LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study
Identifieur interne : 000E90 ( Main/Corpus ); précédent : 000E89; suivant : 000E91LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study
Auteurs : S. Sharma ; R. Bandopadhyay ; T. Lashley ; A. E. M. Renton ; A. E. Kingsbury ; R. Kumaran ; C. Kallis ; C. Vilari O-Güell ; S. S. O'Sullivan ; A. J. Lees ; T. Revesz ; N. W. Wood ; J. L. HoltonSource :
- Neuropathology and Applied Neurobiology [ 0305-1846 ] ; 2011-12.
English descriptors
Abstract
S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) Neuropathology and Applied Neurobiology37, 777–790 LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study Aims: Mutations in the gene encoding leucine‐rich repeat kinase‐2 (LRRK2) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common LRRK2 G2019S mutation. Methods: To further elucidate the role of LRRK2 in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. Results: Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.
Url:
DOI: 10.1111/j.1365-2990.2011.01187.x
Links to Exploration step
ISTEX:F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10FLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title><author><name sortKey="Sharma, S" sort="Sharma, S" uniqKey="Sharma S" first="S." last="Sharma">S. Sharma</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Human Genetics and Health, UCL, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Bandopadhyay, R" sort="Bandopadhyay, R" uniqKey="Bandopadhyay R" first="R." last="Bandopadhyay">R. Bandopadhyay</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Lashley, T" sort="Lashley, T" uniqKey="Lashley T" first="T." last="Lashley">T. Lashley</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Renton, A E M" sort="Renton, A E M" uniqKey="Renton A" first="A. E. M." last="Renton">A. E. M. Renton</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Human Genetics and Health, UCL, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kingsbury, A E" sort="Kingsbury, A E" uniqKey="Kingsbury A" first="A. E." last="Kingsbury">A. E. Kingsbury</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Kumaran, R" sort="Kumaran, R" uniqKey="Kumaran R" first="R." last="Kumaran">R. Kumaran</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Kallis, C" sort="Kallis, C" uniqKey="Kallis C" first="C." last="Kallis">C. Kallis</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Vilari O Ell, C" sort="Vilari O Ell, C" uniqKey="Vilari O Ell C" first="C." last="Vilari O-Güell">C. Vilari O-Güell</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="O Sullivan, S S" sort="O Sullivan, S S" uniqKey="O Sullivan S" first="S. S." last="O'Sullivan">S. S. O'Sullivan</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A. J." last="Lees">A. J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Revesz, T" sort="Revesz, T" uniqKey="Revesz T" first="T." last="Revesz">T. Revesz</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Wood, N W" sort="Wood, N W" uniqKey="Wood N" first="N. W." last="Wood">N. W. Wood</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Holton, J L" sort="Holton, J L" uniqKey="Holton J" first="J. L." last="Holton">J. L. Holton</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1111/j.1365-2990.2011.01187.x</idno><idno type="url">https://api.istex.fr/document/F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000E90</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title><author><name sortKey="Sharma, S" sort="Sharma, S" uniqKey="Sharma S" first="S." last="Sharma">S. Sharma</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Human Genetics and Health, UCL, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Bandopadhyay, R" sort="Bandopadhyay, R" uniqKey="Bandopadhyay R" first="R." last="Bandopadhyay">R. Bandopadhyay</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Lashley, T" sort="Lashley, T" uniqKey="Lashley T" first="T." last="Lashley">T. Lashley</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Renton, A E M" sort="Renton, A E M" uniqKey="Renton A" first="A. E. M." last="Renton">A. E. M. Renton</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation><affiliation><mods:affiliation>Institute of Human Genetics and Health, UCL, London, UK</mods:affiliation></affiliation></author><author><name sortKey="Kingsbury, A E" sort="Kingsbury, A E" uniqKey="Kingsbury A" first="A. E." last="Kingsbury">A. E. Kingsbury</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Kumaran, R" sort="Kumaran, R" uniqKey="Kumaran R" first="R." last="Kumaran">R. Kumaran</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Kallis, C" sort="Kallis, C" uniqKey="Kallis C" first="C." last="Kallis">C. Kallis</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Vilari O Ell, C" sort="Vilari O Ell, C" uniqKey="Vilari O Ell C" first="C." last="Vilari O-Güell">C. Vilari O-Güell</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="O Sullivan, S S" sort="O Sullivan, S S" uniqKey="O Sullivan S" first="S. S." last="O'Sullivan">S. S. O'Sullivan</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Lees, A J" sort="Lees, A J" uniqKey="Lees