Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia
Identifieur interne : 001182 ( Main/Corpus ); précédent : 001181; suivant : 001183Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia
Auteurs : M. J. Hurley ; P. H. Patel ; M. J. Jackson ; L. A. Smith ; S. Rose ; P. JennerSource :
- European Journal of Neuroscience [ 0953-816X ] ; 2007-07.
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- KwdEn :
Abstract
The level of leucine‐rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (Callithrix jacchus) that had l‐3,4‐dihydroxyphenylalanine methyl ester (l‐DOPA)‐induced dyskinesia. The level of striatal Lrrk2 mRNA was increased in MPTP‐treated common marmosets that had l‐DOPA‐induced dyskinesia compared with normal animals that did not receive l‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal Lrrk2 mRNA. Lrrk2 mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in Lrrk2 mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal Lrrk2 mRNA levels in MPTP‐treated common marmoset striatum and l‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause l‐DOPA‐induced dyskinesia.
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DOI: 10.1111/j.1460-9568.2007.05638.x
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ISTEX:AEC367FE37710A5CB8D4CB30A5D9611734837C54Le document en format XML
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Patel</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Jackson, M J" sort="Jackson, M J" uniqKey="Jackson M" first="M. J." last="Jackson">M. J. Jackson</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Smith, L A" sort="Smith, L A" uniqKey="Smith L" first="L. A." last="Smith">L. A. 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Jackson</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Smith, L A" sort="Smith, L A" uniqKey="Smith L" first="L. A." last="Smith">L. A. Smith</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</mods:affiliation></affiliation></author><author><name sortKey="Rose, S" sort="Rose, S" uniqKey="Rose S" first="S." last="Rose">S. 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Jenner</name><affiliation><mods:affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">European Journal of Neuroscience</title><idno type="ISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-07">2007-07</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="171">171</biblScope><biblScope unit="page" to="177">177</biblScope></imprint><idno type="ISSN">0953-816X</idno></series><idno type="istex">AEC367FE37710A5CB8D4CB30A5D9611734837C54</idno><idno type="DOI">10.1111/j.1460-9568.2007.05638.x</idno><idno type="ArticleID">EJN5638</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0953-816X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>basal ganglia</term><term>dopamine receptor signalling</term><term>kinases</term><term>protein phosphorylation</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The level of leucine‐rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (Callithrix jacchus) that had l‐3,4‐dihydroxyphenylalanine methyl ester (l‐DOPA)‐induced dyskinesia. The level of striatal Lrrk2 mRNA was increased in MPTP‐treated common marmosets that had l‐DOPA‐induced dyskinesia compared with normal animals that did not receive l‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal Lrrk2 mRNA. Lrrk2 mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in Lrrk2 mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal Lrrk2 mRNA levels in MPTP‐treated common marmoset striatum and l‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause l‐DOPA‐induced dyskinesia.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. J. 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Jenner</name><affiliations><json:string>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>basal ganglia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine receptor signalling</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>kinases</value></json:item><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>protein phosphorylation</value></json:item></subject><articleId><json:string>EJN5638</json:string></articleId><language><json:string>eng</json:string></language><abstract>The level of leucine‐rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (Callithrix jacchus) that had l‐3,4‐dihydroxyphenylalanine methyl ester (l‐DOPA)‐induced dyskinesia. The level of striatal Lrrk2 mRNA was increased in MPTP‐treated common marmosets that had l‐DOPA‐induced dyskinesia compared with normal animals that did not receive l‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal Lrrk2 mRNA. Lrrk2 mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in Lrrk2 mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal Lrrk2 mRNA levels in MPTP‐treated common marmoset striatum and l‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause l‐DOPA‐induced dyskinesia.