The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study
Identifieur interne : 002506 ( Main/Corpus ); précédent : 002505; suivant : 002507The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study
Auteurs : H. Vefring ; K. Haugarvoll ; O. Tysnes ; J. P. Larsen ; M. W. KurzSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2010-12.
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Abstract
Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S. Objectives – Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. Patients and methods – To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. Results – No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. Conclusion – In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.
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DOI: 10.1111/j.1600-0404.2010.01362.x
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ISTEX:D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2Le document en format XML
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Tysnes</name><affiliation><mods:affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>School of Medicine, University of Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Larsen, J P" sort="Larsen, J P" uniqKey="Larsen J" first="J. P." last="Larsen">J. P. Larsen</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>School of Medicine, University of Bergen, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Kurz, M W" sort="Kurz, M W" uniqKey="Kurz M" first="M. W." last="Kurz">M. W. Kurz</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1111/j.1600-0404.2010.01362.x</idno><idno type="url">https://api.istex.fr/document/D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002506</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study</title><author><name sortKey="Vefring, H" sort="Vefring, H" uniqKey="Vefring H" first="H." last="Vefring">H. Vefring</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Medical Biochemistry, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author><author><name sortKey="Haugarvoll, K" sort="Haugarvoll, K" uniqKey="Haugarvoll K" first="K." last="Haugarvoll">K. Haugarvoll</name><affiliation><mods:affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</mods:affiliation></affiliation></author><author><name sortKey="Tysnes, O" sort="Tysnes, O" uniqKey="Tysnes O" first="O." last="Tysnes">O. 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Kurz</name><affiliation><mods:affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-12">2010-12</date><biblScope unit="volume">122</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="438">438</biblScope><biblScope unit="page" to="441">441</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2</idno><idno type="DOI">10.1111/j.1600-0404.2010.01362.x</idno><idno type="ArticleID">ANE1362</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson’s disease</term><term>apolipoprotein E</term><term>familial</term><term>genetics</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S. Objectives – Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. Patients and methods – To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. Results – No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. Conclusion – In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>H. Vefring</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Department of Medical Biochemistry, Stavanger University Hospital, Stavanger, Norway</json:string></affiliations></json:item><json:item><name>K. Haugarvoll</name><affiliations><json:string>Department of Neurology, Haukeland University Hospital, Bergen, Norway</json:string></affiliations></json:item><json:item><name>O.‐B. Tysnes</name><affiliations><json:string>Department of Neurology, Haukeland University Hospital, Bergen, Norway</json:string><json:string>School of Medicine, University of Bergen, Norway</json:string></affiliations></json:item><json:item><name>J. P. Larsen</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>School of Medicine, University of Bergen, Norway</json:string><json:string>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</json:string></affiliations></json:item><json:item><name>M. W. Kurz</name><affiliations><json:string>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</json:string><json:string>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</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>genetics</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>familial</value></json:item></subject><articleId><json:string>ANE1362</json:string></articleId><language><json:string>eng</json:string></language><abstract>Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S. Objectives – Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. Patients and methods – To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. Results – No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. Conclusion – In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.</abstract><qualityIndicators><score>4.02</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595.276 x 782.362 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1236</abstractCharCount><pdfWordCount>1704</pdfWordCount><pdfCharCount>11691</pdfCharCount><pdfPageCount>4</pdfPageCount><abstractWordCount>193</abstractWordCount></qualityIndicators><title>The role of APOE alleles in incident Parkinson’s disease. 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The Norwegian ParkWest Study</title><author><orgName>for the Norwegian ParkWest Study group</orgName></author><author><persName><forename type="first">H.</forename><surname>Vefring</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Medical Biochemistry, Stavanger University Hospital, Stavanger, Norway</affiliation></author><author><persName><forename type="first">K.</forename><surname>Haugarvoll</surname></persName><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation></author><author><persName><forename type="first">O.‐B.</forename><surname>Tysnes</surname></persName><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><affiliation>School of Medicine, University of Bergen, Norway</affiliation></author><author><persName><forename type="first">J. 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W.</forename><surname>Kurz</surname></persName><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation></author></analytic><monogr><title level="j">Acta Neurologica Scandinavica</title><idno type="pISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><idno type="DOI">10.1111/(ISSN)1600-0404</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2010-12"></date><biblScope unit="volume">122</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="438">438</biblScope><biblScope unit="page" to="441">441</biblScope></imprint></monogr><idno type="istex">D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2</idno><idno type="DOI">10.1111/j.1600-0404.2010.01362.x</idno><idno type="ArticleID">ANE1362</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S. Objectives – Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. Patients and methods – To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. Results – No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. Conclusion – In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson’s disease</term></item><item><term>genetics</term></item><item><term>apolipoprotein E</term></item><item><term>familial</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2/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>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0404</doi><issn type="print">0001-6314</issn><issn type="electronic">1600-0404</issn><idGroup><id type="product" value="ANE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROLOGICA SCANDINAVICA">Acta Neurologica Scandinavica</title></titleGroup></publicationMeta><publicationMeta level="part" position="12106"><doi origin="wiley">10.1111/ane.2010.122.issue-6</doi><numberingGroup><numbering type="journalVolume" number="122">122</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="2010-12">December 2010</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="12" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2010.01362.x</doi><idGroup><id type="unit" value="ANE1362"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="tocHeading1"><i>Short Communication</i></title></titleGroup><copyright>© 2010 John Wiley & Sons A/S</copyright><eventGroup><event type="firstOnline" date="2010-04-29"></event><event type="publishedOnlineAcceptedOrEarlyUnpaginated" date="2010-04-29"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.25 mode:FullText source:FullText result:FullText" date="2010-11-05"></event><event type="publishedOnlineFinalForm" date="2010-10-25"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="438">438</numbering><numbering type="pageLast" number="441">441</numbering></numberingGroup><correspondenceTo>Martin Kurz, Department of Neurology, Stavanger University Hospital, Postboks 8100, 4068 Stavanger, Norway
