Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease
Identifieur interne : 000F11 ( Main/Corpus ); précédent : 000F10; suivant : 000F12Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease
Auteurs : B. Feldman ; J. Chapman ; A. D. KorczynSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2006-01.
English descriptors
Abstract
Background – Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear. Objectives – To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD). Methods – Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis. Results – APOE ɛ3/ɛ4 allele was carried by 20 patients (14 with psychosis), ɛ2/ɛ3 by 11 patients (10 with psychosis), ɛ3/ɛ3 by 55 patients (25 with psychosis) and ɛ2/ɛ4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE ɛ4 allele and 10.1 ± 6.2 years among those who did not carry APOE ɛ4 (n = 35). The APOE ɛ4 allele was significantly associated with earlier onset of psychosis (P < 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE ɛ4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk. Conclusion – Parkinson's disease patients who carry the APOE ɛ4 allele develop psychosis earlier.
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DOI: 10.1111/j.1600-0404.2005.00535.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title><author><name sortKey="Feldman, B" sort="Feldman, B" uniqKey="Feldman B" first="B." last="Feldman">B. Feldman</name><affiliation><mods:affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</mods:affiliation></affiliation></author><author><name sortKey="Chapman, J" sort="Chapman, J" uniqKey="Chapman J" first="J." last="Chapman">J. Chapman</name><affiliation><mods:affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</mods:affiliation></affiliation></author><author><name sortKey="Korczyn, A D" sort="Korczyn, A D" uniqKey="Korczyn A" first="A. D." last="Korczyn">A. D. Korczyn</name><affiliation><mods:affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:64B60B7D001CA197FD7EB87BD1D2E83CD53208EA</idno><date when="2006" year="2006">2006</date><idno type="doi">10.1111/j.1600-0404.2005.00535.x</idno><idno type="url">https://api.istex.fr/document/64B60B7D001CA197FD7EB87BD1D2E83CD53208EA/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000F11</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title><author><name sortKey="Feldman, B" sort="Feldman, B" uniqKey="Feldman B" first="B." last="Feldman">B. Feldman</name><affiliation><mods:affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</mods:affiliation></affiliation></author><author><name sortKey="Chapman, J" sort="Chapman, J" uniqKey="Chapman J" first="J." last="Chapman">J. Chapman</name><affiliation><mods:affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</mods:affiliation></affiliation></author><author><name sortKey="Korczyn, A D" sort="Korczyn, A D" uniqKey="Korczyn A" first="A. D." last="Korczyn">A. D. Korczyn</name><affiliation><mods:affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</mods:affiliation></affiliation><affiliation><mods:affiliation>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</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>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-01">2006-01</date><biblScope unit="volume">113</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="14">14</biblScope><biblScope unit="page" to="17">17</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">64B60B7D001CA197FD7EB87BD1D2E83CD53208EA</idno><idno type="DOI">10.1111/j.1600-0404.2005.00535.x</idno><idno type="ArticleID">ANE535</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>dementia</term><term>neurodegeneration</term><term>psychosis</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background – Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear. Objectives – To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD). Methods – Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis. Results – APOE ɛ3/ɛ4 allele was carried by 20 patients (14 with psychosis), ɛ2/ɛ3 by 11 patients (10 with psychosis), ɛ3/ɛ3 by 55 patients (25 with psychosis) and ɛ2/ɛ4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE ɛ4 allele and 10.1 ± 6.2 years among those who did not carry APOE ɛ4 (n = 35). The APOE ɛ4 allele was significantly associated with earlier onset of psychosis (P < 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE ɛ4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk. Conclusion – Parkinson's disease patients who carry the APOE ɛ4 allele develop psychosis earlier.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>B. Feldman</name><affiliations><json:string>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</json:string></affiliations></json:item><json:item><name>J. Chapman</name><affiliations><json:string>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</json:string></affiliations></json:item><json:item><name>A. D. Korczyn</name><affiliations><json:string>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</json:string><json:string>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</json:string><json:string>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</json:string></affiliations></json:item></author><subject><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>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neurodegeneration</value></json:item><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>psychosis</value></json:item></subject><articleId><json:string>ANE535</json:string></articleId><language><json:string>eng</json:string></language><abstract>Background – Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear. Objectives – To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD). Methods – Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis. Results – APOE ɛ3/ɛ4 allele was carried by 20 patients (14 with psychosis), ɛ2/ɛ3 by 11 patients (10 with psychosis), ɛ3/ɛ3 by 55 patients (25 with psychosis) and ɛ2/ɛ4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE ɛ4 allele and 10.1 ± 6.2 years among those who did not carry APOE ɛ4 (n = 35). The APOE ɛ4 allele was significantly associated with earlier onset of psychosis (P > 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE ɛ4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk. Conclusion – Parkinson's disease patients who carry the APOE ɛ4 allele develop psychosis earlier.