Apolipoprotein E ϵ4 and catechol‐O‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations
Identifieur interne : 000642 ( Main/Corpus ); précédent : 000641; suivant : 000643Apolipoprotein E ϵ4 and catechol‐O‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations
Auteurs : Richard Camicioli ; Ali Rajput ; Michelle Rajput ; Christian Reece ; Haydeh Payami ; Chunhai Hao ; Alex RajputSource :
- Movement Disorders [ 0885-3185 ] ; 2005-08.
English descriptors
- KwdEn :
Abstract
We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐O‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. The observation that males have increased dementia risk and the trend for ApoE4 requires confirmation in larger prospective autopsy studies. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20481
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ISTEX:18A0ACE65619AB988E7D837613A1DD2EB1E0A74CLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Apolipoprotein E ϵ4 and catechol‐O‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations</title><author><name sortKey="Camicioli, Richard" sort="Camicioli, Richard" uniqKey="Camicioli R" first="Richard" last="Camicioli">Richard Camicioli</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Ali" sort="Rajput, Ali" uniqKey="Rajput A" first="Ali" last="Rajput">Ali Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Michelle" sort="Rajput, Michelle" uniqKey="Rajput M" first="Michelle" last="Rajput">Michelle Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author><author><name sortKey="Reece, Christian" sort="Reece, Christian" uniqKey="Reece C" first="Christian" last="Reece">Christian Reece</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><affiliation><mods:affiliation>Wadsworth Center, Albany, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Hao, Chunhai" sort="Hao, Chunhai" uniqKey="Hao C" first="Chunhai" last="Hao">Chunhai Hao</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:18A0ACE65619AB988E7D837613A1DD2EB1E0A74C</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1002/mds.20481</idno><idno type="url">https://api.istex.fr/document/18A0ACE65619AB988E7D837613A1DD2EB1E0A74C/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000642</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Apolipoprotein E ϵ4 and catechol‐O‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations</title><author><name sortKey="Camicioli, Richard" sort="Camicioli, Richard" uniqKey="Camicioli R" first="Richard" last="Camicioli">Richard Camicioli</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Ali" sort="Rajput, Ali" uniqKey="Rajput A" first="Ali" last="Rajput">Ali Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Michelle" sort="Rajput, Michelle" uniqKey="Rajput M" first="Michelle" last="Rajput">Michelle Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author><author><name sortKey="Reece, Christian" sort="Reece, Christian" uniqKey="Reece C" first="Christian" last="Reece">Christian Reece</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Payami, Haydeh" sort="Payami, Haydeh" uniqKey="Payami H" first="Haydeh" last="Payami">Haydeh Payami</name><affiliation><mods:affiliation>Wadsworth Center, Albany, New York, USA</mods:affiliation></affiliation></author><author><name sortKey="Hao, Chunhai" sort="Hao, Chunhai" uniqKey="Hao C" first="Chunhai" last="Hao">Chunhai Hao</name><affiliation><mods:affiliation>University of Alberta, Edmonton, Alberta, Canada</mods:affiliation></affiliation></author><author><name sortKey="Rajput, Alex" sort="Rajput, Alex" uniqKey="Rajput A" first="Alex" last="Rajput">Alex Rajput</name><affiliation><mods:affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="2005-08">2005-08</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="989">989</biblScope><biblScope unit="page" to="994">994</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">18A0ACE65619AB988E7D837613A1DD2EB1E0A74C</idno><idno type="DOI">10.1002/mds.20481</idno><idno type="ArticleID">MDS20481</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apolipoprotein E</term><term>Parkinson's disease</term><term>catechol‐O‐methyltransferase</term><term>dementia</term><term>hallucinations</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐O‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. The observation that males have increased dementia risk and the trend for ApoE4 requires confirmation in larger prospective autopsy studies. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Richard Camicioli MD</name><affiliations><json:string>University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Ali Rajput MD</name><affiliations><json:string>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</json:string></affiliations></json:item><json:item><name>Michelle Rajput PhD</name><affiliations><json:string>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</json:string></affiliations></json:item><json:item><name>Christian Reece MD</name><affiliations><json:string>University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Haydeh Payami PhD</name><affiliations><json:string>Wadsworth Center, Albany, New York, USA</json:string></affiliations></json:item><json:item><name>Chunhai Hao PhD</name><affiliations><json:string>University of Alberta, Edmonton, Alberta, Canada</json:string></affiliations></json:item><json:item><name>Alex Rajput MD</name><affiliations><json:string>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</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>hallucinations</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Apolipoprotein E</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>catechol‐O‐methyltransferase</value></json:item></subject><articleId><json:string>MDS20481</json:string></articleId><language><json:string>eng</json:string></language><abstract>We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐O‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. 