CSF Aβ42 and tau in Parkinson's disease with cognitive impairment
Identifieur interne : 002A15 ( Main/Corpus ); précédent : 002A14; suivant : 002A16CSF Aβ42 and tau in Parkinson's disease with cognitive impairment
Auteurs : Thomas J. Montine ; Min Shi ; Joseph F. Quinn ; Elaine R. Peskind ; Suzanne Craft ; Carmen Ginghina ; Kathryn A. Chung ; Hojoong Kim ; Douglas R. Galasko ; Joseph Jankovic ; Cyrus P. Zabetian ; James B. Leverenz ; Jing ZhangSource :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
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Abstract
We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.23287
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Leverenz</name><affiliation><mods:affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E22F3584401FA8AF62FC70D3542C9D9107AC3FA8</idno><date when="2010" year="2010">2010</date><idno type="doi">10.1002/mds.23287</idno><idno type="url">https://api.istex.fr/document/E22F3584401FA8AF62FC70D3542C9D9107AC3FA8/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">002A15</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">CSF Aβ42 and tau in Parkinson's disease with cognitive impairment</title><author><name sortKey="Montine, Thomas J" sort="Montine, Thomas J" uniqKey="Montine T" first="Thomas J." last="Montine">Thomas J. Montine</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Shi, Min" sort="Shi, Min" uniqKey="Shi M" first="Min" last="Shi">Min Shi</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Quinn, Joseph F" sort="Quinn, Joseph F" uniqKey="Quinn J" first="Joseph F." last="Quinn">Joseph F. Quinn</name><affiliation><mods:affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</mods:affiliation></affiliation></author><author><name sortKey="Peskind, Elaine R" sort="Peskind, Elaine R" uniqKey="Peskind E" first="Elaine R." last="Peskind">Elaine R. Peskind</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Craft, Suzanne" sort="Craft, Suzanne" uniqKey="Craft S" first="Suzanne" last="Craft">Suzanne Craft</name><affiliation><mods:affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Ginghina, Carmen" sort="Ginghina, Carmen" uniqKey="Ginghina C" first="Carmen" last="Ginghina">Carmen Ginghina</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Chung, Kathryn A" sort="Chung, Kathryn A" uniqKey="Chung K" first="Kathryn A." last="Chung">Kathryn A. Chung</name><affiliation><mods:affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</mods:affiliation></affiliation></author><author><name sortKey="Kim, Hojoong" sort="Kim, Hojoong" uniqKey="Kim H" first="Hojoong" last="Kim">Hojoong Kim</name><affiliation><mods:affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Galasko, Douglas R" sort="Galasko, Douglas R" uniqKey="Galasko D" first="Douglas R." last="Galasko">Douglas R. Galasko</name><affiliation><mods:affiliation>Department of Neurosciences, University of California at San Diego, San Diego, California, USA</mods:affiliation></affiliation></author><author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name><affiliation><mods:affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</mods:affiliation></affiliation></author><author><name sortKey="Zabetian, Cyrus P" sort="Zabetian, Cyrus P" uniqKey="Zabetian C" first="Cyrus P." last="Zabetian">Cyrus P. Zabetian</name><affiliation><mods:affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Leverenz, James B" sort="Leverenz, James B" uniqKey="Leverenz J" first="James B." last="Leverenz">James B. Leverenz</name><affiliation><mods:affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author><author><name sortKey="Zhang, Jing" sort="Zhang, Jing" uniqKey="Zhang J" first="Jing" last="Zhang">Jing Zhang</name><affiliation><mods:affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15">2010-11-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2682">2682</biblScope><biblScope unit="page" to="2685">2685</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E22F3584401FA8AF62FC70D3542C9D9107AC3FA8</idno><idno type="DOI">10.1002/mds.23287</idno><idno type="ArticleID">MDS23287</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aβ42</term><term>CSF biomarkers</term><term>Parkinson's disease</term><term>cognitive impairment</term><term>tau</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Thomas J. Montine MD, PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Min Shi MD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Joseph F. Quinn MD</name><affiliations><json:string>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</json:string></affiliations></json:item><json:item><name>Elaine R. Peskind MD</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</json:string><json:string>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Suzanne Craft PhD</name><affiliations><json:string>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</json:string><json:string>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Carmen Ginghina PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Kathryn A. Chung MD</name><affiliations><json:string>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</json:string></affiliations></json:item><json:item><name>Hojoong Kim MD</name><affiliations><json:string>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Douglas R. Galasko MD</name><affiliations><json:string>Department of Neurosciences, University of California at San Diego, San Diego, California, USA</json:string></affiliations></json:item><json:item><name>Joseph Jankovic MD</name><affiliations><json:string>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</json:string></affiliations></json:item><json:item><name>Cyrus P. Zabetian MD, MS</name><affiliations><json:string>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>James B. Leverenz