Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model
Identifieur interne : 000658 ( Istex/Corpus ); précédent : 000657; suivant : 000659Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model
Auteurs : Jay S. Schneider ; Elsa Y. Pioli ; Yang Jianzhong ; Qin Li ; Erwan BezardSource :
- Movement Disorders [ 0885-3185 ] ; 2013-05.
Abstract
Levodopa effectively relieves motor symptoms in Parkinson's disease (PD), but has had inconsistent effects on cognition, even worsening some aspects of cognitive functioning. Therefore, remediation of PD cognitive deficits is a major unmet need. However, drug development efforts have been hampered by lack of an animal model in which motor and cognitive deficits can be examined simultaneously.
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DOI: 10.1002/mds.25258
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Pioli</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Jianzhong, Yang" sort="Jianzhong, Yang" uniqKey="Jianzhong Y" first="Yang" last="Jianzhong">Yang Jianzhong</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, UMR 5293, Bordeaux, France</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950</idno><date when="2013" year="2013">2013</date><idno type="doi">10.1002/mds.25258</idno><idno type="url">https://api.istex.fr/document/F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000658</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000658</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model</title><author><name sortKey="Schneider, Jay S" sort="Schneider, Jay S" uniqKey="Schneider J" first="Jay S." last="Schneider">Jay S. Schneider</name><affiliation><mods:affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Pennsylvania, Philadelphia, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: jay.schneider@jefferson.edu</mods:affiliation></affiliation></author><author><name sortKey="Pioli, Elsa Y" sort="Pioli, Elsa Y" uniqKey="Pioli E" first="Elsa Y." last="Pioli">Elsa Y. Pioli</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Jianzhong, Yang" sort="Jianzhong, Yang" uniqKey="Jianzhong Y" first="Yang" last="Jianzhong">Yang Jianzhong</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Li, Qin" sort="Li, Qin" uniqKey="Li Q" first="Qin" last="Li">Qin Li</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation><mods:affiliation>Motac Cognition Inc, Beijing, China</mods:affiliation></affiliation><affiliation><mods:affiliation>Motac Neuroscience Ltd, Manchester, UK</mods:affiliation></affiliation><affiliation><mods:affiliation>Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, UMR 5293, Bordeaux, France</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>Blackwell Publishing Ltd</publisher><date type="published" when="2013-05">2013-05</date><biblScope unit="volume">28</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="663">663</biblScope><biblScope unit="page" to="667">667</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950</idno><idno type="DOI">10.1002/mds.25258</idno><idno type="ArticleID">MDS25258</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Levodopa effectively relieves motor symptoms in Parkinson's disease (PD), but has had inconsistent effects on cognition, even worsening some aspects of cognitive functioning. Therefore, remediation of PD cognitive deficits is a major unmet need. However, drug development efforts have been hampered by lack of an animal model in which motor and cognitive deficits can be examined simultaneously.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Jay S. Schneider PhD</name><affiliations><json:string>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Pennsylvania, Philadelphia, USA</json:string><json:string>E-mail: jay.schneider@jefferson.edu</json:string></affiliations></json:item><json:item><name>Elsa Y. Pioli PhD</name><affiliations><json:string>Motac Cognition Inc, Beijing, China</json:string><json:string>Motac Neuroscience Ltd, Manchester, UK</json:string></affiliations></json:item><json:item><name>Yang Jianzhong</name><affiliations><json:string>Motac Cognition Inc, Beijing, China</json:string><json:string>Motac Neuroscience Ltd, Manchester, UK</json:string></affiliations></json:item><json:item><name>Qin Li PhD</name><affiliations><json:string>Motac Cognition Inc, Beijing, China</json:string><json:string>Motac Neuroscience Ltd, Manchester, UK</json:string></affiliations></json:item><json:item><name>Erwan Bezard PhD</name><affiliations><json:string>Motac Cognition Inc, Beijing, China</json:string><json:string>Motac Neuroscience Ltd, Manchester, UK</json:string><json:string>Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, UMR 