</abstract><qualityIndicators><score>6.872</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1183</abstractCharCount><pdfWordCount>5656</pdfWordCount><pdfCharCount>35917</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>156</abstractWordCount></qualityIndicators><title>Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>EJN</json:string></publisherId><pages><total>7</total><last>177</last><first>171</first></pages><issn><json:string>0953-816X</json:string></issn><issue>1</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-9568</json:string></eissn><title>European Journal of Neuroscience</title><doi><json:string>10.1111/(ISSN)1460-9568</json:string></doi></host><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1111/j.1460-9568.2007.05638.x</json:string></doi><id>AEC367FE37710A5CB8D4CB30A5D9611734837C54</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/AEC367FE37710A5CB8D4CB30A5D9611734837C54/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/AEC367FE37710A5CB8D4CB30A5D9611734837C54/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/AEC367FE37710A5CB8D4CB30A5D9611734837C54/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2007</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia</title><author><persName><forename type="first">M. J.</forename><surname>Hurley</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">P. H.</forename><surname>Patel</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">M. J.</forename><surname>Jackson</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">L. A.</forename><surname>Smith</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">S.</forename><surname>Rose</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author><author><persName><forename type="first">P.</forename><surname>Jenner</surname></persName><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation></author></analytic><monogr><title level="j">European Journal of Neuroscience</title><idno type="pISSN">0953-816X</idno><idno type="eISSN">1460-9568</idno><idno type="DOI">10.1111/(ISSN)1460-9568</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2007-07"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="171">171</biblScope><biblScope unit="page" to="177">177</biblScope></imprint></monogr><idno type="istex">AEC367FE37710A5CB8D4CB30A5D9611734837C54</idno><idno type="DOI">10.1111/j.1460-9568.2007.05638.x</idno><idno type="ArticleID">EJN5638</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2007</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The level of leucine‐rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (Callithrix jacchus) that had l‐3,4‐dihydroxyphenylalanine methyl ester (l‐DOPA)‐induced dyskinesia. The level of striatal Lrrk2 mRNA was increased in MPTP‐treated common marmosets that had l‐DOPA‐induced dyskinesia compared with normal animals that did not receive l‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal Lrrk2 mRNA. Lrrk2 mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in Lrrk2 mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal Lrrk2 mRNA levels in MPTP‐treated common marmoset striatum and l‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause l‐DOPA‐induced dyskinesia.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>basal ganglia</term></item><item><term>dopamine receptor signalling</term></item><item><term>kinases</term></item><item><term>Parkinson's disease</term></item><item><term>protein phosphorylation</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2007-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AEC367FE37710A5CB8D4CB30A5D9611734837C54/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1460-9568</doi><issn type="print">0953-816X</issn><issn type="electronic">1460-9568</issn><idGroup><id type="product" value="EJN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF NEUROSCIENCE">European Journal of Neuroscience</title></titleGroup></publicationMeta><publicationMeta level="part" position="07001"><doi origin="wiley">10.1111/ejn.2007.26.issue-1</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2007-07">July 2007</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="16" status="forIssue"><doi origin="wiley">10.1111/j.1460-9568.2007.05638.x</doi><idGroup><id type="unit" value="EJN5638"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Research Reports</title></titleGroup><eventGroup><event type="firstOnline" date="2007-07-03"></event><event type="publishedOnlineFinalForm" date="2007-07-03"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.15 mode:FullText" date="2010-07-21"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-12"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="171">171</numbering><numbering type="pageLast" number="177">177</numbering></numberingGroup><correspondenceTo>Dr Michael J. Hurley, as above.
