Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia
Identifieur interne : 000939 ( Main/Corpus ); précédent : 000938; suivant : 000940Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia
Auteurs : Nathan Pankratz ; Lisa Byder ; Cheryl Halter ; Alice Rudolph ; Clifford W. Shults ; P. Michael Conneally ; Tatiana Foroud ; William C. NicholsSource :
- Movement Disorders [ 0885-3185 ] ; 2006-01.
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Abstract
The ε4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; P = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; P = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20663
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Michael Conneally</name><affiliation><mods:affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</mods:affiliation></affiliation></author><author><name sortKey="Foroud, Tatiana" sort="Foroud, Tatiana" uniqKey="Foroud T" first="Tatiana" last="Foroud">Tatiana Foroud</name><affiliation><mods:affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</mods:affiliation></affiliation></author><author><name sortKey="Nichols, William C" sort="Nichols, William C" uniqKey="Nichols W" first="William C." last="Nichols">William C. 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It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; P = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; P = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. 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It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; P = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; P = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. 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Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="10"><doi origin="wiley" registered="yes">10.1002/mds.v21:1</doi><numberingGroup><numbering type="journalVolume" number="21">21</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2006-01">January 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="60" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.20663</doi><idGroup><id type="unit" value="MDS20663"></id></idGroup><countGroup><count type="pageTotal" number="6"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2005 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2005-01-05"></event><event type="manuscriptRevised" date="2005-03-24"></event><event type="manuscriptAccepted" date="2005-04-27"></event><event type="publishedOnlineEarlyUnpaginated" date="2005-08-22"></event><event type="firstOnline" date="2005-08-22"></event><event type="publishedOnlineFinalForm" date="2006-01-13"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></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">45</numbering><numbering type="pageLast">49</numbering></numberingGroup><correspondenceTo>Division of Human Genetics, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229</correspondenceTo><objectNameGroup><objectName elementName="appendix">APPENDIX</objectName></objectNameGroup><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20663.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="3"></count><count type="referenceTotal" number="24"></count><count type="wordTotal" number="4385"></count></countGroup><titleGroup><title type="main" xml:lang="en">Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia</title><title type="short" xml:lang="en">APOE4 Leads to Significantly Earlier PD Onset</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Nathan</givenNames><familyName>Pankratz</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Lisa</givenNames><familyName>Byder</familyName><degrees>BS</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Cheryl</givenNames><familyName>Halter</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Alice</givenNames><familyName>Rudolph</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4 #af5"><personName><givenNames>Clifford W.</givenNames><familyName>Shults</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>P. Michael</givenNames><familyName>Conneally</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Tatiana</givenNames><familyName>Foroud</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af2" corresponding="yes"><personName><givenNames>William C.</givenNames><familyName>Nichols</familyName><degrees>PhD</degrees></personName><contactDetails><email>bill.nichols@chmcc.org</email></contactDetails></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurosciences, University of California, La Jolla, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>VA San Diego Healthcare System, San Diego, California, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">apolipoprotein E</keyword><keyword xml:id="kwd2">age of onset</keyword><keyword xml:id="kwd3">Parkinson's disease</keyword><keyword xml:id="kwd4">dementia</keyword></keywordGroup><fundingInfo><fundingAgency>National Institutes of Health</fundingAgency><fundingNumber>R01 NS37167</fundingNumber></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The ε4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; <i>P</i> = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; <i>P</i> = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>APOE4 Leads to Significantly Earlier PD Onset</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Presence of an APOE4 allele results in significantly earlier onset of Parkinson's disease and a higher risk with dementia</title></titleInfo><name type="personal"><namePart type="given">Nathan</namePart><namePart type="family">Pankratz</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Lisa</namePart><namePart type="family">Byder</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cheryl</namePart><namePart type="family">Halter</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alice</namePart><namePart type="family">Rudolph</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, University of Rochester, Rochester, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Clifford W.</namePart><namePart type="family">Shults</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of California, La Jolla, California, USA</affiliation><affiliation>VA San Diego Healthcare System, San Diego, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P. Michael</namePart><namePart type="family">Conneally</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tatiana</namePart><namePart type="family">Foroud</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Medical and Molecular Genetics, Indiana University Medical Center, Indianapolis, Indiana, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">William C.</namePart><namePart type="family">Nichols</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio, USA</affiliation><description>Correspondence: Division of Human Genetics, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229</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">2006-01</dateIssued><dateCaptured encoding="w3cdtf">2005-01-05</dateCaptured><dateValid encoding="w3cdtf">2005-04-27</dateValid><copyrightDate encoding="w3cdtf">2006</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">24</extent><extent unit="words">4385</extent></physicalDescription><abstract lang="en">The ε4 allele of the apolipoprotein E gene (APOE4) has been consistently associated with a greater risk of Alzheimer's disease (AD) as well as an earlier onset of AD. It is possible that APOE4 may also play a role in the etiology of other neurodegenerative disorders, such as Parkinson's disease (PD). APOE genotype, age of onset, disease duration, smoking history, and dementia status were collected for families with PD, yielding 324 Caucasian families with complete information. Logistic regression employing one individual per family and including age of onset and disease duration as covariates demonstrated a significantly increased risk of dementia for those individuals having inherited at least one ε4 allele (OR = 3.37; P = 0.002). Survival analyses also demonstrated a significantly earlier age of onset for those subjects with at least one ε4 allele (59.7 years) as compared with those homozygous for the more common ε3 allele (62.4 years; P = 0.009). Thus, consistent with previous studies, we find evidence that the presence of an ε4 allele results in significantly earlier onset of PD and a greater likelihood of dementia. It appears the similarities between PD and AD may be due to an overlap in the diseases' genetic etiology. © 2005 Movement Disorder Society</abstract><note type="funding">National Institutes of Health - No. R01 NS37167; </note><subject lang="en"><genre>Keywords</genre><topic>apolipoprotein E</topic><topic>age of onset</topic><topic>Parkinson's disease</topic><topic>dementia</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>2006</date><detail type="volume"><caption>vol.</caption><number>21</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>45</start><end>49</end><total>6</total></extent></part></relatedItem><identifier type="istex">03496D12A5A11B3ABA94FA6B7324EDF14C52CE1F</identifier><identifier type="DOI">10.1002/mds.20663</identifier><identifier type="ArticleID">MDS20663</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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