</abstract><qualityIndicators><score>5.929</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>1803</abstractCharCount><pdfWordCount>2429</pdfWordCount><pdfCharCount>14761</pdfCharCount><pdfPageCount>4</pdfPageCount><abstractWordCount>275</abstractWordCount></qualityIndicators><title>Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>113</volume><publisherId><json:string>ANE</json:string></publisherId><pages><total>4</total><last>17</last><first>14</first></pages><issn><json:string>0001-6314</json:string></issn><issue>1</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1600-0404</json:string></eissn><title>Acta Neurologica Scandinavica</title><doi><json:string>10.1111/(ISSN)1600-0404</json:string></doi></host><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1111/j.1600-0404.2005.00535.x</json:string></doi><id>64B60B7D001CA197FD7EB87BD1D2E83CD53208EA</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/64B60B7D001CA197FD7EB87BD1D2E83CD53208EA/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/64B60B7D001CA197FD7EB87BD1D2E83CD53208EA/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/64B60B7D001CA197FD7EB87BD1D2E83CD53208EA/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title><author><persName><forename type="first">B.</forename><surname>Feldman</surname></persName><affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</affiliation></author><author><persName><forename type="first">J.</forename><surname>Chapman</surname></persName><note type="biography">Present address: Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.</note><affiliation>Present address: Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.</affiliation><affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</affiliation></author><author><persName><forename type="first">A. D.</forename><surname>Korczyn</surname></persName><affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</affiliation><affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</affiliation><affiliation>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</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>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2006-01"></date><biblScope unit="volume">113</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="14">14</biblScope><biblScope unit="page" to="17">17</biblScope></imprint></monogr><idno type="istex">64B60B7D001CA197FD7EB87BD1D2E83CD53208EA</idno><idno type="DOI">10.1111/j.1600-0404.2005.00535.x</idno><idno type="ArticleID">ANE535</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Background – Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear. Objectives – To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD). Methods – Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis. Results – APOE ɛ3/ɛ4 allele was carried by 20 patients (14 with psychosis), ɛ2/ɛ3 by 11 patients (10 with psychosis), ɛ3/ɛ3 by 55 patients (25 with psychosis) and ɛ2/ɛ4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE ɛ4 allele and 10.1 ± 6.2 years among those who did not carry APOE ɛ4 (n = 35). The APOE ɛ4 allele was significantly associated with earlier onset of psychosis (P < 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE ɛ4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk. Conclusion – Parkinson's disease patients who carry the APOE ɛ4 allele develop psychosis earlier.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>apolipoprotein E</term></item><item><term>dementia</term></item><item><term>neurodegeneration</term></item><item><term>Parkinson's disease</term></item><item><term>psychosis</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/64B60B7D001CA197FD7EB87BD1D2E83CD53208EA/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>Munksgaard International Publishers</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="01001"><doi origin="wiley">10.1111/ane.2006.113.issue-1</doi><numberingGroup><numbering type="journalVolume" number="113">113</numbering><numbering type="journalIssue" number="1">1</numbering></numberingGroup><coverDate startDate="2006-01">January 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="3" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2005.00535.x</doi><idGroup><id type="unit" value="ANE535"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="tocHeading1"><i>Original articles</i></title></titleGroup><eventGroup><event type="firstOnline" date="2005-11-18"></event><event type="publishedOnlineFinalForm" date="2005-11-18"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-10"></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="14">14</numbering><numbering type="pageLast" number="17">17</numbering></numberingGroup><correspondenceTo>Amos D. Korczun, Sieratzki Chair of Neurology, Tel‐Aviv University Medical School, Ramat Aviv 69978, Israel
Tel.: +972 3 6974229
Fax: +972 3 6409113
e‐mail: <email>neuro13@post.tau.ac.il</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE535.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication December 16, 2003</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count></countGroup><titleGroup><title type="main">Apolipoprotein <i>ɛ</i>4 advances appearance of psychosis in patients with Parkinson's disease</title><title type="shortAuthors"><b>Feldman et al.</b></title><title type="short"><b>APOE and psychosis in Parkinson's disease</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>B.</givenNames><familyName>Feldman</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2" noteRef="#fn1"><personName><givenNames>J.</givenNames><familyName>Chapman</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2 #a3"><personName><givenNames>A. D.</givenNames><familyName>Korczyn</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="IL"><unparsedAffiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="IL"><unparsedAffiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="IL"><unparsedAffiliation>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">apolipoprotein E</keyword><keyword xml:id="k2">dementia</keyword><keyword xml:id="k3">neurodegeneration</keyword><keyword xml:id="k4">Parkinson's disease</keyword><keyword xml:id="k5">psychosis</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- Feldman B, Chapman J, Korczyn AD. Apolipoprotein ϵ4 advances appearance of psychosis in patients with Parkinson's disease.