MD</name><affiliations><json:string>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</json:string><json:string>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</json:string></affiliations></json:item><json:item><name>Jing Zhang MD, PhD</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, 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>cognitive impairment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CSF biomarkers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Aβ42</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tau</value></json:item></subject><articleId><json:string>MDS23287</json:string></articleId><language><json:string>eng</json:string></language><abstract>We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P > 0.05) and PD‐D (P > 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society</abstract><qualityIndicators><score>6.824</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>5</keywordCount><abstractCharCount>962</abstractCharCount><pdfWordCount>23400</pdfWordCount><pdfCharCount>153211</pdfCharCount><pdfPageCount>37</pdfPageCount><abstractWordCount>152</abstractWordCount></qualityIndicators><title>CSF Aβ42 and tau in Parkinson's disease with cognitive impairment</title><genre><json:string>brief communication</json:string></genre><host><volume>25</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>4</total><last>2685</last><first>2682</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</issue><subject><json:item><value>Brief Report</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>2010</publicationDate><copyrightDate>2010</copyrightDate><doi><json:string>10.1002/mds.23287</json:string></doi><id>E22F3584401FA8AF62FC70D3542C9D9107AC3FA8</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/E22F3584401FA8AF62FC70D3542C9D9107AC3FA8/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/E22F3584401FA8AF62FC70D3542C9D9107AC3FA8/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/E22F3584401FA8AF62FC70D3542C9D9107AC3FA8/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">CSF Aβ42 and tau in Parkinson's disease with cognitive impairment</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>WILEY</p></availability><date>2010</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: Nothing to report.</note><note>NIH - No. ES004696; No. NS057567; No. AG025327; No. AG033398; No. NS060252; No. NS062684; No. AG05136; No. AG08017;</note><note>Michael J. Fox Foundation</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">CSF Aβ42 and tau in Parkinson's disease with cognitive impairment</title><author><persName><forename type="first">Thomas J.</forename><surname>Montine</surname></persName><roleName type="degree">MD, PhD</roleName><note type="biography">Thomas J. Montine and Min Shi contributed equally to this work.</note><affiliation>Thomas J. Montine and Min Shi contributed equally to this work.</affiliation><note type="correspondence"><p>Correspondence: Department of Pathology, University of Washington; 300 9th Ave, Room 713B; Seattle, WA 98104</p></note><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Min</forename><surname>Shi</surname></persName><roleName type="degree">MD</roleName><note type="biography">Thomas J. Montine and Min Shi contributed equally to this work.</note><affiliation>Thomas J. Montine and Min Shi contributed equally to this work.</affiliation><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Joseph F.</forename><surname>Quinn</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</affiliation></author><author><persName><forename type="first">Elaine R.</forename><surname>Peskind</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Suzanne</forename><surname>Craft</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Carmen</forename><surname>Ginghina</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Kathryn A.</forename><surname>Chung</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</affiliation></author><author><persName><forename type="first">Hojoong</forename><surname>Kim</surname></persName><roleName type="degree">MD</roleName><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Douglas R.</forename><surname>Galasko</surname></persName><roleName type="degree">MD</roleName><affiliation>Department of Neurosciences, University of California at San Diego, San Diego, California, USA</affiliation></author><author><persName><forename type="first">Joseph</forename><surname>Jankovic</surname></persName><roleName type="degree">MD</roleName><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</affiliation></author><author><persName><forename type="first">Cyrus P.</forename><surname>Zabetian</surname></persName><roleName type="degree">MD, MS</roleName><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">James B.</forename><surname>Leverenz</surname></persName><roleName type="degree">MD</roleName><affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author><author><persName><forename type="first">Jing</forename><surname>Zhang</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-11-15"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2682">2682</biblScope><biblScope unit="page" to="2685">2685</biblScope></imprint></monogr><idno type="istex">E22F3584401FA8AF62FC70D3542C9D9107AC3FA8</idno><idno type="DOI">10.1002/mds.23287</idno><idno type="ArticleID">MDS23287</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2010</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 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>cognitive impairment</term></item><item><term>CSF biomarkers</term></item><item><term>Aβ42</term></item><item><term>tau</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-03-12">Received</change><change when="2010-05-10">Registration</change><change