E‐mail: <email>michael.j.hurley@kcl.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:EJN.EJN5638.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 22 July 2006, revised 26 April 2007, accepted 21 May 2007</unparsedEditorialHistory><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="1"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="63"></count><count type="wordTotal" number="3708"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (<i>Callithrix jacchus</i>) with <sc>l</sc>‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia</title><title type="shortAuthors">M. J. Hurley <i>et al.</i></title><title type="short"><i>Lrrk2</i> mRNA levels in MPTP‐treated dyskinetic marmosets</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>M. J.</givenNames><familyName>Hurley</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>P. H.</givenNames><familyName>Patel</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>M. J.</givenNames><familyName>Jackson</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#aff-1-1"><personName><givenNames>L. A.</givenNames><familyName>Smith</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#aff-1-1"><personName><givenNames>S.</givenNames><familyName>Rose</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#aff-1-1"><personName><givenNames>P.</givenNames><familyName>Jenner</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="GB"><unparsedAffiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">basal ganglia</keyword><keyword xml:id="k2">dopamine receptor signalling</keyword><keyword xml:id="k3">kinases</keyword><keyword xml:id="k4">Parkinson's disease</keyword><keyword xml:id="k5">protein phosphorylation </keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The level of leucine‐rich repeat kinase 2 (<i>Lrrk2</i>) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (<i>Callithrix jacchus</i>) that had <sc>l</sc>‐3,4‐dihydroxyphenylalanine methyl ester (<sc>l</sc>‐DOPA)‐induced dyskinesia. The level of striatal <i>Lrrk2</i> mRNA was increased in MPTP‐treated common marmosets that had <sc>l</sc>‐DOPA‐induced dyskinesia compared with normal animals that did not receive <sc>l</sc>‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal <i>Lrrk2</i> mRNA. <i>Lrrk2</i> mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in <i>Lrrk2</i> mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal <i>Lrrk2</i> mRNA levels in MPTP‐treated common marmoset striatum and <sc>l</sc>‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause <sc>l</sc>‐DOPA‐induced dyskinesia.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (Callithrix jacchus) with l‐3, 4‐dihydroxyphenylalanine methyl ester‐induced dyskinesia</title></titleInfo><titleInfo type="abbreviated"><title>Lrrk2 mRNA levels in MPTP‐treated dyskinetic marmosets</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Striatal leucine‐rich repeat kinase 2 mRNA is increased in 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine‐lesioned common marmosets (</title></titleInfo><name type="personal"><namePart type="given">M. J.</namePart><namePart type="family">Hurley</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. H.</namePart><namePart type="family">Patel</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. J.</namePart><namePart type="family">Jackson</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">L. A.</namePart><namePart type="family">Smith</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Rose</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Jenner</namePart><affiliation>Neurodegenerative Diseases Research Group, Pharmaceutical Sciences Research Division, School of Biomedical and Health Sciences, King's College, London SE1 1UL, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2007-07</dateIssued><edition>Received 22 July 2006, revised 26 April 2007, accepted 21 May 2007</edition><copyrightDate encoding="w3cdtf">2007</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">4</extent><extent unit="tables">1</extent><extent unit="references">63</extent><extent unit="words">3708</extent></physicalDescription><abstract lang="en">The level of leucine‐rich repeat kinase 2 (Lrrk2) mRNA expression was measured by reverse transcription‐polymerase chain reaction in anterior striatum from normal and 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)‐treated common marmosets (Callithrix jacchus) that had l‐3,4‐dihydroxyphenylalanine methyl ester (l‐DOPA)‐induced dyskinesia. The level of striatal Lrrk2 mRNA was increased in MPTP‐treated common marmosets that had l‐DOPA‐induced dyskinesia compared with normal animals that did not receive l‐DOPA. Marmosets that exhibited higher levels of dyskinesia had the greatest increase in striatal Lrrk2 mRNA. Lrrk2 mRNA expression was also measured in human striatum and substantia nigra from control subjects and patients dying with Parkinson's disease. In contrast to marmoset tissue, no alteration in Lrrk2 mRNA expression was found in parkinsonian human brain. However, the brain was from patients who had an overall low level of dyskinesia. The correlation between striatal Lrrk2 mRNA levels in MPTP‐treated common marmoset striatum and l‐DOPA‐induced dyskinesia indicates that LRRK2 may have a role in the molecular alterations that cause l‐DOPA‐induced dyskinesia.</abstract><subject lang="en"><genre>Keywords</genre><topic>basal ganglia</topic><topic>dopamine receptor signalling</topic><topic>kinases</topic><topic>Parkinson's disease</topic><topic>protein phosphorylation</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neuroscience</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0953-816X</identifier><identifier type="eISSN">1460-9568</identifier><identifier type="DOI">10.1111/(ISSN)1460-9568</identifier><identifier type="PublisherID">EJN</identifier><part><date>2007</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>171</start><end>177</end><total>7</total></extent></part></relatedItem><identifier type="istex">AEC367FE37710A5CB8D4CB30A5D9611734837C54</identifier><identifier type="DOI">10.1111/j.1460-9568.2007.05638.x</identifier><identifier type="ArticleID">EJN5638</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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