Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study
Identifieur interne : 000F58 ( Main/Corpus ); précédent : 000F57; suivant : 000F59Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study
Auteurs : Michael Y. Shino ; Valerie Mcguire ; Stephen K. Van Den Eeden ; Caroline M. Tanner ; Rita Popat ; Amethyst Leimpeter ; Allan L. Bernstein ; Lorene M. NelsonSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
English descriptors
Abstract
To assess the familial aggregation of Parkinson's disease (PD), we compared the cumulative incidence of PD among first‐degree relatives of PD cases and controls. We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; P = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; P = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23361
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15">2010-11-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2587">2587</biblScope><biblScope unit="page" to="2594">2594</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">11D1CEA0D26146D8925CC9EC4E7265AD278D9C39</idno><idno type="DOI">10.1002/mds.23361</idno><idno type="ArticleID">MDS23361</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>case‐control</term><term>epidemiology</term><term>family history</term><term>risk factors</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">To assess the familial aggregation of Parkinson's disease (PD), we compared the cumulative incidence of PD among first‐degree relatives of PD cases and controls. We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; P = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; P = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Michael Y. Shino MD</name><affiliations><json:string>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</json:string><json:string>Current Address: UCLA Med‐Pulmonary and Critical Care, Los Angeles, California, USA</json:string></affiliations></json:item><json:item><name>Valerie McGuire PhD</name><affiliations><json:string>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</json:string></affiliations></json:item><json:item><name>Stephen K. Van Den Eeden PhD</name><affiliations><json:string>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</json:string></affiliations></json:item><json:item><name>Caroline M. Tanner MD, PhD</name><affiliations><json:string>The Parkinson's Institute, Sunnyvale, California, USA</json:string></affiliations></json:item><json:item><name>Rita Popat PhD</name><affiliations><json:string>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</json:string></affiliations></json:item><json:item><name>Amethyst Leimpeter MS</name><affiliations><json:string>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</json:string></affiliations></json:item><json:item><name>Allan L. Bernstein MD</name><affiliations><json:string>Kaiser Santa Rosa Medical Center, Santa Rosa, California, USA</json:string></affiliations></json:item><json:item><name>Lorene M. Nelson PhD</name><affiliations><json:string>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>risk factors</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>family history</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>case‐control</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>epidemiology</value></json:item></subject><articleId><json:string>MDS23361</json:string></articleId><language><json:string>eng</json:string></language><abstract>To assess the familial aggregation of Parkinson's disease (PD), we compared the cumulative incidence of PD among first‐degree relatives of PD cases and controls. We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; P = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; P = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>7.441</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1523</abstractCharCount><pdfWordCount>4537</pdfWordCount><pdfCharCount>29256</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>242</abstractWordCount></qualityIndicators><title>Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study</title><genre><json:string>article</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>8</total><last>2594</last><first>2587</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</issue><subject><json:item><value>Research Article</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><publicationDate>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23361</json:string></doi><id>11D1CEA0D26146D8925CC9EC4E7265AD278D9C39</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/11D1CEA0D26146D8925CC9EC4E7265AD278D9C39/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/11D1CEA0D26146D8925CC9EC4E7265AD278D9C39/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/11D1CEA0D26146D8925CC9EC4E7265AD278D9C39/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.</note><note>NINDS - No. RO1‐NS31964;</note><note>NIEHS - No. R03‐13970;</note><note>Kaiser Permanente Medical Care Program of Northern California</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study</title><author><persName><forename type="first">Michael Y.</forename><surname>Shino</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation><affiliation>Current Address: UCLA Med‐Pulmonary and Critical Care, Los Angeles, California, USA</affiliation></author><author><persName><forename type="first">Valerie</forename><surname>McGuire</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation></author><author><persName><forename type="first">Stephen K.</forename><surname>Van Den Eeden</surname></persName><roleName type="degree">PhD</roleName><affiliation>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</affiliation></author><author><persName><forename type="first">Caroline M.</forename><surname>Tanner</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>The Parkinson's Institute, Sunnyvale, California, USA</affiliation></author><author><persName><forename type="first">Rita</forename><surname>Popat</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation></author><author><persName><forename type="first">Amethyst</forename><surname>Leimpeter</surname></persName><roleName type="degree">MS</roleName><affiliation>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</affiliation></author><author><persName><forename type="first">Allan L.</forename><surname>Bernstein</surname></persName><roleName type="degree">MD</roleName><affiliation>Kaiser Santa Rosa Medical Center, Santa Rosa, California, USA</affiliation></author><author><persName><forename type="first">Lorene M.</forename><surname>Nelson</surname></persName><roleName type="degree">PhD</roleName><note type="correspondence"><p>Correspondence: Department of Health Research and Policy, HRP Redwood Building, Room T223, Stanford University School of Medicine, Stanford, California</p></note><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; P = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; P = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>risk factors</term></item><item><term>family history</term></item><item><term>case‐control</term></item><item><term>epidemiology</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-01-10">Received</change><change when="2010-06-28">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/11D1CEA0D26146D8925CC9EC4E7265AD278D9C39/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. 