Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease
Identifieur interne : 000107 ( Main/Corpus ); précédent : 000106; suivant : 000108Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease
Auteurs : Stewart A. Factor ; N. Kyle Steenland ; Donald S. Higgins ; Eric S. Molho ; Denise M. Kay ; Jennifer Montimurro ; Ami R. Rosen ; Cyrus P. Zabetian ; Haydeh PayamiSource :
- Movement Disorders [ 0885-3185 ] ; 2011-10.
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Abstract
Our aim was to examine disease‐related and genetic correlates of the development of psychotic symptoms in a large population of patients with Parkinson's disease. We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: P = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: P = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: P < 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: P = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (P = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (P < 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23806
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We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: P = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: P = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: P < 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: P = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (P = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (P < 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Stewart A. Factor DO</name><affiliations><json:string>Emory University, Atlanta, Georgia, USA</json:string></affiliations></json:item><json:item><name>N. Kyle Steenland PhD</name><affiliations><json:string>Emory University, Atlanta, Georgia, USA</json:string></affiliations></json:item><json:item><name>Donald S. Higgins MD</name><affiliations><json:string>Samuel Stratton Veterans Affairs Medical Center, Albany, New York, USA</json:string></affiliations></json:item><json:item><name>Eric S. Molho MD</name><affiliations><json:string>Albany Medical Center, Albany, New York, USA</json:string></affiliations></json:item><json:item><name>Denise M. Kay PhD</name><affiliations><json:string>New York State Department of Health, Albany, New York, USA</json:string></affiliations></json:item><json:item><name>Jennifer Montimurro MS</name><affiliations><json:string>New York State Department of Health, Albany, New York, USA</json:string></affiliations></json:item><json:item><name>Ami R. Rosen MS, CGC</name><affiliations><json:string>Emory University, Atlanta, Georgia, USA</json:string></affiliations></json:item><json:item><name>Cyrus P. Zabetian MD</name><affiliations><json:string>Veterans Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Haydeh Payami PhD</name><affiliations><json:string>New York State Department of Health, Albany, New York, USA</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>psychosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>depression</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>sleep</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>freezing of gait</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>risk factors</value></json:item></subject><articleId><json:string>MDS23806</json:string></articleId><language><json:string>eng</json:string></language><abstract>Our aim was to examine disease‐related and genetic correlates of the development of psychotic symptoms in a large population of patients with Parkinson's disease. We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: P = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: P = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: P > 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: P = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (P = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (P > 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society</abstract><qualityIndicators><score>7.944</score><pdfVersion>1.4</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>7</keywordCount><abstractCharCount>1879</abstractCharCount><pdfWordCount>4444</pdfWordCount><pdfCharCount>28766</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>264</abstractWordCount></qualityIndicators><title>Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>6</total><last>2195</last><first>2190</first></pages><issn><json:string>0885-3185</json:string></issn><issue>12</issue><subject><json:item><value>Research Article</value></json:item></subject><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1531-8257</json:string></eissn><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>2011</publicationDate><copyrightDate>2011</copyrightDate><doi><json:string>10.1002/mds.23806</json:string></doi><id>7097244E458A7DAA287CE66C58166160D188172E</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/7097244E458A7DAA287CE66C58166160D188172E/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/7097244E458A7DAA287CE66C58166160D188172E/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/7097244E458A7DAA287CE66C58166160D188172E/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2011</date></publicationStmt><notesStmt><note type="content">*Funding agencies: Michael J. Fox Foundation: Edmond J. Safra Global Genetics Consortia Grant; Close to a Cure Foundation: A Fund for Parkinson's Research of Foundation for the Carolinas; NIH: R01‐NS36960, Department of Veterans Affairs Merit Review Award; New York State Department of Health Wadsworth Center; The Sartain Lanier Family Foundation; and the Riley Family Chair in Parkinson's Disease.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Stewart A. Factor has research grants from Teva Neurosciences, Ipsen, Ceregene, the Michael J. Fox Foundation, and the Consolidated Anti‐aging Foundation and also was a consultant for Boehringer‐Ingelheim. Eric S. Molho has received research grants from Teva Neurosciences, Allergan, EMD Serono, Impax Pharmaceuticals, and Acadia Pharmaceuticals and has received consulting fees from Allergan, Merz Pharmaceuticals, and Ipsen.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease</title><author><persName><forename type="first">Stewart A.</forename><surname>Factor</surname></persName><roleName type="degree">DO</roleName><note type="correspondence"><p>Correspondence: Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA</p></note><affiliation>Emory University, Atlanta, Georgia, USA</affiliation></author><author><persName><forename type="first">N. Kyle</forename><surname>Steenland</surname></persName><roleName type="degree">PhD</roleName><affiliation>Emory University, Atlanta, Georgia, USA</affiliation></author><author><persName><forename type="first">Donald S.