type="personal"><namePart type="given">T</namePart><namePart type="family">Seifert</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Bauer</namePart></name><name type="personal"><namePart type="given">R</namePart><namePart type="family">Weissert</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Fazekas</namePart></name><name type="personal"><namePart type="given">MK</namePart><namePart type="family">Storch</namePart></name><genre>journal</genre><note>SeifertTBauerJWeissertRFazekasFStorchMKNotch1 and its ligand Jagged1 are present in remyelination in a T-cell- and antibody-mediated model of inflammatory demyelinationActa Neuropathol2007113195203</note><relatedItem type="host"><titleInfo><title>Acta Neuropathol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>113</number></detail><extent unit="pages"><start>195</start><end>203</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B119"><titleInfo><title>Inflammation stimulates myelination by transplanted oligodendrocyte precursor cells</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Setzu</namePart></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Lathia</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Wells</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Rao</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Ffrench-Constant</namePart></name><genre>journal</genre><note>SetzuALathiaJDZhaoCWellsKRaoMSFfrench-ConstantCInflammation stimulates myelination by transplanted oligodendrocyte precursor cellsGlia200654297303</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><extent unit="pages"><start>297</start><end>303</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B120"><titleInfo><title>A ‘GAG’ reflex prevents repair of the damaged CNS</title></titleInfo><name type="personal"><namePart type="given">LS</namePart><namePart type="family">Sherman</namePart></name><name type="personal"><namePart type="given">SA</namePart><namePart type="family">Back</namePart></name><genre>journal</genre><note>ShermanLSBackSAA ‘GAG’ reflex prevents repair of the damaged CNSTrends Neurosci2008314452</note><relatedItem type="host"><titleInfo><title>Trends Neurosci</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>31</number></detail><extent unit="pages"><start>44</start><end>52</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B121"><titleInfo><title>Complementary patterns of gene expression by human oligodendrocyte progenitors and their environment predict determinants of progenitor maintenance and differentiation</title></titleInfo><name type="personal"><namePart type="given">FJ</namePart><namePart type="family">Sim</namePart></name><name type="personal"><namePart type="given">JK</namePart><namePart type="family">Lang</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Waldau</namePart></name><name type="personal"><namePart type="given">NS</namePart><namePart type="family">Roy</namePart></name><name type="personal"><namePart type="given">TE</namePart><namePart type="family">Schwartz</namePart></name><name type="personal"><namePart type="given">WH</namePart><namePart type="family">Pilcher</namePart></name><genre>journal</genre><note>SimFJLangJKWaldauBRoyNSSchwartzTEPilcherWHComplementary patterns of gene expression by human oligodendrocyte progenitors and their environment predict determinants of progenitor maintenance and differentiationAnn Neurol20065976379</note><relatedItem type="host"><titleInfo><title>Ann Neurol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>59</number></detail><extent unit="pages"><start>763</start><end>79</end><list>763-79</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B122"><titleInfo><title>The age-related decrease in CNS remyelination efficiency is attributable to an impairment of both oligodendrocyte progenitor recruitment and differentiation</title></titleInfo><name type="personal"><namePart type="given">FJ</namePart><namePart type="family">Sim</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Penderis</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>SimFJZhaoCPenderisJFranklinRJThe age-related decrease in CNS remyelination efficiency is attributable to an impairment of both oligodendrocyte progenitor recruitment and differentiationJ Neurosci20022224519</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>2451</start><end>9</end><list>2451-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B123"><titleInfo><title>Axonal protection in multiple sclerosis – a particular need during remyelination?