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Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-08"></date><biblScope unit="volume">20</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="989">989</biblScope><biblScope unit="page" to="994">994</biblScope></imprint></monogr><idno type="istex">18A0ACE65619AB988E7D837613A1DD2EB1E0A74C</idno><idno type="DOI">10.1002/mds.20481</idno><idno type="ArticleID">MDS20481</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐O‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. The observation that males have increased dementia risk and the trend for ApoE4 requires confirmation in larger prospective autopsy studies. © 2005 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>hallucinations</term></item><item><term>dementia</term></item><item><term>Apolipoprotein E</term></item><item><term>catechol‐O‐methyltransferase</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="2004-05-26">Received</change><change when="2004-11-23">Registration</change><change when="2005-08">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/18A0ACE65619AB988E7D837613A1DD2EB1E0A74C/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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type="figureTotal" number="0"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="43"></count><count type="wordTotal" number="4946"></count></countGroup><titleGroup><title type="main" xml:lang="en">Apolipoprotein E ϵ4 and catechol‐<i>O</i>‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations</title><title type="short" xml:lang="en">ApoE ϵ4 and COMT Alleles in Autopsy‐Proven PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Richard</givenNames><familyName>Camicioli</familyName><degrees>MD</degrees></personName><contactDetails><email>rcamicio@ualberta.ca</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Ali</givenNames><familyName>Rajput</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Michelle</givenNames><familyName>Rajput</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Christian</givenNames><familyName>Reece</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Haydeh</givenNames><familyName>Payami</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Chunhai</givenNames><familyName>Hao</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Alex</givenNames><familyName>Rajput</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="CA" type="organization"><unparsedAffiliation>University of Alberta, Edmonton, Alberta, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="CA" type="organization"><unparsedAffiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Wadsworth Center, Albany, New York, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">hallucinations</keyword><keyword xml:id="kwd3">dementia</keyword><keyword xml:id="kwd4">Apolipoprotein E</keyword><keyword xml:id="kwd5">catechol‐<i>O</i>‐methyltransferase</keyword></keywordGroup><fundingInfo><fundingAgency>Parkinson Disease Foundation (New York)</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐<i>O</i>‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. The observation that males have increased dementia risk and the trend for ApoE4 requires confirmation in larger prospective autopsy studies. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Apolipoprotein E ϵ4 and catechol‐O‐methyltransferase alleles in autopsy‐proven Parkinson's disease: Relationship to dementia and hallucinations</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ApoE ϵ4 and COMT Alleles in Autopsy‐Proven PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Apolipoprotein E ϵ4 and catechol‐</title></titleInfo><name type="personal"><namePart type="given">Richard</namePart><namePart type="family">Camicioli</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Alberta, Edmonton, Alberta, Canada</affiliation><description>Correspondence: E223, Glenrose Rehabilitation Hospital, 10230 111th Avenue, Edmonton, Alberta, Canada T5G 0B7</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ali</namePart><namePart type="family">Rajput</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michelle</namePart><namePart type="family">Rajput</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christian</namePart><namePart type="family">Reece</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Haydeh</namePart><namePart type="family">Payami</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Wadsworth Center, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chunhai</namePart><namePart type="family">Hao</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>University of Alberta, Edmonton, Alberta, Canada</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alex</namePart><namePart type="family">Rajput</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>University of Saskatchewan, Saskatoon, Saskatchewan, Canada</affiliation><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">2005-08</dateIssued><dateCaptured encoding="w3cdtf">2004-05-26</dateCaptured><dateValid encoding="w3cdtf">2004-11-23</dateValid><copyrightDate encoding="w3cdtf">2005</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="tables">3</extent><extent unit="references">43</extent><extent unit="words">4946</extent></physicalDescription><abstract lang="en">We determined whether apolipoprotein E ϵ4 (ApoE4) or catechol‐O‐methyltransferase (COMT) genotypes were associated with dementia, hallucinations, Alzheimer's disease pathological findings (AP), or cortical Lewy bodies (CLBs) in autopsy‐confirmed cases of Parkinson's disease (PD). Outcomes were obtained from medical records. Pathology reports identified AP and CLBs. Brain tissue was genotyped. A total of 47 subjects (33 men, 14 women) had PD onset at 62.4 ± 8.7 years of age and died at 77.8 ± 5.6 years of age. Demented and hallucinating patients did not differ in age at onset (AO) of PD or age at death, or the proportion ApoE4+, AP+, or CLB+ compared to nondemented patients or nonhallucinating patients. ApoE4 and COMT (low metabolizer [LH], intermediate metabolizer [HL], or high metabolizer [HH]) did not influence AO, death, or dementia‐ or hallucination‐free survival, based on age or duration of treatment. All seven subjects with AP were demented and had hallucinations. CLBs were associated with dementia but not hallucinations. In Cox regression models adjusting for AO and duration of treatment, increased risk of dementia was associated with male sex but not significantly with ApoE4; inclusion of AP in the model did not affect the results; COMT was not a risk factor for dementia. Psychosis risk was not associated with ApoE4, COMT, or sex. The observation that males have increased dementia risk and the trend for ApoE4 requires confirmation in larger prospective autopsy studies. © 2005 Movement Disorder Society</abstract><note type="funding">Parkinson Disease Foundation (New York)</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>hallucinations</topic><topic>dementia</topic><topic>Apolipoprotein E</topic><topic>catechol‐O‐methyltransferase</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></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>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>8</number></detail><extent unit="pages"><start>989</start><end>994</end><total>6</total></extent></part></relatedItem><identifier type="istex">18A0ACE65619AB988E7D837613A1DD2EB1E0A74C</identifier><identifier type="DOI">10.1002/mds.20481</identifier><identifier type="ArticleID">MDS20481</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 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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