A" first="A. J." last="Lees">A. J. Lees</name><affiliation><mods:affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Revesz, T" sort="Revesz, T" uniqKey="Revesz T" first="T." last="Revesz">T. Revesz</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Wood, N W" sort="Wood, N W" uniqKey="Wood N" first="N. W." last="Wood">N. W. Wood</name><affiliation><mods:affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author><author><name sortKey="Holton, J L" sort="Holton, J L" uniqKey="Holton J" first="J. L." last="Holton">J. L. Holton</name><affiliation><mods:affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuropathology and Applied Neurobiology</title><idno type="ISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-12">2011-12</date><biblScope unit="volume">37</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="777">777</biblScope><biblScope unit="page" to="790">790</biblScope></imprint><idno type="ISSN">0305-1846</idno></series><idno type="istex">F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F</idno><idno type="DOI">10.1111/j.1365-2990.2011.01187.x</idno><idno type="ArticleID">NAN1187</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0305-1846</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>G2019S mutation</term><term>LRRK2</term><term>LRRK2 mRNA</term><term>LRRK2 protein</term><term>Lewy bodies</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) Neuropathology and Applied Neurobiology37, 777–790 LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study Aims: Mutations in the gene encoding leucine‐rich repeat kinase‐2 (LRRK2) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common LRRK2 G2019S mutation. Methods: To further elucidate the role of LRRK2 in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. Results: Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>S. Sharma</name><affiliations><json:string>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string><json:string>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string><json:string>Institute of Human Genetics and Health, UCL, London, UK</json:string></affiliations></json:item><json:item><name>R. Bandopadhyay</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>T. Lashley</name><affiliations><json:string>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>A. E. M. Renton</name><affiliations><json:string>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string><json:string>Institute of Human Genetics and Health, UCL, London, UK</json:string></affiliations></json:item><json:item><name>A. E. Kingsbury</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>R. Kumaran</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>C. Kallis</name><affiliations><json:string>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>C. Vilariño‐Güell</name><affiliations><json:string>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>S. S. O'Sullivan</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>A. J. Lees</name><affiliations><json:string>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>T. Revesz</name><affiliations><json:string>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>N. W. Wood</name><affiliations><json:string>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item><json:item><name>J. L. Holton</name><affiliations><json:string>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>G2019S mutation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Lewy bodies</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LRRK2</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LRRK2 mRNA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LRRK2 protein</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><articleId><json:string>NAN1187</json:string></articleId><language><json:string>eng</json:string></language><abstract>S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) Neuropathology and Applied Neurobiology37, 777–790 LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study Aims: Mutations in the gene encoding leucine‐rich repeat kinase‐2 (LRRK2) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common LRRK2 G2019S mutation. Methods: To further elucidate the role of LRRK2 in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. Results: Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1951</abstractCharCount><pdfWordCount>7685</pdfWordCount><pdfCharCount>47233</pdfCharCount><pdfPageCount>14</pdfPageCount><abstractWordCount>287</abstractWordCount></qualityIndicators><title>LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title><genre><json:string>article</json:string></genre><host><volume>37</volume><publisherId><json:string>NAN</json:string></publisherId><pages><total>14</total><last>790</last><first>777</first></pages><issn><json:string>0305-1846</json:string></issn><issue>7</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1365-2990</json:string></eissn><title>Neuropathology and Applied Neurobiology</title><doi><json:string>10.1111/(ISSN)1365-2990</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1111/j.1365-2990.2011.01187.x</json:string></doi><id>F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title><author><persName><forename type="first">S.