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href="file:MDS.MDS23361.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="49"></count><count type="wordTotal" number="5994"></count></countGroup><titleGroup><title type="main" xml:lang="en">Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study<link href="#fn1"></link></title><title type="short" xml:lang="en">Familial Aggregation and Risk of PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" currentRef="#curr1"><personName><givenNames>Michael Y.</givenNames><familyName>Shino</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Valerie</givenNames><familyName>McGuire</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Stephen K.</givenNames><familyName>Van Den Eeden</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Caroline M.</givenNames><familyName>Tanner</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Rita</givenNames><familyName>Popat</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Amethyst</givenNames><familyName>Leimpeter</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Allan L.</givenNames><familyName>Bernstein</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Lorene M.</givenNames><familyName>Nelson</familyName><degrees>PhD</degrees></personName><contactDetails><email>lnelson@stanford.edu</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>The Parkinson's Institute, Sunnyvale, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Kaiser Santa Rosa Medical Center, Santa Rosa, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="curr1" countryCode="US"><unparsedAffiliation>UCLA Med‐Pulmonary and Critical Care, Los Angeles, California, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">risk factors</keyword><keyword xml:id="kwd3">family history</keyword><keyword xml:id="kwd4">case‐control</keyword><keyword xml:id="kwd5">epidemiology</keyword></keywordGroup><fundingInfo><fundingAgency>NINDS</fundingAgency><fundingNumber>RO1‐NS31964</fundingNumber></fundingInfo><fundingInfo><fundingAgency>NIEHS</fundingAgency><fundingNumber>R03‐13970</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Kaiser Permanente Medical Care Program of Northern California</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>To assess the familial aggregation of Parkinson's disease (PD), we compared the cumulative incidence of PD among first‐degree relatives of PD cases and controls. We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; <i>P</i> = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; <i>P</i> = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Familial Aggregation and Risk of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Familial aggregation of Parkinson's disease in a multiethnic community‐based case‐control study</title></titleInfo><name type="personal"><namePart type="given">Michael Y.</namePart><namePart type="family">Shino</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation><affiliation>Current Address: UCLA Med‐Pulmonary and Critical Care, Los Angeles, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Valerie</namePart><namePart type="family">McGuire</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephen K.</namePart><namePart type="family">Van Den Eeden</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Caroline M.</namePart><namePart type="family">Tanner</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>The Parkinson's Institute, Sunnyvale, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rita</namePart><namePart type="family">Popat</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Amethyst</namePart><namePart type="family">Leimpeter</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Division of Research, Kaiser Foundation Research Institute, Oakland, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Allan L.</namePart><namePart type="family">Bernstein</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Kaiser Santa Rosa Medical Center, Santa Rosa, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lorene M.</namePart><namePart type="family">Nelson</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Health Research and Policy, Division of Epidemiology, Stanford University School of Medicine, Stanford, California, USA</affiliation><description>Correspondence: Department of Health Research and Policy, HRP Redwood Building, Room T223, Stanford University School of Medicine, Stanford, California</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-01-10</dateCaptured><dateValid encoding="w3cdtf">2010-06-28</dateValid><copyrightDate encoding="w3cdtf">2010</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">3</extent><extent unit="references">49</extent><extent unit="words">5994</extent></physicalDescription><abstract lang="en">To assess the familial aggregation of Parkinson's disease (PD), we compared the cumulative incidence of PD among first‐degree relatives of PD cases and controls. We identified newly diagnosed patients with PD (n = 573) during 1994 to 1995 within Kaiser Permanente Medical Care Program of Northern California and recruited 496 cases (87%) for the case‐control study. Of 720 eligible controls matched by birth year and sex to cases, 541 (75%) agreed to participate. Information on family history of PD and other neurodegenerative diseases was obtained by in‐person structured interview. We used the reconstructed cohort approach that provides a better estimate of the risk. The cumulative incidence of PD was significantly higher among relatives of PD patients compared with relatives of controls (2.0 vs. 0.7%; relative risk (RR) = 3.4, 95% confidence interval (CI) 1.9–5.9; P = 0.0001). The degree of familial aggregation was higher among first‐degree relatives of Hispanic PD cases compared with Hispanic controls (3.7% vs. 0.4%; RR = 8.5, 95% CI 1.0–68.9) than it was among non‐Hispanic Caucasian cases and controls (2.0% vs. 0.8%; RR = 2.7, 95% CI 1.5–5.1; P = 0.02). The familial aggregation of PD was stronger among the siblings of PD cases (RR = 5.4, 95% CI 1.8–16.0) than among parents (RR = 2.7, 95% CI 1.3–5.2). The incidence and familial aggregation of PD is highest among Hispanics, warranting further studies of genetic and environmental risk factors in the Hispanic population. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><note type="funding">NINDS - No. RO1‐NS31964; </note><note type="funding">NIEHS - No. R03‐13970; </note><note type="funding">Kaiser Permanente Medical Care Program of Northern California</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>risk factors</topic><topic>family history</topic><topic>case‐control</topic><topic>epidemiology</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>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>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2587</start><end>2594</end><total>8</total></extent></part></relatedItem><identifier type="istex">11D1CEA0D26146D8925CC9EC4E7265AD278D9C39</identifier><identifier type="DOI">10.1002/mds.23361</identifier><identifier type="ArticleID">MDS23361</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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