5293, Bordeaux, France</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MPTP</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>primate</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cognition</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>motor</value></json:item></subject><articleId><json:string>MDS25258</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><qualityIndicators><score>4.212</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 809.972 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Neurol</title></host><title>Dopamine: a key regulator to adapt action, emotion, motivation, and cognition</title></json:item></refBibs><genre><json:string>article</json:string></genre><host><volume>28</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>5</total><last>667</last><first>663</first></pages><issn><json:string>0885-3185</json:string></issn><issue>5</issue><subject><json:item><value>Brief Report</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><categories><wos><json:string>science</json:string><json:string>clinical neurology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>neurology & 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model</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><availability><p>Copyright © 2012 Movement Disorders SocietyCopyright © 2012 Movement Disorders Society</p></availability><date>2013-05-13</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model</title><author xml:id="author-1"><persName><forename type="first">Jay S.</forename><surname>Schneider</surname></persName><roleName type="degree">PhD</roleName><email>jay.schneider@jefferson.edu</email><affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Pennsylvania, Philadelphia, USA</affiliation></author><author xml:id="author-2"><persName><forename type="first">Elsa Y.</forename><surname>Pioli</surname></persName><roleName type="degree">PhD</roleName><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation></author><author xml:id="author-3"><persName><forename type="first">Yang</forename><surname>Jianzhong</surname></persName><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation></author><author xml:id="author-4"><persName><forename type="first">Qin</forename><surname>Li</surname></persName><roleName type="degree">PhD</roleName><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation></author><author xml:id="author-5"><persName><forename type="first">Erwan</forename><surname>Bezard</surname></persName><roleName type="degree">PhD</roleName><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation><affiliation>Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, UMR 5293, Bordeaux, France</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>Blackwell Publishing Ltd</publisher><date type="published" when="2013-05"></date><biblScope unit="volume">28</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="663">663</biblScope><biblScope unit="page" to="667">667</biblScope></imprint></monogr><idno type="istex">F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950</idno><idno type="DOI">10.1002/mds.25258</idno><idno type="ArticleID">MDS25258</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2013-05-13</date></creation><langUsage><language ident="en">en</language></langUsage><abstract><p>Levodopa effectively relieves motor symptoms in Parkinson's disease (PD), but has had inconsistent effects on cognition, even worsening some aspects of cognitive functioning. Therefore, remediation of PD cognitive deficits is a major unmet need. However, drug development efforts have been hampered by lack of an animal model in which motor and cognitive deficits can be examined simultaneously.</p></abstract><abstract><p>Cynomolgus monkeys were trained to perform cognitive tasks and then chronically exposed to MPTP to slowly produce cognitive and motor deficits of parkinsonism.</p></abstract><abstract><p>Administration of L‐dopa to these animals dose dependently improved motor functioning, but did not significantly improve cognitive performance. At doses that maximally improved motor function, additional cognitive deficits were observed. The present model of MPTP‐induced parkinsonism recapitulates important motor and cognitive aspects of PD. Results with L‐dopa mirror data derived from PD patients.</p></abstract><abstract><p>This model should allow more efficient testing of potential PD therapeutics to evaluate motor and cognitive functions simultaneously. © 2012 Movement Disorder Society</p></abstract><textClass><keywords scheme="keyword"><list><head>keywords</head><item><term>levodopa</term></item><item><term>MPTP</term></item><item><term>primate</term></item><item><term>cognition</term></item><item><term>motor</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article-category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2012-08-08">Received</change><change when="2012-09-27">Registration</change><change when="2013-05-13">Created</change><change when="2013-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950/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" xml:id="mds25258"><header><publicationMeta