Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach
Identifieur interne : 002180 ( Main/Corpus ); précédent : 002179; suivant : 002181Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach
Auteurs : Bart F. L. Van Nuenen ; Thilo Van Eimeren ; Joyce P. M. Van Der Vegt ; Carsten Buhmann ; Christine Klein ; Bastiaan R. Bloem ; Hartwig R. SiebnerSource :
- Movement Disorders [ 0885-3185 ] ; 2009.
English descriptors
- KwdEn :
Abstract
Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22635
Links to Exploration step
ISTEX:F66C6C81895FF6DEEF5935F830EA716D1D03F785Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title><author><name sortKey="Van Nuenen, Bart F L" sort="Van Nuenen, Bart F L" uniqKey="Van Nuenen B" first="Bart F. L." last="Van Nuenen">Bart F. L. Van Nuenen</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Van Eimeren, Thilo" sort="Van Eimeren, Thilo" uniqKey="Van Eimeren T" first="Thilo" last="Van Eimeren">Thilo Van Eimeren</name><affiliation><mods:affiliation>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Van Der Vegt, Joyce P M" sort="Van Der Vegt, Joyce P M" uniqKey="Van Der Vegt J" first="Joyce P. M." last="Van Der Vegt">Joyce P. M. Van Der Vegt</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhmann, Carsten" sort="Buhmann, Carsten" uniqKey="Buhmann C" first="Carsten" last="Buhmann">Carsten Buhmann</name><affiliation><mods:affiliation>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R." last="Bloem">Bastiaan R. Bloem</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R." last="Siebner">Hartwig R. Siebner</name><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F66C6C81895FF6DEEF5935F830EA716D1D03F785</idno><date when="2009" year="2009">2009</date><idno type="doi">10.1002/mds.22635</idno><idno type="url">https://api.istex.fr/document/F66C6C81895FF6DEEF5935F830EA716D1D03F785/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002180</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title><author><name sortKey="Van Nuenen, Bart F L" sort="Van Nuenen, Bart F L" uniqKey="Van Nuenen B" first="Bart F. L." last="Van Nuenen">Bart F. L. Van Nuenen</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Van Eimeren, Thilo" sort="Van Eimeren, Thilo" uniqKey="Van Eimeren T" first="Thilo" last="Van Eimeren">Thilo Van Eimeren</name><affiliation><mods:affiliation>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</mods:affiliation></affiliation></author><author><name sortKey="Van Der Vegt, Joyce P M" sort="Van Der Vegt, Joyce P M" uniqKey="Van Der Vegt J" first="Joyce P. M." last="Van Der Vegt">Joyce P. M. Van Der Vegt</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation></author><author><name sortKey="Buhmann, Carsten" sort="Buhmann, Carsten" uniqKey="Buhmann C" first="Carsten" last="Buhmann">Carsten Buhmann</name><affiliation><mods:affiliation>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</mods:affiliation></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><mods:affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</mods:affiliation></affiliation></author><author><name sortKey="Bloem, Bastiaan R" sort="Bloem, Bastiaan R" uniqKey="Bloem B" first="Bastiaan R." last="Bloem">Bastiaan R. Bloem</name><affiliation><mods:affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</mods:affiliation></affiliation></author><author><name sortKey="Siebner, Hartwig R" sort="Siebner, Hartwig R" uniqKey="Siebner H" first="Hartwig R." last="Siebner">Hartwig R. Siebner</name><affiliation><mods:affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</mods:affiliation></affiliation><affiliation><mods:affiliation>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009">2009</date><biblScope unit="volume">24</biblScope><biblScope unit="issue">S2</biblScope><biblScope unit="page" from="S703">S703</biblScope><biblScope unit="page" to="S710">S710</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">F66C6C81895FF6DEEF5935F830EA716D1D03F785</idno><idno type="DOI">10.1002/mds.22635</idno><idno type="ArticleID">MDS22635</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PINK1 gene</term><term>Parkinson's disease</term><term>compensation</term><term>functional magnetic resonance imaging</term><term>motor cortex</term><term>parkin gene</term><term>presymptomatic parkinsonism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Bart F.L. van Nuenen MD</name><affiliations><json:string>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</json:string><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Thilo van Eimeren MD</name><affiliations><json:string>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</json:string></affiliations></json:item><json:item><name>Joyce P.M. van der Vegt MD</name><affiliations><json:string>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</json:string><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string></affiliations></json:item><json:item><name>Carsten Buhmann