</forename><surname>Sharma</surname></persName><note type="correspondence"><p>Correspondence: Janice Holton, Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, 1 Wakefield Street, UCL, London WC1N 1PJ, UK. Tel: +44 0207 676 2168; Fax: +44 0207 676 2157; E‐mail:</p></note><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Institute of Human Genetics and Health, UCL, London, UK</affiliation></author><author><persName><forename type="first">R.</forename><surname>Bandopadhyay</surname></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">T.</forename><surname>Lashley</surname></persName><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">A. E. M.</forename><surname>Renton</surname></persName><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Institute of Human Genetics and Health, UCL, London, UK</affiliation></author><author><persName><forename type="first">A. E.</forename><surname>Kingsbury</surname></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">R.</forename><surname>Kumaran</surname></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">C.</forename><surname>Kallis</surname></persName><note type="biography">Current address: Forensic Psychiatry Research Unit, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.</note><affiliation>Current address: Forensic Psychiatry Research Unit, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.</affiliation><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">C.</forename><surname>Vilariño‐Güell</surname></persName><note type="biography">Current address: Centre for Applied Neurogenetics, Centre for Molecular Medicine and Therapeutics, 3011‐950 West 28th Avenue, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.</note><affiliation>Current address: Centre for Applied Neurogenetics, Centre for Molecular Medicine and Therapeutics, 3011‐950 West 28th Avenue, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.</affiliation><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">S. S.</forename><surname>O'Sullivan</surname></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">A. J.</forename><surname>Lees</surname></persName><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">T.</forename><surname>Revesz</surname></persName><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">N. W.</forename><surname>Wood</surname></persName><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author><author><persName><forename type="first">J. L.</forename><surname>Holton</surname></persName><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation></author></analytic><monogr><title level="j">Neuropathology and Applied Neurobiology</title><idno type="pISSN">0305-1846</idno><idno type="eISSN">1365-2990</idno><idno type="DOI">10.1111/(ISSN)1365-2990</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2011-12"></date><biblScope unit="volume">37</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="777">777</biblScope><biblScope unit="page" to="790">790</biblScope></imprint></monogr><idno type="istex">F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F</idno><idno type="DOI">10.1111/j.1365-2990.2011.01187.x</idno><idno type="ArticleID">NAN1187</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2011</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) Neuropathology and Applied Neurobiology37, 777–790 LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study Aims: Mutations in the gene encoding leucine‐rich repeat kinase‐2 (LRRK2) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common LRRK2 G2019S mutation. Methods: To further elucidate the role of LRRK2 in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. Results: Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>G2019S mutation</term></item><item><term>Lewy bodies</term></item><item><term>LRRK2</term></item><item><term>LRRK2 mRNA</term></item><item><term>LRRK2 protein</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F/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)1365-2990</doi><issn type="print">0305-1846</issn><issn type="electronic">1365-2990</issn><idGroup><id type="product" value="NAN"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY APPLIED NEUROBIOLOGY">Neuropathology and Applied Neurobiology</title></titleGroup></publicationMeta><publicationMeta level="part" position="12107"><doi origin="wiley">10.1111/nan.2011.37.issue-7</doi><numberingGroup><numbering type="journalVolume" number="37">37</numbering><numbering type="journalIssue" number="7">7</numbering></numberingGroup><coverDate startDate="2011-12">December 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley">10.1111/j.1365-2990.2011.01187.x</doi><idGroup><id type="unit" value="NAN1187"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><copyright>© 2011 The Authors. Neuropathology and Applied Neurobiology © 2011 British Neuropathological Society</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.10 mode:FullText" date="2011-10-27"></event><event type="publishedOnlineAccepted" date="2011-06-23"></event><event type="firstOnline" date="2011-10-27"></event><event type="publishedOnlineFinalForm" date="2011-10-27"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></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" number="777">777</numbering><numbering type="pageLast" number="790">790</numbering></numberingGroup><correspondenceTo>Janice Holton, Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, 1 Wakefield Street, UCL, London WC1N 1PJ, UK. Tel: +44 0207 676 2168; Fax: +44 0207 676 2157; E‐mail: <email>j.holton@ion.ucl.