</title></titleInfo><name type="personal"><namePart type="given">KJ</namePart><namePart type="family">Smith</namePart></name><genre>journal</genre><note>SmithKJAxonal protection in multiple sclerosis – a particular need during remyelination?Brain200612931479</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>129</number></detail><extent unit="pages"><start>3147</start><end>9</end><list>3147-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B124"><titleInfo><title>Dysmyelination revealed through MRI as increased radial (but unchanged axial) diffusion of water</title></titleInfo><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Song</namePart></name><name type="personal"><namePart type="given">SW</namePart><namePart type="family">Sun</namePart></name><name type="personal"><namePart type="given">MJ</namePart><namePart type="family">Ramsbottom</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Chang</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Russell</namePart></name><name type="personal"><namePart type="given">AH</namePart><namePart type="family">Cross</namePart></name><genre>journal</genre><note>SongSKSunSWRamsbottomMJChangCRussellJCrossAHDysmyelination revealed through MRI as increased radial (but unchanged axial) diffusion of waterNeuroimage200217142936</note><relatedItem type="host"><titleInfo><title>Neuroimage</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>1429</start><end>36</end><list>1429-36</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B125"><titleInfo><title>Demyelination increases radial diffusivity in corpus callosum of mouse brain</title></titleInfo><name type="personal"><namePart type="given">SK</namePart><namePart type="family">Song</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Yoshino</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Lin</namePart></name><name type="personal"><namePart type="given">SW</namePart><namePart type="family">Sun</namePart></name><name type="personal"><namePart type="given">AH</namePart><namePart type="family">Cross</namePart></name><genre>journal</genre><note>SongSKYoshinoJLeTQLinSJSunSWCrossAHDemyelination increases radial diffusivity in corpus callosum of mouse brainNeuroimage20052613240</note><relatedItem type="host"><titleInfo><title>Neuroimage</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><extent unit="pages"><start>132</start><end>40</end><list>132-40</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B126"><titleInfo><title>Directional guidance of oligodendroglial migration by class 3 semaphorins and netrin-1</title></titleInfo><name type="personal"><namePart type="given">N</namePart><namePart type="family">Spassky</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">de Castro</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Le Bras</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Heydon</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Queraud-LeSaux</namePart></name><name type="personal"><namePart type="given">E</namePart><namePart type="family">Bloch-Gallego</namePart></name><genre>journal</genre><note>SpasskyNde CastroFLe BrasBHeydonKQueraud-LeSauxFBloch-GallegoEDirectional guidance of oligodendroglial migration by class 3 semaphorins and netrin-1J Neurosci20022259926004</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>5992</start><end>6004</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B127"><titleInfo><title>Ciliary neurotrophic factor (CNTF) enhances myelin formation: a novel role for CNTF and CNTF-related molecules</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stankoff</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Noel</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Wattilliaux</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Lubetzki</namePart></name><genre>journal</genre><note>StankoffBAigrotMSNoelFWattilliauxAZalcBLubetzkiCCiliary neurotrophic factor (CNTF) enhances myelin formation: a novel role for CNTF and CNTF-related moleculesJ Neurosci20022292217</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>22</number></detail><extent unit="pages"><start>9221</start><end>7</end><list>9221-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B128"><titleInfo><title>Imaging of CNS myelin by positron-emission tomography</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stankoff</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wang</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Bottlaender</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Dolle</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Wu</namePart></name><genre>journal</genre><note>StankoffBWangYBottlaenderMAigrotMSDolleFWuCImaging of CNS myelin by positron-emission tomographyProc Natl Acad Sci USA200610393049</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>103</number></detail><extent unit="pages"><start>9304</start><end>9</end><list>9304-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B129"><titleInfo><title>Adenosine: a neuron-glial transmitter promoting myelination in the