MD</name><affiliations><json:string>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</json:string></affiliations></json:item><json:item><name>Christine Klein MD, PhD</name><affiliations><json:string>Department of Neurology, University of Lübeck, Lübeck, Germany</json:string></affiliations></json:item><json:item><name>Bastiaan R. Bloem MD, PhD</name><affiliations><json:string>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</json:string></affiliations></json:item><json:item><name>Hartwig R. Siebner MD</name><affiliations><json:string>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</json:string><json:string>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>compensation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>functional magnetic resonance imaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PINK1 gene</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>parkin gene</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>presymptomatic parkinsonism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><articleId><json:string>MDS22635</json:string></articleId><language><json:string>eng</json:string></language><abstract>Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society</abstract><qualityIndicators><score>8</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1904</abstractCharCount><pdfWordCount>5035</pdfWordCount><pdfCharCount>32907</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>275</abstractWordCount></qualityIndicators><title>Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title><genre><json:string>article</json:string></genre><host><volume>24</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>8</total><last>S710</last><first>S703</first></pages><issn><json:string>0885-3185</json:string></issn><issue>S2</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/mds.22635</json:string></doi><id>F66C6C81895FF6DEEF5935F830EA716D1D03F785</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/F66C6C81895FF6DEEF5935F830EA716D1D03F785/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/F66C6C81895FF6DEEF5935F830EA716D1D03F785/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F66C6C81895FF6DEEF5935F830EA716D1D03F785/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>BMBF - No. 01GO 0511;</note><note>NWO - No. VIDI research grant #016.076.352;</note><note>Volkswagen Foundation</note><note>Hermann and Lilly Schilling Foundation</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title><author><persName><forename type="first">Bart F.L.</forename><surname>van Nuenen</surname></persName><roleName type="degree">MD</roleName><note type="biography">The first two authors contributed equally to this manuscript.</note><affiliation>The first two authors contributed equally to this manuscript.</affiliation><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation></author><author><persName><forename type="first">Thilo</forename><surname>van Eimeren</surname></persName><roleName type="degree">MD</roleName><note type="biography">The first two authors contributed equally to this manuscript.</note><affiliation>The first two authors contributed equally to this manuscript.</affiliation><affiliation>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</affiliation></author><author><persName><forename type="first">Joyce P.M.</forename><surname>van der Vegt</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation></author><author><persName><forename type="first">Carsten</forename><surname>Buhmann</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</affiliation></author><author><persName><forename type="first">Christine</forename><surname>Klein</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation></author><author><persName><forename type="first">Bastiaan R.</forename><surname>Bloem</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation></author><author><persName><forename type="first">Hartwig R.</forename><surname>Siebner</surname></persName><roleName type="degree">MD</roleName><note type="correspondence"><p>Correspondence: Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre Kettegaard Allé 30, DK‐2650 Hvidovre, Denmark</p></note><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><affiliation>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2009"></date><biblScope unit="volume">24</biblScope><biblScope unit="issue">S2</biblScope><biblScope unit="page" from="S703">S703</biblScope><biblScope unit="page" to="S710">S710</biblScope></imprint></monogr><idno type="istex">F66C6C81895FF6DEEF5935F830EA716D1D03F785</idno><idno type="DOI">10.1002/mds.22635</idno><idno type="ArticleID">MDS22635</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>compensation</term></item><item><term>functional magnetic resonance imaging</term></item><item><term>motor cortex</term></item><item><term>PINK1 gene</term></item><item><term>parkin gene</term></item><item><term>presymptomatic