The effect of drug treatment on neurogenesis in Parkinson's disease
Identifieur interne : 001C23 ( Istex/Corpus ); précédent : 001C22; suivant : 001C24The effect of drug treatment on neurogenesis in Parkinson's disease
Auteurs : Sean S. O'Sullivan ; Mary Johnson ; David R. Williams ; Tamas Revesz ; Janice L. Holton ; Andrew J. Lees ; Elaine K. PerrySource :
- Movement Disorders [ 0885-3185 ] ; 2011-01.
English descriptors
- KwdEn :
Abstract
There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic L‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.
Url:
DOI: 10.1002/mds.23340
Links to Exploration step
ISTEX:20400833E0FC8F49CC3E88C9892ACBD539242333Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The effect of drug treatment on neurogenesis in Parkinson's disease</title><author><name sortKey="O Sullivan, Sean S" sort="O Sullivan, Sean S" uniqKey="O Sullivan S" first="Sean S." last="O'Sullivan">Sean S. O'Sullivan</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Johnson, Mary" sort="Johnson, Mary" uniqKey="Johnson M" first="Mary" last="Johnson">Mary Johnson</name><affiliation><mods:affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Williams, David R" sort="Williams, David R" uniqKey="Williams D" first="David R." last="Williams">David R. Williams</name><affiliation><mods:affiliation>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</mods:affiliation></affiliation></author><author><name sortKey="Revesz, Tamas" sort="Revesz, Tamas" uniqKey="Revesz T" first="Tamas" last="Revesz">Tamas Revesz</name><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Holton, Janice L" sort="Holton, Janice L" uniqKey="Holton J" first="Janice L." last="Holton">Janice L. Holton</name><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Perry, Elaine K" sort="Perry, Elaine K" uniqKey="Perry E" first="Elaine K." last="Perry">Elaine K. Perry</name><affiliation><mods:affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:20400833E0FC8F49CC3E88C9892ACBD539242333</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23340</idno><idno type="url">https://api.istex.fr/document/20400833E0FC8F49CC3E88C9892ACBD539242333/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001C23</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The effect of drug treatment on neurogenesis in Parkinson's disease</title><author><name sortKey="O Sullivan, Sean S" sort="O Sullivan, Sean S" uniqKey="O Sullivan S" first="Sean S." last="O'Sullivan">Sean S. O'Sullivan</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Johnson, Mary" sort="Johnson, Mary" uniqKey="Johnson M" first="Mary" last="Johnson">Mary Johnson</name><affiliation><mods:affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Williams, David R" sort="Williams, David R" uniqKey="Williams D" first="David R." last="Williams">David R. Williams</name><affiliation><mods:affiliation>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</mods:affiliation></affiliation></author><author><name sortKey="Revesz, Tamas" sort="Revesz, Tamas" uniqKey="Revesz T" first="Tamas" last="Revesz">Tamas Revesz</name><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Holton, Janice L" sort="Holton, Janice L" uniqKey="Holton J" first="Janice L." last="Holton">Janice L. Holton</name><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Lees, Andrew J" sort="Lees, Andrew J" uniqKey="Lees A" first="Andrew J." last="Lees">Andrew J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</mods:affiliation></affiliation><affiliation><mods:affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Perry, Elaine K" sort="Perry, Elaine K" uniqKey="Perry E" first="Elaine K." last="Perry">Elaine K. Perry</name><affiliation><mods:affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</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="2011-01">2011-01</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="50">50</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">20400833E0FC8F49CC3E88C9892ACBD539242333</idno><idno type="DOI">10.1002/mds.23340</idno><idno type="ArticleID">MDS23340</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>neurogenesis</term><term>neuroprotection</term><term>stem cells</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic L‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Sean S. O'Sullivan PhD, MRCPI</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</json:string><json:string>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Mary Johnson</name><affiliations><json:string>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</json:string></affiliations></json:item><json:item><name>David R. Williams PhD</name><affiliations><json:string>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</json:string></affiliations></json:item><json:item><name>Tamas Revesz FRCPath</name><affiliations><json:string>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Janice L. Holton FRCPath</name><affiliations><json:string>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Andrew J. Lees MD</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</json:string><json:string>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</json:string></affiliations></json:item><json:item><name>Elaine K. Perry PhD</name><affiliations><json:string>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurogenesis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuroprotection</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>stem cells</value></json:item></subject><language><json:string>eng</json:string></language><abstract>There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic L‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.