CNS in response to action potentials</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Stevens</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Porta</namePart></name><name type="personal"><namePart type="given">LL</namePart><namePart type="family">Haak</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Gallo</namePart></name><name type="personal"><namePart type="given">RD</namePart><namePart type="family">Fields</namePart></name><genre>journal</genre><note>StevensBPortaSHaakLLGalloVFieldsRDAdenosine: a neuron-glial transmitter promoting myelination in the CNS in response to action potentialsNeuron20023685568</note><relatedItem type="host"><titleInfo><title>Neuron</title></titleInfo><part><date>2002</date><detail type="volume"><caption>vol.</caption><number>36</number></detail><extent unit="pages"><start>855</start><end>68</end><list>855-68</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B130"><titleInfo><title>Type III neuregulin-1 promotes oligodendrocyte myelination</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Taveggia</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Thaker</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Petrylak</namePart></name><name type="personal"><namePart type="given">GL</namePart><namePart type="family">Caporaso</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Toews</namePart></name><name type="personal"><namePart type="given">DL</namePart><namePart type="family">Falls</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Einheber</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Salzer</namePart></name><genre>journal</genre><note>TaveggiaCThakerPPetrylakACaporasoGLToewsAFallsDLEinheberSSalzerJLType III neuregulin-1 promotes oligodendrocyte myelinationGlia20085628493</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>56</number></detail><extent unit="pages"><start>284</start><end>93</end><list>284-93</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B131"><titleInfo><title>Correlation of apparent myelin measures obtained in multiple sclerosis patients and controls from magnetization transfer and multicompartmental T2 analysis</title></titleInfo><name type="personal"><namePart type="given">DJ</namePart><namePart type="family">Tozer</namePart></name><name type="personal"><namePart type="given">GR</namePart><namePart type="family">Davies</namePart></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Altmann</namePart></name><name type="personal"><namePart type="given">DH</namePart><namePart type="family">Miller</namePart></name><name type="personal"><namePart type="given">PS</namePart><namePart type="family">Tofts</namePart></name><genre>journal</genre><note>TozerDJDaviesGRAltmannDRMillerDHToftsPSCorrelation of apparent myelin measures obtained in multiple sclerosis patients and controls from magnetization transfer and multicompartmental T2 analysisMagn Reson Med200553141522</note><relatedItem type="host"><titleInfo><title>Magn Reson Med</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><extent unit="pages"><start>1415</start><end>22</end><list>1415-22</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B132"><titleInfo><title>Optic nerve magnetization transfer imaging and measures of axonal loss and demyelination in optic neuritis</title></titleInfo><name type="personal"><namePart type="given">SA</namePart><namePart type="family">Trip</namePart></name><name type="personal"><namePart type="given">PG</namePart><namePart type="family">Schlottmann</namePart></name><name type="personal"><namePart type="given">SJ</namePart><namePart type="family">Jones</namePart></name><name type="personal"><namePart type="given">WY</namePart><namePart type="family">Li</namePart></name><name type="personal"><namePart type="given">DF</namePart><namePart type="family">Garway-Heath</namePart></name><name type="personal"><namePart type="given">AJ</namePart><namePart type="family">Thompson</namePart></name><genre>journal</genre><note>TripSASchlottmannPGJonesSJLiWYGarway-HeathDFThompsonAJOptic nerve magnetization transfer imaging and measures of axonal loss and demyelination in optic neuritisMult Scler2007138759</note><relatedItem type="host"><titleInfo><title>Mult Scler</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>875</start><end>9</end><list>875-9</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B133"><titleInfo><title>Transplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient rat</title></titleInfo><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Utzschneider</namePart></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Archer</namePart></name><name type="personal"><namePart type="given">JD</namePart><namePart type="family">Kocsis</namePart></name><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Waxman</namePart></name><name type="personal"><namePart type="given">ID</namePart><namePart type="family">Duncan</namePart></name><genre>journal</genre><note>UtzschneiderDAArcherDRKocsisJDWaxmanSGDuncanIDTransplantation of glial cells enhances action potential conduction of amyelinated spinal cord axons in the myelin-deficient ratProc Natl Acad Sci USA199491537</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>1994</date><detail type="volume"><caption>vol.