Complex interactions in Parkinson's disease: A two‐phased approach
Identifieur interne : 001E32 ( Istex/Corpus ); précédent : 001E31; suivant : 001E33Complex interactions in Parkinson's disease: A two‐phased approach
Auteurs : Demetrius M. Maraganore ; Mariza De Andrade ; Timothy G. Lesnick ; Matthew J. Farrer ; James H. Bower ; John A. Hardy ; Walter A. RoccaSource :
- Movement Disorders [ 0885-3185 ] ; 2003-06.
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- KwdEn :
Abstract
The identification of pathogenic mutations in the three genes α‐synuclein, parkin, and ubiquitin carboxy‐terminal hydrolase L1 (UCHL1) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two‐phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and α‐synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS. © 2003 Movement Disorder Society
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DOI: 10.1002/mds.10431
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ISTEX:6D2F0F2002A2C9CA6122A9E865C7C8B5D95EB5E0Le document en format XML
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In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two‐phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and α‐synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS. © 2003 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Demetrius M. 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In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two‐phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and α‐synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). 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xml:id="kwd5">epistasis</keyword><keyword xml:id="kwd6">interactions</keyword></keywordGroup><fundingInfo><fundingAgency>National Institute of Environmental Health Sciences</fundingAgency><fundingNumber>ES10751</fundingNumber></fundingInfo><fundingInfo><fundingAgency>National Institute of Neurological Disorders and Stroke</fundingAgency><fundingNumber>NS33978</fundingNumber><fundingNumber>NS40256</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Mayo Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The identification of pathogenic mutations in the three genes α‐<i>synuclein</i>, <i>parkin</i>, and <i>ubiquitin carboxy‐terminal hydrolase L1</i> (<i>UCHL1</i>) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two‐phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of <i>UCHL1</i> and α‐<i>synuclein</i> genotypes with significant effects on PD risk (odds ratio = 2.42; <i>P</i> = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS. © 2003 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Complex interactions in Parkinson's disease: A two‐phased approach</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Interactions in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Complex interactions in Parkinson's disease: A two‐phased approach</title></titleInfo><name type="personal"><namePart type="given">Demetrius M.</namePart><namePart type="family">Maraganore</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><description>Correspondence: Department of Neurology, Mayo Clinic and Mayo Foundation, 200 First Street S.W., Rochester, MN 55905</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mariza</namePart><namePart type="family">de Andrade</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Health Sciences Research, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Timothy G.</namePart><namePart type="family">Lesnick</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Health Sciences Research, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matthew J.</namePart><namePart type="family">Farrer</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neuroscience, Mayo Clinic and Mayo Foundation, Jacksonville, Florida, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James H.</namePart><namePart type="family">Bower</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John A.</namePart><namePart type="family">Hardy</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Walter A.</namePart><namePart type="family">Rocca</namePart><namePart type="termsOfAddress">MD, MPH</namePart><affiliation>Department of Neurology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><affiliation>Department of Health Sciences Research, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2003-06</dateIssued><dateCaptured encoding="w3cdtf">2002-07-03</dateCaptured><dateValid encoding="w3cdtf">2002-11-07</dateValid><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">40</extent><extent unit="words">4401</extent></physicalDescription><abstract lang="en">The identification of pathogenic mutations in the three genes α‐synuclein, parkin, and ubiquitin carboxy‐terminal hydrolase L1 (UCHL1) has elucidated the ubiquitin proteasome system (UPS) and its potential role as a causal pathway in Parkinson's disease (PD). In addition, polymorphisms of these three genes have been shown to be independently associated with PD. In a sample of 298 unrelated PD cases and 185 controls, we applied a two‐phased approach of recursive partitioning and logistic regression analyses to explore complex interactions. For women only, we observed an epistatic interaction of UCHL1 and α‐synuclein genotypes with significant effects on PD risk (odds ratio = 2.42; P = 0.003). Our findings are consistent with the hypothesis that PD is a multigenic disorder of the UPS. © 2003 Movement Disorder Society</abstract><note type="funding">National Institute of Environmental Health Sciences - No. ES10751; </note><note type="funding">National Institute of Neurological Disorders and Stroke - No. NS33978; No. NS40256; </note><note type="funding">Mayo Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>susceptibility genes</topic><topic>ubiquitin proteasome system</topic><topic>recursive partitioning</topic><topic>epistasis</topic><topic>interactions</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>631</start><end>636</end><total>6</total></extent></part></relatedItem><identifier type="istex">6D2F0F2002A2C9CA6122A9E865C7C8B5D95EB5E0</identifier><identifier type="DOI">10.1002/mds.10431</identifier><identifier type="ArticleID">MDS10431</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2003 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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