Tel.: 0047‐51518426
Fax: 0047‐51519916
e‐mail: <email>kuma@sus.no</email></correspondenceTo><objectNameGroup><objectName elementName="appendix">Appendix</objectName></objectNameGroup><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE1362.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication March 8, 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="2"></count></countGroup><titleGroup><title type="main">The role of <i>APOE</i> alleles in incident Parkinson’s disease. The Norwegian ParkWest Study</title><title type="shortAuthors"><b>Vefring et al.</b></title><title type="short"><b><i>APOE</i> alleles in the Norwegian ParkWest study</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2"><personName><givenNames>H.</givenNames><familyName>Vefring</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a3"><personName><givenNames>K.</givenNames><familyName>Haugarvoll</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3 #a4"><personName><givenNames>O.‐B.</givenNames><familyName>Tysnes</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1 #a4 #a5"><personName><givenNames>J. P.</givenNames><familyName>Larsen</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1 #a5"><personName><givenNames>M. W.</givenNames><familyName>Kurz</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" noteRef="#fn1"><groupName>for the Norwegian ParkWest Study group</groupName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="NO"><unparsedAffiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="NO"><unparsedAffiliation>Department of Medical Biochemistry, Stavanger University Hospital, Stavanger, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="NO"><unparsedAffiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="NO"><unparsedAffiliation>School of Medicine, University of Bergen, Norway</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="NO"><unparsedAffiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson’s disease</keyword><keyword xml:id="k2">genetics</keyword><keyword xml:id="k3">apolipoprotein E</keyword><keyword xml:id="k4">familial</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of <i>APOE</i> alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S.</p><p><b>Objectives – </b> <i>Apolipoprotein E</i> (<i>APOE</i>) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between <i>APOE</i> alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on <i>APOE</i> alleles in an unselected cohort of patients with incident PD.</p><p><b>Patients and methods – </b> To determine the role of <i>APOE</i> alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their <i>APOE</i> allele status.</p><p><b>Results – </b> No association was observed between any <i>APOE</i> alleles and susceptibility to PD or age at onset in PD.</p><p><b>Conclusion – </b> In our cohort of unselected, incident PD patients <i>APOE</i> alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between <i>APOE</i> alleles and clinical and neuropsychological progression in PD.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p> Members of the Norwegian ParkWest Study group are listed in the Appendix.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study</title></titleInfo><titleInfo type="abbreviated"><title>APOE alleles in the Norwegian ParkWest study</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The role of</title></titleInfo><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Vefring</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Medical Biochemistry, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Haugarvoll</namePart><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.‐B.</namePart><namePart type="family">Tysnes</namePart><affiliation>Department of Neurology, Haukeland University Hospital, Bergen, Norway</affiliation><affiliation>School of Medicine, University of Bergen, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J. P.</namePart><namePart type="family">Larsen</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>School of Medicine, University of Bergen, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. W.</namePart><namePart type="family">Kurz</namePart><affiliation>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway</affiliation><affiliation>Department of Neurology, Stavanger University Hospital, Stavanger, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="corporate"><namePart>for the Norwegian ParkWest Study group</namePart><description>The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Stavanger, NorwayDepartment of Medical Biochemistry, Stavanger University Hospital, Stavanger, NorwayDepartment of Neurology, Haukeland University Hospital, Bergen, NorwaySchool of Medicine, University of Bergen, NorwayDepartment of Neurology, Stavanger University Hospital, Stavanger, Norway</description></name><typeOfResource>text</typeOfResource><genre type="brief communication" displayLabel="shortCommunication"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-12</dateIssued><edition>Accepted for publication March 8, 2010</edition><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="tables">2</extent></physicalDescription><abstract lang="en">Vefring H, Haugarvoll K, Tysnes O‐B, Larsen JP, Kurz MW, for the Norwegian ParkWest Study group. The role of APOE alleles in incident Parkinson’s disease. The Norwegian ParkWest Study.
Acta Neurol Scand: 2010: 122: 438–441.
© 2010 John Wiley & Sons A/S. Objectives – Apolipoprotein E (APOE) gene alleles have been associated with various neurodegenerative disorders. However, there have been conflicting reports on associations between APOE alleles and Parkinson’s disease (PD) and age at onset in PD. There exist no data on APOE alleles in an unselected cohort of patients with incident PD. Patients and methods – To determine the role of APOE alleles in PD and age of onset in PD at time of diagnosis, 203 patients with incident PD and 187 healthy control subjects from Western and Southern Norway were investigated according to their APOE allele status. Results – No association was observed between any APOE alleles and susceptibility to PD or age at onset in PD. Conclusion – In our cohort of unselected, incident PD patients APOE alleles do not seem to play a role for development of PD. Prospective, long‐term follow‐up may still reveal associations between APOE alleles and clinical and neuropsychological progression in PD.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson’s disease</topic><topic>genetics</topic><topic>apolipoprotein E</topic><topic>familial</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neurologica Scandinavica</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0001-6314</identifier><identifier type="eISSN">1600-0404</identifier><identifier type="DOI">10.1111/(ISSN)1600-0404</identifier><identifier type="PublisherID">ANE</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>122</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>438</start><end>441</end><total>4</total></extent></part></relatedItem><identifier type="istex">D4C8953173A8D70C907CC8036F5A62BF5AEEE5A2</identifier><identifier type="DOI">10.1111/j.1600-0404.2010.01362.x</identifier><identifier type="ArticleID">ANE1362</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 John Wiley & Sons A/S</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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