</forename><surname>Higgins</surname></persName><roleName type="degree">MD</roleName><affiliation>Samuel Stratton Veterans Affairs Medical Center, Albany, New York, USA</affiliation></author><author><persName><forename type="first">Eric S.</forename><surname>Molho</surname></persName><roleName type="degree">MD</roleName><affiliation>Albany Medical Center, Albany, New York, USA</affiliation></author><author><persName><forename type="first">Denise M.</forename><surname>Kay</surname></persName><roleName type="degree">PhD</roleName><affiliation>New York State Department of Health, Albany, New York, USA</affiliation></author><author><persName><forename type="first">Jennifer</forename><surname>Montimurro</surname></persName><roleName type="degree">MS</roleName><affiliation>New York State Department of Health, Albany, New York, USA</affiliation></author><author><persName><forename type="first">Ami R.</forename><surname>Rosen</surname></persName><roleName type="degree">MS, CGC</roleName><affiliation>Emory University, Atlanta, Georgia, USA</affiliation></author><author><persName><forename type="first">Cyrus P.</forename><surname>Zabetian</surname></persName><roleName type="degree">MD</roleName><affiliation>Veterans Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Haydeh</forename><surname>Payami</surname></persName><roleName type="degree">PhD</roleName><affiliation>New York State Department of Health, Albany, New York, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: P = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: P = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: P < 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: P = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (P = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (P < 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>psychosis</term></item><item><term>depression</term></item><item><term>sleep</term></item><item><term>freezing of gait</term></item><item><term>genetics</term></item><item><term>risk factors</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2011-01-24">Received</change><change when="2011-04-28">Registration</change><change when="2011-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/7097244E458A7DAA287CE66C58166160D188172E/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="120"><doi origin="wiley" registered="yes">10.1002/mds.v26.12</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue">12</numbering></numberingGroup><coverDate startDate="2011-10">October 2011</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="130" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23806</doi><idGroup><id type="unit" value="MDS23806"></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 © 2011 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2011-01-24"></event><event type="manuscriptRevised" date="2011-04-18"></event><event type="manuscriptAccepted" date="2011-04-28"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:3.0.1 mode:FullText" date="2012-01-04"></event><event type="publishedOnlineEarlyUnpaginated" date="2011-06-28"></event><event type="publishedOnlineFinalForm" date="2011-10-21"></event><event type="firstOnline" date="2011-06-28"></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">2190</numbering><numbering type="pageLast">2195</numbering></numberingGroup><correspondenceTo>Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS23806.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="49"></count><count type="wordTotal" number="6308"></count></countGroup><titleGroup><title type="main" xml:lang="en">Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease<link href="#fn1"></link><link href="#fn2"></link><link href="#fn3"></link></title><title type="short" xml:lang="en">Risks for Psychosis in Parkinson's Disease</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Stewart A.</givenNames><familyName>Factor</familyName><degrees>DO</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>N. Kyle</givenNames><familyName>Steenland</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Donald S.</givenNames><familyName>Higgins</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Eric S.</givenNames><familyName>Molho</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Denise M.</givenNames><familyName>Kay</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Jennifer</givenNames><familyName>Montimurro</familyName><degrees>MS</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Ami R.</givenNames><familyName>Rosen</familyName><degrees>MS, CGC</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5"><personName><givenNames>Cyrus P.</givenNames><familyName>Zabetian</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af4"><personName><givenNames>Haydeh</givenNames><familyName>Payami</familyName><degrees>PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Emory University, Atlanta, Georgia, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Samuel Stratton Veterans Affairs Medical Center, Albany, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Albany Medical Center, Albany, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>New York State Department of Health, Albany, New York, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Veterans Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">psychosis</keyword><keyword xml:id="kwd3">depression</keyword><keyword xml:id="kwd4">sleep</keyword><keyword xml:id="kwd5">freezing of gait</keyword><keyword xml:id="kwd6">genetics</keyword><keyword xml:id="kwd7">risk factors</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Our aim was to examine disease‐related and genetic correlates of the development of psychotic symptoms in a large population of patients with Parkinson's disease. We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: <i>P</i> = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: <i>P</i> = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: <i>P</i> < 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: <i>P</i> = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (<i>P</i> = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (<i>P</i> < 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Funding agencies:</b> Michael J. Fox Foundation: Edmond J. Safra Global Genetics Consortia Grant; Close to a Cure Foundation: A Fund for Parkinson's Research of Foundation for the Carolinas; NIH: R01‐NS36960, Department of Veterans Affairs Merit Review Award; New York State Department of Health Wadsworth Center; The Sartain Lanier Family Foundation; and the Riley Family Chair in Parkinson's Disease.