parkinsonism</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-12-22">Received</change><change when="2009-03-27">Registration</change><change when="2009">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F66C6C81895FF6DEEF5935F830EA716D1D03F785/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="145"><doi origin="wiley" registered="yes">10.1002/mds.v24.2s</doi><numberingGroup><numbering type="journalVolume" number="24">24</numbering><numbering type="journalIssue">S2</numbering></numberingGroup><coverDate startDate="2009">2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="90" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.22635</doi><idGroup><id type="unit" value="MDS22635"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2009 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2008-12-22"></event><event type="manuscriptRevised" date="2009-03-20"></event><event type="manuscriptAccepted" date="2009-03-27"></event><event type="firstOnline" date="2009-10-28"></event><event type="publishedOnlineFinalForm" date="2009-10-28"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.4 mode:FullText" date="2010-12-14"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">S703</numbering><numbering type="pageLast">S710</numbering></numberingGroup><correspondenceTo>Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre Kettegaard Allé 30, DK‐2650 Hvidovre, Denmark</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS22635.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="2"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="43"></count><count type="wordTotal" number="5283"></count></countGroup><titleGroup><title type="main" xml:lang="en">Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach<link href="#fn1"></link></title><title type="short" xml:lang="en">Preclinical Compensation in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" noteRef="#fn2"><personName><givenNames>Bart F.L.</givenNames><familyName>van Nuenen</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3" noteRef="#fn2"><personName><givenNames>Thilo</givenNames><familyName>van Eimeren</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Joyce P.M.</givenNames><familyName>van der Vegt</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Carsten</givenNames><familyName>Buhmann</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Christine</givenNames><familyName>Klein</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Bastiaan R.</givenNames><familyName>Bloem</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2 #af6" corresponding="yes"><personName><givenNames>Hartwig R.</givenNames><familyName>Siebner</familyName><degrees>MD</degrees></personName><contactDetails><email>hartwig.siebner@drcmr.dk</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="NL" type="organization"><unparsedAffiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="CA" type="organization"><unparsedAffiliation>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="DE" type="organization"><unparsedAffiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="DK" type="organization"><unparsedAffiliation>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">compensation</keyword><keyword xml:id="kwd2">functional magnetic resonance imaging</keyword><keyword xml:id="kwd3">motor cortex</keyword><keyword xml:id="kwd4"><i>PINK1</i> gene</keyword><keyword xml:id="kwd5"><i>parkin</i> gene</keyword><keyword xml:id="kwd6">presymptomatic parkinsonism</keyword><keyword xml:id="kwd7">Parkinson's disease</keyword></keywordGroup><fundingInfo><fundingAgency>BMBF</fundingAgency><fundingNumber>01GO 0511</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NWO</fundingAgency><fundingNumber>VIDI research grant #016.076.352</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Volkswagen Foundation</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Hermann and Lilly Schilling Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Mutations in the <i>Parkin</i> (PARK2) and <i>PINK1</i> gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single <i>Parkin</i> or <i>PINK1</i> mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant <i>Parkin</i> or <i>PINK1</i> allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, <i>Parkin</i> mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous <i>PINK1</i> mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: None reported.</p></note><note xml:id="fn2"><p>The first two authors contributed equally to this manuscript.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Preclinical Compensation in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach</title></titleInfo><name type="personal"><namePart type="given">Bart F.L.</namePart><namePart type="family">van Nuenen</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><description>The first two authors contributed equally to this manuscript.