level="product"><doi origin="wiley" 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" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov Disord</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi>10.1002/mds.v28.5</doi><copyright ownership="thirdParty">Copyright © 2012 Movement Disorders Society</copyright><numberingGroup><numbering type="journalVolume" number="28">28</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2013-05">May 2013</coverDate></publicationMeta><publicationMeta level="unit" position="220" type="article" status="forIssue"><doi>10.1002/mds.25258</doi><idGroup><id type="unit" value="MDS25258"></id></idGroup><countGroup><count type="pageTotal" number="5"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2012 Movement Disorders Society</copyright><eventGroup><event type="manuscriptReceived" date="2012-08-08"></event><event type="manuscriptRevised" date="2012-09-12"></event><event type="manuscriptAccepted" date="2012-09-27"></event><event type="xmlCreated" agent="Cenveo Publisher Services" date="2013-05-13"></event><event type="publishedOnlineEarlyUnpaginated" date="2012-12-12"></event><event type="publishedOnlineFinalForm" date="2013-05-15"></event><event type="firstOnline" date="2012-12-12"></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:4.6.4 mode:FullText" date="2015-10-02"></event></eventGroup><numberingGroup><numbering type="pageFirst">663</numbering><numbering type="pageLast">667</numbering></numberingGroup><correspondenceTo>Correspondence to: Jay S. Schneider, PhD, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, 1020 Locust Street, Philadelphia, PA 19107, USA. E-mail: <email>jay.schneider@jefferson.edu</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS25258.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model</title><title type="short">Cognition in a Macaque PD Model</title></titleGroup><creators><creator affiliationRef="#mds25258-aff-0001" corresponding="yes" creatorRole="author" xml:id="mds25258-cr-0001"><personName><givenNames>Jay S.</givenNames><familyName>Schneider</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25258-aff-0002 #mds25258-aff-0003" creatorRole="author" xml:id="mds25258-cr-0002"><personName><givenNames>Elsa Y.</givenNames><familyName>Pioli</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25258-aff-0002 #mds25258-aff-0003" creatorRole="author" xml:id="mds25258-cr-0003"><personName><givenNames>Yang</givenNames><familyName>Jianzhong</familyName></personName></creator><creator affiliationRef="#mds25258-aff-0002 #mds25258-aff-0003" creatorRole="author" xml:id="mds25258-cr-0004"><personName><givenNames>Qin</givenNames><familyName>Li</familyName><degrees>PhD</degrees></personName></creator><creator affiliationRef="#mds25258-aff-0002 #mds25258-aff-0003 #mds25258-aff-0004" creatorRole="author" xml:id="mds25258-cr-0005"><personName><givenNames>Erwan</givenNames><familyName>Bezard</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation type="organization" xml:id="mds25258-aff-0001" countryCode="US"><orgDiv>Department of Pathology, Anatomy and Cell Biology</orgDiv><orgName>Thomas Jefferson University</orgName><address><city>Philadelphia</city><countryPart>Pennsylvania</countryPart><country>USA</country></address></affiliation><affiliation type="organization" xml:id="mds25258-aff-0002" countryCode="CN"><orgName>Motac Cognition Inc</orgName><address><city>Beijing</city><country>China</country></address></affiliation><affiliation type="organization" xml:id="mds25258-aff-0003" countryCode="GB"><orgName>Motac Neuroscience Ltd</orgName><address><city>Manchester</city><country>UK</country></address></affiliation><affiliation type="organization" xml:id="mds25258-aff-0004" countryCode="FR"><orgName>Institute of Neurodegenerative Diseases</orgName><orgName>Université Victor Ségalen‐Bordeaux II</orgName><orgDiv>Centre National de la Recherche Scientifique</orgDiv><address><street>UMR 5293</street><city>Bordeaux</city><country>France</country></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="mds25258-kwd-0001">levodopa</keyword><keyword xml:id="mds25258-kwd-0002">MPTP</keyword><keyword xml:id="mds25258-kwd-0003">primate</keyword><keyword xml:id="mds25258-kwd-0004">cognition</keyword><keyword xml:id="mds25258-kwd-0005">motor</keyword></keywordGroup><abstractGroup><abstract type="main"><section xml:id="mds25258-sec-0001"><title type="main">Background</title><p>Levodopa effectively relieves motor symptoms in Parkinson's disease (PD), but has had inconsistent effects on cognition, even worsening some aspects of cognitive functioning. Therefore, remediation of PD cognitive deficits is a major unmet need. However, drug development efforts have been hampered by lack of an animal model in which motor and cognitive deficits can be examined simultaneously.