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NAN.NAN1187.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 9 November 2010; Accepted after revision 26 April 2011; Published online Article Accepted on 09 May 2011</unparsedEditorialHistory><countGroup><count type="figureTotal" number="5"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="71"></count><count type="wordTotal" number="8543"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title><title type="shortAuthors">S. Sharma <i>et al</i>.</title><title type="short">LRRK2 expression in Parkinson's disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a4" corresponding="yes"><personName><givenNames>S.</givenNames><familyName>Sharma</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a3"><personName><givenNames>R.</givenNames><familyName>Bandopadhyay</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>T.</givenNames><familyName>Lashley</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a2 #a4"><personName><givenNames>A. E. M.</givenNames><familyName>Renton</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a3"><personName><givenNames>A. E.</givenNames><familyName>Kingsbury</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a3"><personName><givenNames>R.</givenNames><familyName>Kumaran</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a2" noteRef="#fn1"><personName><givenNames>C.</givenNames><familyName>Kallis</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a2" noteRef="#fn2"><personName><givenNames>C.</givenNames><familyName>Vilariño‐Güell</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a3"><personName><givenNames>S. S.</givenNames><familyName>O'Sullivan</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a3"><personName><givenNames>A. J.</givenNames><familyName>Lees</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a1"><personName><givenNames>T.</givenNames><familyName>Revesz</familyName></personName></creator><creator creatorRole="author" xml:id="cr12" affiliationRef="#a2"><personName><givenNames>N. W.</givenNames><familyName>Wood</familyName></personName></creator><creator creatorRole="author" xml:id="cr13" affiliationRef="#a1"><personName><givenNames>J. L.</givenNames><familyName>Holton</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="GB"><unparsedAffiliation>Institute of Human Genetics and Health, UCL, London, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">G2019S mutation</keyword><keyword xml:id="k2">Lewy bodies</keyword><keyword xml:id="k3"><i>LRRK2</i></keyword><keyword xml:id="k4">LRRK2 mRNA</keyword><keyword xml:id="k5">LRRK2 protein</keyword><keyword xml:id="k6">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) <i>Neuropathology and Applied Neurobiology</i><b>37,</b> 777–790</p><p><b>LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</b></p><p><b>Aims:</b> Mutations in the gene encoding leucine‐rich repeat kinase‐2 (<i>LRRK2</i>) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common <i>LRRK2</i> G2019S mutation. <b>Methods:</b> To further elucidate the role of <i>LRRK2</i> in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. <b>Results:</b> Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. <b>Conclusions:</b> Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p> Current address: Forensic Psychiatry Research Unit, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.</p></note><note xml:id="fn2"><p> Current address: Centre for Applied Neurogenetics, Centre for Molecular Medicine and Therapeutics, 3011‐950 West 28th Avenue, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title></titleInfo><titleInfo type="abbreviated"><title>LRRK2 expression in Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study</title></titleInfo><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Sharma</namePart><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Institute of Human Genetics and Health, UCL, London, UK</affiliation><description>Correspondence: Janice Holton, Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, 1 Wakefield Street, UCL, London WC1N 1PJ, UK. Tel: +44 0207 676 2168; Fax: +44 0207 676 2157; E‐mail: </description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Bandopadhyay</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Lashley</namePart><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. E. M.</namePart><namePart type="family">Renton</namePart><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><affiliation>Institute of Human Genetics and Health, UCL, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. E.</namePart><namePart type="family">Kingsbury</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">R.