</caption><number>91</number></detail><extent unit="pages"><start>53</start><end>7</end><list>53-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B134"><titleInfo><title>Platelet-derived growth factor promotes repair of chronically demyelinated white matter</title></titleInfo><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Vana</namePart></name><name type="personal"><namePart type="given">NC</namePart><namePart type="family">Flint</namePart></name><name type="personal"><namePart type="given">NE</namePart><namePart type="family">Harwood</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Fruttiger</namePart></name><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Armstrong</namePart></name><genre>journal</genre><note>VanaACFlintNCHarwoodNELeTQFruttigerMArmstrongRCPlatelet-derived growth factor promotes repair of chronically demyelinated white matterJ Neuropathol Exp Neurol20076697588</note><relatedItem type="host"><titleInfo><title>J Neuropathol Exp Neurol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>66</number></detail><extent unit="pages"><start>975</start><end>88</end><list>975-88</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B135"><titleInfo><title>Myelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNS</title></titleInfo><name type="personal"><namePart type="given">AC</namePart><namePart type="family">Vana</namePart></name><name type="personal"><namePart type="given">CF</namePart><namePart type="family">Lucchinetti</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Armstrong</namePart></name><genre>journal</genre><note>VanaACLucchinettiCFLeTQArmstrongRCMyelin transcription factor 1 (Myt1) expression in demyelinated lesions of rodent and human CNSGlia20075568797</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>55</number></detail><extent unit="pages"><start>687</start><end>97</end><list>687-97</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B136"><titleInfo><title>Leukemia inhibitory factor is produced by myelin-reactive T cells from multiple sclerosis patients and protects against tumor necrosis factor-alpha-induced oligodendrocyte apoptosis</title></titleInfo><name type="personal"><namePart type="given">J</namePart><namePart type="family">Vanderlocht</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Hellings</namePart></name><name type="personal"><namePart type="given">JJ</namePart><namePart type="family">Hendriks</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Vandenabeele</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Moreels</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Buntinx</namePart></name><genre>journal</genre><note>VanderlochtJHellingsNHendriksJJVandenabeeleFMoreelsMBuntinxMLeukemia inhibitory factor is produced by myelin-reactive T cells from multiple sclerosis patients and protects against tumor necrosis factor-alpha-induced oligodendrocyte apoptosisJ Neurosci Res20068376374</note><relatedItem type="host"><titleInfo><title>J Neurosci Res</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>83</number></detail><extent unit="pages"><start>763</start><end>74</end><list>763-74</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B137"><titleInfo><title>alphaII-spectrin is essential for assembly of the nodes of Ranvier in myelinated axons</title></titleInfo><name type="personal"><namePart type="given">MG</namePart><namePart type="family">Voas</namePart></name><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Lyons</namePart></name><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Naylor</namePart></name><name type="personal"><namePart type="given">N</namePart><namePart type="family">Arana</namePart></name><name type="personal"><namePart type="given">MN</namePart><namePart type="family">Rasband</namePart></name><name type="personal"><namePart type="given">WS</namePart><namePart type="family">Talbot</namePart></name><genre>journal</genre><note>VoasMGLyonsDANaylorSGAranaNRasbandMNTalbotWSalphaII-spectrin is essential for assembly of the nodes of Ranvier in myelinated axonsCurr Biol2007175628</note><relatedItem type="host"><titleInfo><title>Curr Biol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>17</number></detail><extent unit="pages"><start>562</start><end>8</end><list>562-8</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B138"><titleInfo><title>The