</p></note><note xml:id="fn2"><p><b>Relevant conflicts of interest/financial disclosures</b>: Stewart A. Factor has research grants from Teva Neurosciences, Ipsen, Ceregene, the Michael J. Fox Foundation, and the Consolidated Anti‐aging Foundation and also was a consultant for Boehringer‐Ingelheim. Eric S. Molho has received research grants from Teva Neurosciences, Allergan, EMD Serono, Impax Pharmaceuticals, and Acadia Pharmaceuticals and has received consulting fees from Allergan, Merz Pharmaceuticals, and Ipsen.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Risks for Psychosis in Parkinson's Disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Disease‐related and genetic correlates of psychotic symptoms in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Stewart A.</namePart><namePart type="family">Factor</namePart><namePart type="termsOfAddress">DO</namePart><affiliation>Emory University, Atlanta, Georgia, USA</affiliation><description>Correspondence: Department of Neurology, Emory University School of Medicine, 1841 Clifton Road NE, Atlanta, GA 30329, USA</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">N. Kyle</namePart><namePart type="family">Steenland</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Emory University, Atlanta, Georgia, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donald S.</namePart><namePart type="family">Higgins</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Samuel Stratton Veterans Affairs Medical Center, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eric S.</namePart><namePart type="family">Molho</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Albany Medical Center, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Denise M.</namePart><namePart type="family">Kay</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>New York State Department of Health, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jennifer</namePart><namePart type="family">Montimurro</namePart><namePart type="termsOfAddress">MS</namePart><affiliation>New York State Department of Health, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Ami R.</namePart><namePart type="family">Rosen</namePart><namePart type="termsOfAddress">MS, CGC</namePart><affiliation>Emory University, Atlanta, Georgia, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Cyrus P.</namePart><namePart type="family">Zabetian</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Veterans Affairs Puget Sound Health Care System and University of Washington, Seattle, Washington, USA</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>New York State Department of Health, Albany, New York, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-10</dateIssued><dateCaptured encoding="w3cdtf">2011-01-24</dateCaptured><dateValid encoding="w3cdtf">2011-04-28</dateValid><copyrightDate encoding="w3cdtf">2011</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">1</extent><extent unit="references">49</extent><extent unit="words">6308</extent></physicalDescription><abstract lang="en">Our aim was to examine disease‐related and genetic correlates of the development of psychotic symptoms in a large population of patients with Parkinson's disease. We studied 500 patients with Parkinson's disease from the NeuroGenetics Research Consortium using logistic regression models. Predictors were demographic, clinical (motor/nonmotor features), and genetic, measured as continuous or dichotomous variables. Continuous measures were divided into population‐based tertiles. Results are given as odds ratios (95% confidence intervals) for dichotomous variables and by ascending tertile for continuous variables. Psychotic symptoms were associated with increasing age: 4.86 (1.62–14.30) and 6.25 (2.09–18.74) (test for trend: P = 0.01); and duration of disease: 3.81 (1.23–11.76) and 5.33 (1.68–16.89) (test for trend: P = 0.03). For nonmotor features, we demonstrated positive trends with depression: 1.31 (0.47–3.61) and 5.01 (2.04–12.33) (test for trend: P < 0.0001); cognitive dysfunction: 0.69 (0.26–1.84) and 2.51 (1.00–6.29) (test for trend: P = 0.03); and an excess for those with sleep disorders: 2.00 (1.03–3.89) (P = 0.04). Psychotic symptoms were not associated with tremor or postural instability scores, but there was an association with freezing of gait: 3.83 (1.67–8.75) (P < 0.002). Psychotic symptoms were not associated with the presence of any examined polymorphisms in the apolipoprotein, alpha‐synuclein, or microtubule associated protein tau genes. This is the largest study to examine correlates of psychotic symptoms in Parkinson's disease. We discovered a novel association with freezing of gait. We demonstrated an association with depression and duration of disease, both of which were inconsistently related in previous studies, and confirmed the association with age, cognitive dysfunction, and sleep disorders. © 2011 Movement Disorder Society</abstract><note type="content">*Funding agencies: Michael J. Fox Foundation: Edmond J. Safra Global Genetics Consortia Grant; Close to a Cure Foundation: A Fund for Parkinson's Research of Foundation for the Carolinas; NIH: R01‐NS36960, Department of Veterans Affairs Merit Review Award; New York State Department of Health Wadsworth Center; The Sartain Lanier Family Foundation; and the Riley Family Chair in Parkinson's Disease.</note><note type="content">*Relevant conflicts of interest/financial disclosures: Stewart A. Factor has research grants from Teva Neurosciences, Ipsen, Ceregene, the Michael J. Fox Foundation, and the Consolidated Anti‐aging Foundation and also was a consultant for Boehringer‐Ingelheim. Eric S. Molho has received research grants from Teva Neurosciences, Allergan, EMD Serono, Impax Pharmaceuticals, and Acadia Pharmaceuticals and has received consulting fees from Allergan, Merz Pharmaceuticals, and Ipsen.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>psychosis</topic><topic>depression</topic><topic>sleep</topic><topic>freezing of gait</topic><topic>genetics</topic><topic>risk factors</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. 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