</namePart><namePart type="family">Kumaran</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Kallis</namePart><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><description>Current address: Forensic Psychiatry Research Unit, Queen Mary, University of London, Charterhouse Square, London EC1M 6BQ, UK.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Vilariño‐Güell</namePart><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><description>Current address: Centre for Applied Neurogenetics, Centre for Molecular Medicine and Therapeutics, 3011‐950 West 28th Avenue, University of British Columbia, Vancouver, British Columbia, Canada V5Z 4H4.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S. S.</namePart><namePart type="family">O'Sullivan</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. J.</namePart><namePart type="family">Lees</namePart><affiliation>Reta Lila Weston Institute of Neurological Studies, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">T.</namePart><namePart type="family">Revesz</namePart><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. W.</namePart><namePart type="family">Wood</namePart><affiliation>Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. L.</namePart><namePart type="family">Holton</namePart><affiliation>Queen Square Brain Bank, Department of Molecular Neuroscience, UCL Institute of Neurology, UCL</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">2011-12</dateIssued><edition>Received 9 November 2010; Accepted after revision 26 April 2011; Published online Article Accepted on 09 May 2011</edition><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">5</extent><extent unit="tables">2</extent><extent unit="references">71</extent><extent unit="words">8543</extent></physicalDescription><abstract lang="en">S. Sharma, R. Bandopadhyay, T. Lashley, A. E. M. Renton, A. E. Kingsbury, R. Kumaran, C. Kallis, C. Vilariño‐Güell, S. S. O'Sullivan, A. J. Lees, T. Revesz, N. W. Wood and J. L. Holton (2011) Neuropathology and Applied Neurobiology37, 777–790 LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study Aims: Mutations in the gene encoding leucine‐rich repeat kinase‐2 (LRRK2) have been established as a common genetic cause of Parkinson's disease (PD). The distribution of LRRK2 mRNA and protein in the human brain has previously been described, although it has not been reported in PD cases with the common LRRK2 G2019S mutation. Methods: To further elucidate the role of LRRK2 in PD, we determined the localization of LRRK2 mRNA and protein in post‐mortem brain tissue from control, idiopathic PD (IPD) and G2019S positive PD cases. Results: Widespread neuronal expression of LRRK2 mRNA and protein was recorded and no difference was observed in the morphological localization of LRRK2 mRNA or protein between control, IPD and G2019S positive PD cases. Using quantitative real‐time polymerase chain reaction, we demonstrated that there is no regional variation in LRRK2 mRNA in normal human brain, but we have identified differential expression of LRRK2 mRNA with significant reductions recorded in limbic and neocortical regions of IPD cases compared with controls. Semi‐quantitative analysis of LRRK2 immunohistochemical staining demonstrated regional variation in staining intensity, with weak LRRK2 immunoreactivity consistently recorded in the striatum and substantia nigra. No clear differences were identified in LRRK2 immunoreactivity between control, IPD and G2019S positive PD cases. LRRK2 protein was identified in a small proportion of Lewy bodies. Conclusions: Our data suggest that widespread dysregulation of LRRK2 mRNA expression may contribute to the pathogenesis of IPD.</abstract><subject lang="en"><genre>Keywords</genre><topic>G2019S mutation</topic><topic>Lewy bodies</topic><topic>LRRK2</topic><topic>LRRK2 mRNA</topic><topic>LRRK2 protein</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology and Applied Neurobiology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0305-1846</identifier><identifier type="eISSN">1365-2990</identifier><identifier type="DOI">10.1111/(ISSN)1365-2990</identifier><identifier type="PublisherID">NAN</identifier><part><date>2011</date><detail type="volume"><caption>vol.</caption><number>37</number></detail><detail type="issue"><caption>no.</caption><number>7</number></detail><extent unit="pages"><start>777</start><end>790</end><total>14</total></extent></part></relatedItem><identifier type="istex">F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F</identifier><identifier type="DOI">10.1111/j.1365-2990.2011.01187.x</identifier><identifier type="ArticleID">NAN1187</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 The Authors. Neuropathology and Applied Neurobiology © 2011 British Neuropathological Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</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 000E90 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Corpus/biblio.hfd -nk 000E90 | 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:F7C0B09C4EA0A2C84EB135FFFCD43E70853BC10F
|texte= LRRK2 expression in idiopathic and G2019S positive Parkinson's disease subjects: a morphological and quantitative study
}}
| This area was generated with Dilib version V0.6.23. |  |