see-through medaka: a fish model that is transparent throughout life</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Wakamatsu</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Pristyazhnyuk</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Kinoshita</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Tanaka</namePart></name><name type="personal"><namePart type="given">K</namePart><namePart type="family">Ozato</namePart></name><genre>journal</genre><note>WakamatsuYPristyazhnyukSKinoshitaMTanakaMOzatoKThe see-through medaka: a fish model that is transparent throughout lifeProc Natl Acad Sci USA2001981004650</note><relatedItem type="host"><titleInfo><title>Proc Natl Acad Sci USA</title></titleInfo><part><date>2001</date><detail type="volume"><caption>vol.</caption><number>98</number></detail><extent unit="pages"><start>10046</start><end>50</end><list>10046-50</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B139"><titleInfo><title>Axonal conduction and injury in multiple sclerosis: the role of sodium channels</title></titleInfo><name type="personal"><namePart type="given">SG</namePart><namePart type="family">Waxman</namePart></name><genre>journal</genre><note>WaxmanSGAxonal conduction and injury in multiple sclerosis: the role of sodium channelsNat Rev Neurosci2006793241</note><relatedItem type="host"><titleInfo><title>Nat Rev Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>7</number></detail><extent unit="pages"><start>932</start><end>41</end><list>932-41</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B140"><titleInfo><title>Semaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Williams</namePart></name><name type="personal"><namePart type="given">G</namePart><namePart type="family">Piaton</namePart></name><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Aigrot</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Belhadi</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Theaudin</namePart></name><name type="personal"><namePart type="given">F</namePart><namePart type="family">Petermann</namePart></name><genre>journal</genre><note>WilliamsAPiatonGAigrotMSBelhadiATheaudinMPetermannFSemaphorin 3A and 3F: key players in myelin repair in multiple sclerosis?Brain2007130255465</note><relatedItem type="host"><titleInfo><title>Brain</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>130</number></detail><extent unit="pages"><start>2554</start><end>65</end><list>2554-65</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B141"><titleInfo><title>Fetal and adult human oligodendrocyte progenitor cell isolates myelinate the congenitally dysmyelinated brain</title></titleInfo><name type="personal"><namePart type="given">MS</namePart><namePart type="family">Windrem</namePart></name><name type="personal"><namePart type="given">MC</namePart><namePart type="family">Nunes</namePart></name><name type="personal"><namePart type="given">WK</namePart><namePart type="family">Rashbaum</namePart></name><name type="personal"><namePart type="given">TH</namePart><namePart type="family">Schwartz</namePart></name><name type="personal"><namePart type="given">RA</namePart><namePart type="family">Goodman</namePart></name><name type="personal"><namePart type="given">2nd</namePart><namePart type="family">McKhann G</namePart></name><genre>journal</genre><note>WindremMSNunesMCRashbaumWKSchwartzTHGoodmanRAMcKhann G2ndFetal and adult human oligodendrocyte progenitor cell isolates myelinate the congenitally dysmyelinated brainNat Med200410937</note><relatedItem type="host"><titleInfo><title>Nat Med</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>10</number></detail><extent unit="pages"><start>93</start><end>7</end><list>93-7</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B142"><titleInfo><title>Myelination and remyelination in the regenerating visual system of the goldfish</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Wolburg</namePart></name><genre>journal</genre><note>WolburgHMyelination and remyelination in the regenerating visual system of the goldfishExp Brain Res198143199206</note><relatedItem type="host"><titleInfo><title>Exp Brain Res</title></titleInfo><part><date>1981</date><detail type="volume"><caption>vol.