Modulation of the age at onset of Parkinson's disease by apolipoprotein E genotypes
Identifieur interne : 002C93 ( Main/Corpus ); précédent : 002C92; suivant : 002C94Modulation of the age at onset of Parkinson's disease by apolipoprotein E genotypes
Auteurs : Zareparsi ; Jeffrey Kaye ; Richard Camicioli ; Holly Grimslid ; Barry Oken ; Michael Litt ; John Nutt ; Thomas Bird ; Gerard Schellenberg ; Haydeh PayamiSource :
- Annals of Neurology [ 0364-5134 ] ; 1997-10.
Abstract
Parkinson's disease (PD) patients often develop dementia, and Alzheimer's disease (AD) patients frequently develop parkinsonian signs. The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. These preliminary results suggest that apolipoprotein E genotypes modulate the age at onset of PD.
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DOI: 10.1002/ana.410420417
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The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. These preliminary results suggest that apolipoprotein E genotypes modulate the age at onset of PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Zareparsi MS</name><affiliations><json:string>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>Jeffrey Kaye PhD</name><affiliations><json:string>Department of Neurology, Oregon Health Sciences University, Portland, OR</json:string><json:string>Portland Veterans Affairs Medical Center, Portland, OR</json:string></affiliations></json:item><json:item><name>Richard Camicioli PhD</name><affiliations><json:string>Department of Neurology, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>Holly Grimslid BS</name><affiliations><json:string>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>Barry Oken PhD</name><affiliations><json:string>Department of Neurology, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>Michael Litt PhD</name><affiliations><json:string>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</json:string><json:string>Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>John Nutt PhD</name><affiliations><json:string>Department of Neurology, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item><json:item><name>Thomas Bird PhD</name><affiliations><json:string>Neurology Section, University of Washington, Seattle, WA</json:string><json:string>Department of Neurology, University of Washington, Seattle, WA</json:string></affiliations></json:item><json:item><name>Gerard Schellenberg PhD</name><affiliations><json:string>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle, WA</json:string><json:string>Department of Medicine, University of Washington, Seattle, WA</json:string><json:string>Department of Pharmacology, University of Washington, Seattle, WA</json:string></affiliations></json:item><json:item><name>Haydeh Payami PhD</name><affiliations><json:string>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</json:string><json:string>Department of Neurology, Oregon Health Sciences University, Portland, OR</json:string></affiliations></json:item></author><articleId><json:string>ANA410420417</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson's disease (PD) patients often develop dementia, and Alzheimer's disease (AD) patients frequently develop parkinsonian signs. The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. 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The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. 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affiliationRef="#af1 #af3"><personName><givenNames>Michael</givenNames><familyName>Litt</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>John</givenNames><familyName>Nutt</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5 #af7"><personName><givenNames>Thomas</givenNames><familyName>Bird</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af6 #af8 #af9"><personName><givenNames>Gerard</givenNames><familyName>Schellenberg</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af1 #af2"><personName><givenNames>Haydeh</givenNames><familyName>Payami</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland, OR</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>Portland Veterans Affairs Medical Center, Portland, OR</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Neurology Section, University of Washington, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, University of Washington, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Department of Medicine, University of Washington, Seattle, WA</unparsedAffiliation></affiliation><affiliation xml:id="af9" countryCode="US" type="organization"><unparsedAffiliation>Department of Pharmacology, University of Washington, Seattle, WA</unparsedAffiliation></affiliation></affiliationGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Parkinson's disease (PD) patients often develop dementia, and Alzheimer's disease (AD) patients frequently develop parkinsonian signs. The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. These preliminary results suggest that apolipoprotein E genotypes modulate the age at onset of PD.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Modulation of the age at onset of Parkinson's disease by apolipoprotein E genotypes</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>ApoE and Onset of PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Modulation of the age at onset of Parkinson's disease by apolipoprotein E genotypes</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Zareparsi</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</affiliation><description>Correspondence: CDW‐2, Oregon Health Sciences University, 745 SW Gaines Rd, Portland, OR 97201</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jeffrey</namePart><namePart type="family">Kaye</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</affiliation><affiliation>Portland Veterans Affairs Medical Center, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Richard</namePart><namePart type="family">Camicioli</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Holly</namePart><namePart type="family">Grimslid</namePart><namePart type="termsOfAddress">BS</namePart><affiliation>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Barry</namePart><namePart type="family">Oken</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Litt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</affiliation><affiliation>Department of Biochemistry and Molecular Biology, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John</namePart><namePart type="family">Nutt</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Thomas</namePart><namePart type="family">Bird</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Neurology Section, University of Washington, Seattle, WA</affiliation><affiliation>Department of Neurology, University of Washington, Seattle, WA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Gerard</namePart><namePart type="family">Schellenberg</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Geriatric Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, University of Washington, Seattle, WA</affiliation><affiliation>Department of Medicine, University of Washington, Seattle, WA</affiliation><affiliation>Department of Pharmacology, University of Washington, Seattle, WA</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>Department of Molecular and Medical Genetics, Oregon Health Sciences University, Portland, OR</affiliation><affiliation>Department of Neurology, Oregon Health Sciences University, Portland, OR</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief communication" displayLabel="shortCommunication"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1997-10</dateIssued><dateCaptured encoding="w3cdtf">1997-01-21</dateCaptured><dateValid encoding="w3cdtf">1997-04-23</dateValid><copyrightDate encoding="w3cdtf">1997</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">2</extent><extent unit="tables">1</extent><extent unit="references">24</extent></physicalDescription><abstract lang="en">Parkinson's disease (PD) patients often develop dementia, and Alzheimer's disease (AD) patients frequently develop parkinsonian signs. The apolipoprotein E σ4 allele is associated with increased risk and earlier onset of AD. We studied 137 unrelated white PD patients. Those with σ4 had the earliest onset (52.7 · 9.8 years), σ3/σ3 patients had an intermediate onset (56.1 · 11.1 years), and those with σ2 had the latest onset (59.1 · 13.4 years). The age at onset distribution for σ4/σ – was significantly earlier than for σ3/σ3 and σ2/σ3. These preliminary results suggest that apolipoprotein E genotypes modulate the age at onset of PD.</abstract><relatedItem type="host"><titleInfo><title>Annals of Neurology</title><subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Ann Neurol.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Brief Communication</topic></subject><identifier type="ISSN">0364-5134</identifier><identifier type="eISSN">1531-8249</identifier><identifier type="DOI">10.1002/(ISSN)1531-8249</identifier><identifier type="PublisherID">ANA</identifier><part><date>1997</date><detail type="volume"><caption>vol.</caption><number>42</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>655</start><end>658</end><total>4</total></extent></part></relatedItem><identifier type="istex">7C1965F6D823174EEB123043772ED6988AA5A620</identifier><identifier type="DOI">10.1002/ana.410420417</identifier><identifier type="ArticleID">ANA410420417</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1997 the American Neurological Association</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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