</abstract><qualityIndicators><score>5.646</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1044</abstractCharCount><pdfWordCount>3858</pdfWordCount><pdfCharCount>24696</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>149</abstractWordCount></qualityIndicators><title>The effect of drug treatment on neurogenesis in Parkinson's disease</title><genre><json:string>Serial article</json:string></genre><host><volume>26</volume><pages><total>6</total><last>50</last><first>45</first></pages><issn><json:string>0885-3185</json:string></issn><issue>1</issue><subject><json:item><value>Research Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23340</json:string></doi><id>20400833E0FC8F49CC3E88C9892ACBD539242333</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/20400833E0FC8F49CC3E88C9892ACBD539242333/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/20400833E0FC8F49CC3E88C9892ACBD539242333/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/20400833E0FC8F49CC3E88C9892ACBD539242333/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">The effect of drug treatment on neurogenesis in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: The authors have no conflicts of interest and no financial disclosures to make.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The effect of drug treatment on neurogenesis in Parkinson's disease</title><author><persName><forename type="first">Sean S.</forename><surname>O'Sullivan</surname><roleName type="degree">PhD, MRCPI</roleName></persName><note type="correspondence"><p>Correspondence: Reta Lila Weston Institute of Neurological Studies, University College London, 1 Wakefield Street, London WC1N 1PJ, United Kingdom</p></note><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation></author><author><persName><forename type="first">Mary</forename><surname>Johnson</surname></persName><affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</affiliation></author><author><persName><forename type="first">David R.</forename><surname>Williams</surname><roleName type="degree">PhD</roleName></persName><affiliation>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</affiliation></author><author><persName><forename type="first">Tamas</forename><surname>Revesz</surname><roleName type="degree">FRCPath</roleName></persName><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation></author><author><persName><forename type="first">Janice L.</forename><surname>Holton</surname><roleName type="degree">FRCPath</roleName></persName><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation></author><author><persName><forename type="first">Andrew J.</forename><surname>Lees</surname><roleName type="degree">MD</roleName></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation></author><author><persName><forename type="first">Elaine K.</forename><surname>Perry</surname><roleName type="degree">PhD</roleName></persName><affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</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="2011-01"></date><biblScope unit="vol">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="45">45</biblScope><biblScope unit="page" to="50">50</biblScope></imprint></monogr><idno type="istex">20400833E0FC8F49CC3E88C9892ACBD539242333</idno><idno type="DOI">10.1002/mds.23340</idno><idno type="ArticleID">MDS23340</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic L‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>neurogenesis</term></item><item><term>neuroprotection</term></item><item><term>stem cells</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="2009-10-14">Received</change><change when="2010-06-10">Registration</change><change when="2011-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/20400833E0FC8F49CC3E88C9892ACBD539242333/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="10"><doi origin="wiley" registered="yes">10.1002/mds.v26.1</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2011-01">January 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="120" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23340</doi><idGroup><id type="unit" value="MDS23340"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2009-10-14"></event><event type="manuscriptRevised" date="2010-02-22"></event><event type="manuscriptAccepted" date="2010-06-10"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.1.6 mode:FullText" date="2012-07-17"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-11-16"></event><event type="publishedOnlineFinalForm" date="2011-02-14"></event><event type="firstOnline" date="2010-11-16"></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">45</numbering><numbering type="pageLast">50</numbering></numberingGroup><correspondenceTo>Reta Lila Weston Institute of Neurological Studies, University College London, 1 Wakefield Street, London WC1N 1PJ, United Kingdom</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23340.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="33"></count><count type="wordTotal" number="4478"></count></countGroup><titleGroup><title type="main" xml:lang="en">The effect of drug treatment on neurogenesis in Parkinson's disease<link href="#fn1"></link></title><title type="short" xml:lang="en">PD Treatments and Neurogenesis</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1 #af2" corresponding="yes"><personName><givenNames>Sean S.</givenNames><familyName>O'Sullivan</familyName><degrees>PhD, MRCPI</degrees></personName><contactDetails><email>sosulliv@ion.ucl.ac.uk</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Mary</givenNames><familyName>Johnson</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af4"><personName><givenNames>David R.