</caption><number>43</number></detail><extent unit="pages"><start>199</start><end>206</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B143"><titleInfo><title>Demyelination and remyelination of the caudal cerebellar peduncle of adult rats following stereotaxic injections of lysolecithin, ethidium bromide, and complement/anti-galactocerebroside: a comparative study</title></titleInfo><name type="personal"><namePart type="given">RH</namePart><namePart type="family">Woodruff</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>WoodruffRHFranklinRJDemyelination and remyelination of the caudal cerebellar peduncle of adult rats following stereotaxic injections of lysolecithin, ethidium bromide, and complement/anti-galactocerebroside: a comparative studyGlia19992521628</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>1999</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><extent unit="pages"><start>216</start><end>28</end><list>216-28</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B144"><titleInfo><title>nsf is essential for organization of myelinated axons in zebrafish</title></titleInfo><name type="personal"><namePart type="given">IG</namePart><namePart type="family">Woods</namePart></name><name type="personal"><namePart type="given">DA</namePart><namePart type="family">Lyons</namePart></name><name type="personal"><namePart type="given">MG</namePart><namePart type="family">Voas</namePart></name><name type="personal"><namePart type="given">HM</namePart><namePart type="family">Pogoda</namePart></name><name type="personal"><namePart type="given">WS</namePart><namePart type="family">Talbot</namePart></name><genre>journal</genre><note>WoodsIGLyonsDAVoasMGPogodaHMTalbotWSnsf is essential for organization of myelinated axons in zebrafishCurr Biol20061663648</note><relatedItem type="host"><titleInfo><title>Curr Biol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><extent unit="pages"><start>636</start><end>48</end><list>636-48</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B145"><titleInfo><title>A novel fluorescent probe that is brain permeable and selectively binds to myelin</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Wu</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Tian</namePart></name><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Feng</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Polak</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Wei</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Sharp</namePart></name><genre>journal</genre><note>WuCTianDFengYPolakPWeiJSharpAA novel fluorescent probe that is brain permeable and selectively binds to myelinJ Histochem Cytochem2006549971004</note><relatedItem type="host"><titleInfo><title>J Histochem Cytochem</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><extent unit="pages"><start>997</start><end>1004</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B146"><titleInfo><title>Detection of myelination using a novel histological probe</title></titleInfo><name type="personal"><namePart type="given">Z</namePart><namePart type="family">Xiang</namePart></name><name type="personal"><namePart type="given">EE</namePart><namePart type="family">Nesterov</namePart></name><name type="personal"><namePart type="given">J</namePart><namePart type="family">Skoch</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Lin</namePart></name><name type="personal"><namePart type="given">BT</namePart><namePart type="family">Hyman</namePart></name><name type="personal"><namePart type="given">TM</namePart><namePart type="family">Swager</namePart></name><genre>journal</genre><note>XiangZNesterovEESkochJLinTHymanBTSwagerTMDetection of myelination using a novel histological probeJ Histochem Cytochem20055315116</note><relatedItem type="host"><titleInfo><title>J Histochem Cytochem</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>53</number></detail><extent unit="pages"><start>1511</start><end>6</end><list>1511-6</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B147"><titleInfo><title>The acquisition of myelin: a success story.</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><genre>journal</genre><note>discussion 21–5, 54–7, 275–81</note><note>ZalcBThe acquisition of myelin: a success story.Novartis Found Symp20062761521discussion 21–5, 54–7, 275–81</note><relatedItem type="host"><titleInfo><title>Novartis Found Symp</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>276</number></detail><extent unit="pages"><start>15</start><end>21</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B148"><titleInfo><title>Origin of vertebrate success</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Colman</namePart></name><genre>journal</genre><note>ZalcBColmanDROrigin of vertebrate successScience20002882712</note><relatedItem type="host"><titleInfo><title>Science</title></titleInfo><part><date>2000</date><detail type="volume"><caption>vol.