</p></section><section xml:id="mds25258-sec-0002"><title type="main">Methods</title><p>Cynomolgus monkeys were trained to perform cognitive tasks and then chronically exposed to MPTP to slowly produce cognitive and motor deficits of parkinsonism.</p></section><section xml:id="mds25258-sec-0003"><title type="main">Results</title><p>Administration of <sc>L</sc>‐dopa to these animals dose dependently improved motor functioning, but did not significantly improve cognitive performance. At doses that maximally improved motor function, additional cognitive deficits were observed. The present model of MPTP‐induced parkinsonism recapitulates important motor and cognitive aspects of PD. Results with <sc>L</sc>‐dopa mirror data derived from PD patients.</p></section><section xml:id="mds25258-sec-0004"><title type="main">Conclusion</title><p>This model should allow more efficient testing of potential PD therapeutics to evaluate motor and cognitive functions simultaneously. © 2012 Movement Disorder Society</p></section></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="mds25258-note-0001"><p><b>Funding agencies:</b> This research was supported by an unrestricted grant from Motac Holding, Inc.</p></note><note xml:id="mds25258-note-0002"><p><b>Relevant conflicts of interest/financial disclosures:</b> Nothing to report.</p></note><note xml:id="mds25258-note-0003"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Cognition in a Macaque PD Model</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Levodopa improves motor deficits but can further disrupt cognition in a macaque parkinson model</title></titleInfo><name type="personal"><namePart type="given">Jay S.</namePart><namePart type="family">Schneider</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Pennsylvania, Philadelphia, USA</affiliation><affiliation>E-mail: jay.schneider@jefferson.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elsa Y.</namePart><namePart type="family">Pioli</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yang</namePart><namePart type="family">Jianzhong</namePart><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Qin</namePart><namePart type="family">Li</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Erwan</namePart><namePart type="family">Bezard</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Motac Cognition Inc, Beijing, China</affiliation><affiliation>Motac Neuroscience Ltd, Manchester, UK</affiliation><affiliation>Centre National de la Recherche Scientifique, Institute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, UMR 5293, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2013-05</dateIssued><dateCreated encoding="w3cdtf">2013-05-13</dateCreated><dateCaptured encoding="w3cdtf">2012-08-08</dateCaptured><dateValid encoding="w3cdtf">2012-09-27</dateValid><copyrightDate encoding="w3cdtf">2013</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract>Levodopa effectively relieves motor symptoms in Parkinson's disease (PD), but has had inconsistent effects on cognition, even worsening some aspects of cognitive functioning. Therefore, remediation of PD cognitive deficits is a major unmet need. However, drug development efforts have been hampered by lack of an animal model in which motor and cognitive deficits can be examined simultaneously.</abstract><abstract>Cynomolgus monkeys were trained to perform cognitive tasks and then chronically exposed to MPTP to slowly produce cognitive and motor deficits of parkinsonism.</abstract><abstract>Administration of L‐dopa to these animals dose dependently improved motor functioning, but did not significantly improve cognitive performance. At doses that maximally improved motor function, additional cognitive deficits were observed. The present model of MPTP‐induced parkinsonism recapitulates important motor and cognitive aspects of PD. Results with L‐dopa mirror data derived from PD patients.</abstract><abstract>This model should allow more efficient testing of potential PD therapeutics to evaluate motor and cognitive functions simultaneously. © 2012 Movement Disorder Society</abstract><subject><genre>keywords</genre><topic>levodopa</topic><topic>MPTP</topic><topic>primate</topic><topic>cognition</topic><topic>motor</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>Brief Report</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>2013</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>663</start><end>667</end><total>5</total></extent></part></relatedItem><identifier type="istex">F043B1F7A3E6ABE8FE272426DA5F6F196C0F3950</identifier><identifier type="DOI">10.1002/mds.25258</identifier><identifier type="ArticleID">MDS25258</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2012 Movement Disorders SocietyCopyright © 2012 Movement Disorders Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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