</givenNames><familyName>Williams</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Tamas</givenNames><familyName>Revesz</familyName><degrees>FRCPath</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Janice L.</givenNames><familyName>Holton</familyName><degrees>FRCPath</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Andrew J.</givenNames><familyName>Lees</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Elaine K.</givenNames><familyName>Perry</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="GB" type="organization"><unparsedAffiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="GB" type="organization"><unparsedAffiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="GB" type="organization"><unparsedAffiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="AU" type="organization"><unparsedAffiliation>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">neurogenesis</keyword><keyword xml:id="kwd3">neuroprotection</keyword><keyword xml:id="kwd4">stem cells</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic <sc>L</sc>‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: The authors have no conflicts of interest and no financial disclosures to make.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>The effect of drug treatment on neurogenesis in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>PD Treatments and Neurogenesis</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The effect of drug treatment on neurogenesis in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Sean S.</namePart><namePart type="family">O'Sullivan</namePart><namePart type="termsOfAddress">PhD, MRCPI</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation><description>Correspondence: Reta Lila Weston Institute of Neurological Studies, University College London, 1 Wakefield Street, London WC1N 1PJ, United Kingdom</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mary</namePart><namePart type="family">Johnson</namePart><affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">David R.</namePart><namePart type="family">Williams</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Faculty of Medicine (Neuroscience), Monash University (Alfred Hospital Campus), Melbourne, Australia</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tamas</namePart><namePart type="family">Revesz</namePart><namePart type="termsOfAddress">FRCPath</namePart><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Janice L.</namePart><namePart type="family">Holton</namePart><namePart type="termsOfAddress">FRCPath</namePart><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew J.</namePart><namePart type="family">Lees</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, University College London, London, United Kingdom</affiliation><affiliation>Queen Square Brain Bank for Neurological Disorders and Institute of Neurology, University College London, London, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elaine K.</namePart><namePart type="family">Perry</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle‐upon‐Tyne, United Kingdom</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-01</dateIssued><dateCaptured encoding="w3cdtf">2009-10-14</dateCaptured><dateValid encoding="w3cdtf">2010-06-10</dateValid><copyrightDate encoding="w3cdtf">2011</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">1</extent><extent unit="tables">1</extent><extent unit="references">33</extent><extent unit="words">4478</extent></physicalDescription><abstract lang="en">There has been recent interest in the possibility that impaired neurogenesis may contribute to the decline in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease (PD). We have investigated the effects of commonly used treatments for PD on neural stem cell (NSC) activity in nondemented patients. Postmortem of brain tissue containing the subventricular zone (SVZ) and ependymal layer cells was obtained from 32 nondemented patients with PD. NSC activity was assessed by immunohistochemical staining for RNA‐binding protein Musashi1. Regression analyses were then used to identify which clinical factors independently influenced NSC activity. Disease duration was negatively associated with SVZ Musashi1 staining, whereas lifetime levodopa was positively associated in this region. Our findings suggest a positive impact of chronic L‐dopa use on the number of NSC in the SVZ of PD patients, which may have relevance for future studies on neuroprotection in neurodegenerative diseases. © 2010 Movement Disorder Society.</abstract><note type="content">*Potential conflict of interest: The authors have no conflicts of interest and no financial disclosures to make.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>neurogenesis</topic><topic>neuroprotection</topic><topic>stem cells</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><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>2011</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>45</start><end>50</end><total>6</total></extent></part></relatedItem><identifier type="istex">20400833E0FC8F49CC3E88C9892ACBD539242333</identifier><identifier type="DOI">10.1002/mds.23340</identifier><identifier type="ArticleID">MDS23340</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001C23 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001C23 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:20400833E0FC8F49CC3E88C9892ACBD539242333
|texte= The effect of drug treatment on neurogenesis in Parkinson's disease
}}
| This area was generated with Dilib version V0.6.23. |  |