</caption><number>288</number></detail><extent unit="pages"><start>271</start><end>2</end><list>271-2</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B149"><titleInfo><title>The origin of the myelination program in vertebrates</title></titleInfo><name type="personal"><namePart type="given">B</namePart><namePart type="family">Zalc</namePart></name><name type="personal"><namePart type="given">D</namePart><namePart type="family">Goujet</namePart></name><name type="personal"><namePart type="given">DR</namePart><namePart type="family">Colman</namePart></name><genre>journal</genre><note>in press</note><note>ZalcBGoujetDColmanDRThe origin of the myelination program in vertebratesCurrent Biol2008in press</note><relatedItem type="host"><titleInfo><title>Current Biol</title></titleInfo><part><date>2008</date></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B150"><titleInfo><title>Ontogeny of the immune system of fish</title></titleInfo><name type="personal"><namePart type="given">A</namePart><namePart type="family">Zapata</namePart></name><name type="personal"><namePart type="given">B</namePart><namePart type="family">Diez</namePart></name><name type="personal"><namePart type="given">T</namePart><namePart type="family">Cejalvo</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Gutierrez-de Frias</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Cortes</namePart></name><genre>journal</genre><note>ZapataADiezBCejalvoTGutierrez-de FriasCCortesAOntogeny of the immune system of fishFish Shellfish Immunol20062012636</note><relatedItem type="host"><titleInfo><title>Fish Shellfish Immunol</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>126</start><end>36</end><list>126-36</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B151"><titleInfo><title>Myelin regeneration in demyelinating disorders: new developments in biology and clinical pathology</title></titleInfo><name type="personal"><namePart type="given">M</namePart><namePart type="family">Zawadzka</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>ZawadzkaMFranklinRJMyelin regeneration in demyelinating disorders: new developments in biology and clinical pathologyCurr Opin Neurol2007202948</note><relatedItem type="host"><titleInfo><title>Curr Opin Neurol</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><extent unit="pages"><start>294</start><end>8</end><list>294-8</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B152"><titleInfo><title>A role for the polysialic acid-neural cell adhesion molecule in PDGF-induced chemotaxis of oligodendrocyte precursor cells</title></titleInfo><name type="personal"><namePart type="given">H</namePart><namePart type="family">Zhang</namePart></name><name type="personal"><namePart type="given">L</namePart><namePart type="family">Vutskits</namePart></name><name type="personal"><namePart type="given">V</namePart><namePart type="family">Calaora</namePart></name><name type="personal"><namePart type="given">P</namePart><namePart type="family">Durbec</namePart></name><name type="personal"><namePart type="given">JZ</namePart><namePart type="family">Kiss</namePart></name><genre>journal</genre><note>ZhangHVutskitsLCalaoraVDurbecPKissJZA role for the polysialic acid-neural cell adhesion molecule in PDGF-induced chemotaxis of oligodendrocyte precursor cellsJ Cell Sci200411793103</note><relatedItem type="host"><titleInfo><title>J Cell Sci</title></titleInfo><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>117</number></detail><extent unit="pages"><start>93</start><end>103</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B153"><titleInfo><title>Interleukin-11 potentiates oligodendrocyte survival and maturation, and myelin formation</title></titleInfo><name type="personal"><namePart type="given">Y</namePart><namePart type="family">Zhang</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Taveggia</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Melendez-Vasquez</namePart></name><name type="personal"><namePart type="given">S</namePart><namePart type="family">Einheber</namePart></name><name type="personal"><namePart type="given">CS</namePart><namePart type="family">Raine</namePart></name><name type="personal"><namePart type="given">JL</namePart><namePart type="family">Salzer</namePart></name><genre>journal</genre><note>ZhangYTaveggiaCMelendez-VasquezCEinheberSRaineCSSalzerJLInterleukin-11 potentiates oligodendrocyte survival and maturation, and myelin formationJ Neurosci2006261217485</note><relatedItem type="host"><titleInfo><title>J Neurosci</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><extent unit="pages"><start>12174</start><end>85</end><list>12174-85</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B154"><titleInfo><title>Mechanisms of CNS remyelination – the key to therapeutic advances</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">SP</namePart><namePart type="family">Fancy</namePart></name><name type="personal"><namePart type="given">MR</namePart><namePart type="family">Kotter</namePart></name><name type="personal"><namePart type="given">WW</namePart><namePart