From fish to man: understanding endogenous remyelination in CNS demyelinating diseases
Identifieur interne : 000117 ( Ncbi/Merge ); précédent : 000116; suivant : 000118From fish to man: understanding endogenous remyelination in CNS demyelinating diseases
Auteurs : Monique Dubois-Dalcq [États-Unis] ; Anna Williams [Royaume-Uni] ; Christine Stadelmann [Allemagne] ; Bruno Stankoff [France] ; Bernard Zalc [France] ; Catherine Lubetzki [France]Source :
- Brain : a journal of neurology [ 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.
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DOI: 10.1093/brain/awn076
PubMed: 18474520
PubMed Central: 2516372
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France</nlm:aff><wicri:noCountry code="subfield">75013 Paris. France</wicri:noCountry></affiliation><affiliation wicri:level="3"><nlm:aff id="A5"> Université Pierre & Marie Curie, Faculté de médecine, IFR 70, 75013 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea> Université Pierre & Marie Curie, Faculté de médecine, IFR 70, 75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:aff id="A6"> AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea> AP-HP, Hôpital de la Salpêtrière, 75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Lubetzki, Catherine" sort="Lubetzki, Catherine" uniqKey="Lubetzki C" first="Catherine" last="Lubetzki">Catherine Lubetzki</name><affiliation><nlm:aff id="A4"> Inserm, U711, 75013 Paris. France</nlm:aff><wicri:noCountry code="subfield">75013 Paris. France</wicri:noCountry></affiliation><affiliation wicri:level="3"><nlm:aff id="A5"> Université Pierre & Marie Curie, Faculté de médecine, IFR 70, 75013 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea> Université Pierre & Marie Curie, Faculté de médecine, IFR 70, 75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation><affiliation wicri:level="3"><nlm:aff id="A6"> AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</nlm:aff><country xml:lang="fr">France</country><wicri:regionArea> AP-HP, Hôpital de la Salpêtrière, 75013 Paris</wicri:regionArea><placeName><region type="region" nuts="2">Île-de-France</region><settlement type="city">Paris</settlement></placeName></affiliation></author></analytic><series><title level="j">Brain : a journal of neurology</title><idno type="ISSN">0006-8950</idno><idno type="eISSN">1460-2156</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="P1">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></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0372537</journal-id><journal-id journal-id-type="pubmed-jr-id">1917</journal-id><journal-id journal-id-type="nlm-ta">Brain</journal-id><journal-id journal-id-type="iso-abbrev">Brain</journal-id><journal-title-group><journal-title>Brain : a journal of neurology</journal-title></journal-title-group><issn pub-type="ppub">0006-8950</issn><issn pub-type="epub">1460-2156</issn></journal-meta><article-meta><article-id pub-id-type="pmid">18474520</article-id><article-id pub-id-type="pmc">2516372</article-id><article-id pub-id-type="doi">10.1093/brain/awn076</article-id><article-id pub-id-type="manuscript">NIHMS48275</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>From fish to man: understanding endogenous remyelination in CNS demyelinating diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Dubois-Dalcq</surname><given-names>Monique</given-names></name><xref ref-type="aff" rid="A1">#</xref></contrib><contrib contrib-type="author"><name><surname>Williams</surname><given-names>Anna</given-names></name><xref ref-type="aff" rid="A2">+</xref></contrib><contrib contrib-type="author"><name><surname>Stadelmann</surname><given-names>Christine</given-names></name><xref ref-type="aff" rid="A3">*</xref></contrib><contrib contrib-type="author"><name><surname>Stankoff</surname><given-names>Bruno</given-names></name><xref ref-type="aff" rid="A4">°</xref><xref ref-type="aff" rid="A5">$</xref><xref ref-type="aff" rid="A6">§</xref></contrib><contrib contrib-type="author"><name><surname>Zalc</surname><given-names>Bernard</given-names></name><xref ref-type="aff" rid="A4">°</xref><xref ref-type="aff" rid="A5">$</xref><xref ref-type="aff" rid="A6">§</xref></contrib><contrib contrib-type="author"><name><surname>Lubetzki</surname><given-names>Catherine</given-names></name><xref ref-type="aff" rid="A4">°</xref><xref ref-type="aff" rid="A5">$</xref><xref ref-type="aff" rid="A6">§</xref></contrib></contrib-group><aff id="A1"><label>#</label> National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA</aff><aff id="A2"><label>+</label> Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK</aff><aff id="A3"><label>*</label> Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany</aff><aff id="A4"><label>°</label> Inserm, U711, 75013 Paris. France</aff><aff id="A5"><label>$</label> Université Pierre & Marie Curie, Faculté de médecine, IFR 70, 75013 Paris, France</aff><aff id="A6"><label>§</label> AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France</aff><author-notes><corresp id="FN1">Corresponding author: 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, Tel 301-4027669 or 4511428, Fax 301-4802737, <email>mdalcq@pasteur.fr</email>, <email>dalcqm@mail.nih.gov</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>1</day><month>5</month><year>2008</year></pub-date><pub-date pub-type="epub"><day>12</day><month>5</month><year>2008</year></pub-date><pub-date pub-type="ppub"><month>7</month><year>2008</year></pub-date><pub-date pub-type="pmc-release"><day>14</day><month>8</month><year>2008</year></pub-date><volume>131</volume><issue>Pt 7</issue><fpage>1686</fpage><lpage>1700</lpage><abstract><p id="P1">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><funding-group><award-group><funding-source country="United States">National Institute of Neurological Disorders and Stroke : NINDS</funding-source><award-id>Z99 NS999999 || NS</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list><country><li>Allemagne</li><li>France</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Basse-Saxe</li><li>Écosse</li><li>Île-de-France</li></region><settlement><li>Göttingen</li><li>Paris</li><li>Édimbourg</li></settlement></list><tree><country name="États-Unis"><noRegion><name sortKey="Dubois Dalcq, Monique" sort="Dubois Dalcq, Monique" uniqKey="Dubois Dalcq M" first="Monique" last="Dubois-Dalcq">Monique Dubois-Dalcq</name></noRegion></country><country name="Royaume-Uni"><region name="Écosse"><name sortKey="Williams, Anna" sort="Williams, Anna" uniqKey="Williams A" first="Anna" last="Williams">Anna Williams</name></region></country><country name="Allemagne"><region name="Basse-Saxe"><name sortKey="Stadelmann, Christine" sort="Stadelmann, Christine" uniqKey="Stadelmann C" first="Christine" last="Stadelmann">Christine Stadelmann</name></region></country><country name="France"><region name="Île-de-France"><name sortKey="Stankoff, Bruno" sort="Stankoff, Bruno" uniqKey="Stankoff B" first="Bruno" last="Stankoff">Bruno Stankoff</name></region><name sortKey="Lubetzki, Catherine" sort="Lubetzki, Catherine" uniqKey="Lubetzki C" first="Catherine" last="Lubetzki">Catherine Lubetzki</name><name sortKey="Lubetzki, Catherine" sort="Lubetzki, Catherine" uniqKey="Lubetzki C" first="Catherine" last="Lubetzki">Catherine Lubetzki</name><name sortKey="Stankoff, Bruno" sort="Stankoff, Bruno" uniqKey="Stankoff B" first="Bruno" last="Stankoff">Bruno Stankoff</name><name sortKey="Zalc, Bernard" sort="Zalc, Bernard" uniqKey="Zalc B" first="Bernard" last="Zalc">Bernard Zalc</name><name sortKey="Zalc, Bernard" sort="Zalc, Bernard" uniqKey="Zalc B" first="Bernard" last="Zalc">Bernard Zalc</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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