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thilo</namePart><namePart type="family">van Eimeren</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>CAMH‐PET Centre, Toronto Western Research Institute and Movement Disorders Centre, University of Toronto, Canada</affiliation><description>The first two authors contributed equally to this manuscript.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joyce P.M.</namePart><namePart type="family">van der Vegt</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carsten</namePart><namePart type="family">Buhmann</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology and Human Genetics, University Clinic Eppendorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christine</namePart><namePart type="family">Klein</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, University of Lübeck, Lübeck, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bastiaan R.</namePart><namePart type="family">Bloem</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hartwig R.</namePart><namePart type="family">Siebner</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Christian‐Albrechts‐University, Kiel, Germany</affiliation><affiliation>Danish Research Centre for Magnetic Resonance, Hvidovre University Hospital, Copenhagen Medical School, Copenhagen, Denmark</affiliation><description>Correspondence: Danish Research Centre for Magnetic Resonance, Copenhagen University Hospital, Hvidovre Kettegaard Allé 30, DK‐2650 Hvidovre, Denmark</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009</dateIssued><dateCaptured encoding="w3cdtf">2008-12-22</dateCaptured><dateValid encoding="w3cdtf">2009-03-27</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="references">43</extent><extent unit="words">5283</extent></physicalDescription><abstract lang="en">Mutations in the Parkin (PARK2) and PINK1 gene (PARK 6) can cause recessively inherited Parkinson's disease (PD). The presence of a single Parkin or PINK1 mutation is associated with a dopaminergic nigrostriatal dysfunction and conveys an increased risk to develop PD throughout lifetime. Therefore neuroimaging of non‐manifesting individuals with a mutant Parkin or PINK1 allele opens up a window for the investigation of preclinical and very early phases of PD in vivo. Here we review how functional magnetic resonance imaging (fMRI) can be used to identify compensatory mechanisms that help to prevent development of overt disease. In two separate experiments, Parkin mutation carriers displayed stronger activation of rostral supplementary motor area (SMA) and right dorsal premotor cortex (PMd) during a simple motor sequence task and anterior cingulate motor area and left rostral PMd during internal movement selection as opposed to externally cued movements. The additional recruitment of the rostral SMA and right rostral PMd during the finger sequence task was also observed in a separate group of nonmanifesting mutation carriers with a single heterozygous PINK1 mutation. Because mutation carriers were not impaired at performing the task, the additional recruitment of motor cortical areas indicates a compensatory mechanism that effectively counteracts the nigrostriatal dysfunction. These first results warrant further studies that use these imaging genomics approach to tap into preclinical compensation of PD. Extensions of this line of research involve fMRI paradigms probing nonmotor brain functions. Additionally, the same fMRI paradigms should be applied to nonmanifesting mutation carriers in genes linked to autosomal dominant PD. This will help to determine how “generically” the human brain compensates for a preclinical dopaminergic dysfunction. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">BMBF - No. 01GO 0511; </note><note type="funding">NWO - No. VIDI research grant #016.076.352; </note><note type="funding">Volkswagen Foundation</note><note type="funding">Hermann and Lilly Schilling Foundation</note><subject lang="en"><genre>Keywords</genre><topic>compensation</topic><topic>functional magnetic resonance imaging</topic><topic>motor cortex</topic><topic>PINK1 gene</topic><topic>parkin gene</topic><topic>presymptomatic parkinsonism</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>S2</number></detail><extent unit="pages"><start>S703</start><end>S710</end><total>8</total></extent></part></relatedItem><identifier type="istex">F66C6C81895FF6DEEF5935F830EA716D1D03F785</identifier><identifier type="DOI">10.1002/mds.22635</identifier><identifier type="ArticleID">MDS22635</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonV1/Data/Main/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002180 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 002180 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Sante
|area= ParkinsonV1
|flux= Main
|étape= Corpus
|type= RBID
|clé= ISTEX:F66C6C81895FF6DEEF5935F830EA716D1D03F785
|texte= Mapping preclinical compensation in Parkinson's disease: An imaging genomics approach
}}
| This area was generated with Dilib version V0.6.23. |  |