type="family">Li</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>ZhaoCFancySPKotterMRLiWWFranklinRJMechanisms of CNS remyelination – the key to therapeutic advancesJ Neurol Sci20052338791</note><relatedItem type="host"><titleInfo><title>J Neurol Sci</title></titleInfo><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>233</number></detail><extent unit="pages"><start>87</start><end>91</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B155"><titleInfo><title>Promoting remyelination in multiple sclerosis by endogenous adult neural stem/precursor cells: defining cellular targets</title></titleInfo><name type="personal"><namePart type="given">C</namePart><namePart type="family">Zhao</namePart></name><name type="personal"><namePart type="given">M</namePart><namePart type="family">Zawadzka</namePart></name><name type="personal"><namePart type="given">AJ</namePart><namePart type="family">Roulois</namePart></name><name type="personal"><namePart type="given">CC</namePart><namePart type="family">Bruce</namePart></name><name type="personal"><namePart type="given">RJ</namePart><namePart type="family">Franklin</namePart></name><genre>journal</genre><note>ZhaoCZawadzkaMRouloisAJBruceCCFranklinRJPromoting remyelination in multiple sclerosis by endogenous adult neural stem/precursor cells: defining cellular targetsJ Neurol Sci20082651216</note><relatedItem type="host"><titleInfo><title>J Neurol Sci</title></titleInfo><part><date>2008</date><detail type="volume"><caption>vol.</caption><number>265</number></detail><extent unit="pages"><start>12</start><end>16</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B156"><titleInfo><title>Retroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiation</title></titleInfo><name type="personal"><namePart type="given">YX</namePart><namePart type="family">Zhou</namePart></name><name type="personal"><namePart type="given">NC</namePart><namePart type="family">Flint</namePart></name><name type="personal"><namePart type="given">JC</namePart><namePart type="family">Murtie</namePart></name><name type="personal"><namePart type="given">TQ</namePart><namePart type="family">Le</namePart></name><name type="personal"><namePart type="given">RC</namePart><namePart type="family">Armstrong</namePart></name><genre>journal</genre><note>ZhouYXFlintNCMurtieJCLeTQArmstrongRCRetroviral lineage analysis of fibroblast growth factor receptor signaling in FGF2 inhibition of oligodendrocyte progenitor differentiationGlia20065457890</note><relatedItem type="host"><titleInfo><title>Glia</title></titleInfo><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>54</number></detail><extent unit="pages"><start>578</start><end>90</end><list>578-90</list></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B157"><titleInfo><title>Can imaging techniques measure neuroprotection and remyelination in multiple sclerosis?</title></titleInfo><name type="personal"><namePart type="given">R</namePart><namePart type="family">Zivadinov</namePart></name><genre>journal</genre><note>discussion S91–6</note><note>ZivadinovRCan imaging techniques measure neuroprotection and remyelination in multiple sclerosis?Neurology200768S7282discussion S91–6</note><relatedItem type="host"><titleInfo><title>Neurology</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>68</number></detail><extent unit="pages"><start>S72</start><end>82</end></extent></part></relatedItem></relatedItem><relatedItem type="references" displayLabel="B158"><titleInfo><title>Remyelination of the central nervous system: a valuable contribution from the periphery</title></titleInfo><name type="personal"><namePart type="given">V</namePart><namePart type="family">Zujovic</namePart></name><name type="personal"><namePart type="given">C</namePart><namePart type="family">Bachelin</namePart></name><name type="personal"><namePart type="given">A</namePart><namePart type="family">Baron-Van Evercooren</namePart></name><genre>journal</genre><note>ZujovicVBachelinCBaron-Van EvercoorenARemyelination of the central nervous system: a valuable contribution from the peripheryNeuroscientist20071338391</note><relatedItem type="host"><titleInfo><title>Neuroscientist</title></titleInfo><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><extent unit="pages"><start>383</start><end>91</end><list>383-91</list></extent></part></relatedItem></relatedItem><identifier type="istex">C2CA6E337E425395BB40CEA63368993F4A8FCEA1</identifier><identifier type="ark">ark:/67375/HXZ-K7JKPH5G-5</identifier><identifier type="DOI">10.1093/brain/awn076</identifier><identifier type="ArticleID">awn076</identifier><accessCondition type="use and reproduction" contentType="copyright">Published by Oxford University Press on behalf of the Guarantors of Brain. 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