Acta Neurol Scand 2005: DOI: 10.1111/j.1600-0404.2005.00535.x.
© Blackwell Munksgaard 2005. --><p><b>Background – </b> Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear.</p><p><b>Objectives – </b> To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD).</p><p><b>Methods – </b> Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis.</p><p><b>Results – </b> APOE <i>ɛ</i>3/<i>ɛ</i>4 allele was carried by 20 patients (14 with psychosis), <i>ɛ</i>2/<i>ɛ</i>3 by 11 patients (10 with psychosis), <i>ɛ</i>3/<i>ɛ</i>3 by 55 patients (25 with psychosis) and <i>ɛ</i>2/<i>ɛ</i>4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE <i>ɛ</i>4 allele and 10.1 ± 6.2 years among those who did not carry APOE <i>ɛ</i>4 (<i>n</i> = 35). The APOE <i>ɛ</i>4 allele was significantly associated with earlier onset of psychosis (<i>P</i> < 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE <i>ɛ</i>4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk.</p><p><b>Conclusion – </b> Parkinson's disease patients who carry the APOE <i>ɛ</i>4 allele develop psychosis earlier.</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><label>*</label><p> Present address: Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Apolipoprotein ɛ4 advances appearance of psychosis in patients with Parkinson's disease</title></titleInfo><titleInfo type="abbreviated"><title>APOE and psychosis in Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Apolipoprotein</title></titleInfo><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Feldman</namePart><affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Chapman</namePart><affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</affiliation><description>Present address: Department of Neurology, Sheba Medical Center, Tel Hashomer, Israel.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A. D.</namePart><namePart type="family">Korczyn</namePart><affiliation>Be'er Yakov Mental Health Center, Be'er Yakov, Israel</affiliation><affiliation>Department of Neurology, Tel Aviv Sourasky Medical Center, Sackler School of Medicine, Tel Aviv University, Tel‐Aviv, Israel</affiliation><affiliation>Sieratzky Chair of Neurology, Tel Aviv University, Ramat Aviv, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-01</dateIssued><edition>Accepted for publication December 16, 2003</edition><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="figures">1</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">Background – Psychosis is one of the most serious complications of advanced parkinsonism, but many patients are spared. The genetic factors predisposing to psychosis are unclear. Objectives – To assess the association between apolipoprotein E (APOE) polymorphism and the development of psychosis in patients with Parkinson's disease (PD). Methods – Eighty‐seven patients with advanced PD were assessed. Psychosis was diagnosed in 50 patients who manifested paranoid delusions, hallucinations without insight, or disorders of perception. Time of onset of psychosis was retrieved from the medical records and caregivers’ recall. APOE genotype was determined by restriction enzyme digests of amplified alleles. Cox models of logistic regression and Kaplan–Meier survival curves were used to assess factors determining early development of psychosis. Results – APOE ɛ3/ɛ4 allele was carried by 20 patients (14 with psychosis), ɛ2/ɛ3 by 11 patients (10 with psychosis), ɛ3/ɛ3 by 55 patients (25 with psychosis) and ɛ2/ɛ4 by one patient who had psychosis. The mean age of onset of PD symptoms was 60.0 ± 12.5 years. The mean duration of motor symptoms at the onset of psychosis was 7.3 ± 4.3 years for the 15 patients harboring an APOE ɛ4 allele and 10.1 ± 6.2 years among those who did not carry APOE ɛ4 (n = 35). The APOE ɛ4 allele was significantly associated with earlier onset of psychosis (P < 0.05) when the age of onset of motor symptoms and presence of dementia were included in the Cox regression model. Carrying the APOE ɛ4 allele was a significant risk factor for earlier appearance of psychosis with a hazard ratio of 3.24 (95% CI 1.62–6.46) while dementia by itself did not increase the risk. Conclusion – Parkinson's disease patients who carry the APOE ɛ4 allele develop psychosis earlier.</abstract><subject lang="en"><genre>Keywords</genre><topic>apolipoprotein E</topic><topic>dementia</topic><topic>neurodegeneration</topic><topic>Parkinson's disease</topic><topic>psychosis</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>2006</date><detail type="volume"><caption>vol.</caption><number>113</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>14</start><end>17</end><total>4</total></extent></part></relatedItem><identifier type="istex">64B60B7D001CA197FD7EB87BD1D2E83CD53208EA</identifier><identifier type="DOI">10.1111/j.1600-0404.2005.00535.x</identifier><identifier type="ArticleID">ANE535</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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