when="2010-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/E22F3584401FA8AF62FC70D3542C9D9107AC3FA8/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="150"><doi origin="wiley" registered="yes">10.1002/mds.v25:15</doi><numberingGroup><numbering type="journalVolume" number="25">25</numbering><numbering type="journalIssue">15</numbering></numberingGroup><coverDate startDate="2010-11-15">15 November 2010</coverDate></publicationMeta><publicationMeta level="unit" type="shortCommunication" position="320" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.23287</doi><idGroup><id type="unit" value="MDS23287"></id></idGroup><countGroup><count type="pageTotal" number="4"></count></countGroup><titleGroup><title type="articleCategory">Brief Report</title><title type="tocHeading1">Brief Reports</title></titleGroup><copyright ownership="thirdParty">Copyright © 2010 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2010-03-12"></event><event type="manuscriptRevised" date="2010-04-09"></event><event 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type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="19"></count><count type="wordTotal" number="3140"></count></countGroup><titleGroup><title type="main" xml:lang="en">CSF Aβ<sub>42</sub> and tau in Parkinson's disease with cognitive impairment<link href="#fn4"></link></title><title type="short" xml:lang="en">CSF Biomarkers for PD with CI or Dementia</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes" noteRef="#fn3"><personName><givenNames>Thomas J.</givenNames><familyName>Montine</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>tmontine@uw.edu</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" noteRef="#fn3"><personName><givenNames>Min</givenNames><familyName>Shi</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Joseph F.</givenNames><familyName>Quinn</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3 #af4"><personName><givenNames>Elaine R.</givenNames><familyName>Peskind</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af3 #af5"><personName><givenNames>Suzanne</givenNames><familyName>Craft</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Carmen</givenNames><familyName>Ginghina</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Kathryn A.</givenNames><familyName>Chung</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af5 #af6"><personName><givenNames>Hojoong</givenNames><familyName>Kim</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af7"><personName><givenNames>Douglas R.</givenNames><familyName>Galasko</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au10" creatorRole="author" affiliationRef="#af8"><personName><givenNames>Joseph</givenNames><familyName>Jankovic</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au11" creatorRole="author" affiliationRef="#af5 #af6"><personName><givenNames>Cyrus P.</givenNames><familyName>Zabetian</familyName><degrees>MD, MS</degrees></personName></creator><creator xml:id="au12" creatorRole="author" affiliationRef="#af4 #af6"><personName><givenNames>James B.</givenNames><familyName>Leverenz</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au13" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Jing</givenNames><familyName>Zhang</familyName><degrees>MD, PhD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="US" type="organization"><unparsedAffiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="US" type="organization"><unparsedAffiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</unparsedAffiliation></affiliation><affiliation xml:id="af4" countryCode="US" type="organization"><unparsedAffiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</unparsedAffiliation></affiliation><affiliation xml:id="af5" countryCode="US" type="organization"><unparsedAffiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</unparsedAffiliation></affiliation><affiliation xml:id="af6" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</unparsedAffiliation></affiliation><affiliation xml:id="af7" countryCode="US" type="organization"><unparsedAffiliation>Department of Neurosciences, University of California at San Diego, San Diego, California, USA</unparsedAffiliation></affiliation><affiliation xml:id="af8" countryCode="US" type="organization"><unparsedAffiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">cognitive impairment</keyword><keyword xml:id="kwd3">CSF biomarkers</keyword><keyword xml:id="kwd4">Aβ<sub>42</sub></keyword><keyword xml:id="kwd5">tau</keyword></keywordGroup><fundingInfo><fundingAgency>NIH</fundingAgency><fundingNumber>ES004696</fundingNumber><fundingNumber>NS057567</fundingNumber><fundingNumber>AG025327</fundingNumber><fundingNumber>AG033398</fundingNumber><fundingNumber>NS060252</fundingNumber><fundingNumber>NS062684</fundingNumber><fundingNumber>AG05136</fundingNumber><fundingNumber>AG08017</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Michael J. Fox Foundation</fundingAgency></fundingInfo><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ<sub>42</sub>, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (<i>n</i>): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ<sub>42</sub> was reduced in PD‐CIND (<i>P</i> < 0.05) and PD‐D (<i>P</i> < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ<sub>42</sub> may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn4"><p>Potential conflict of interest: Nothing to report.</p></note><note xml:id="fn3"><p>Thomas J. Montine and Min Shi contributed equally to this work.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>CSF Aβ42 and tau in Parkinson's disease with cognitive impairment</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CSF Biomarkers for PD with CI or Dementia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>CSF Aβ</title></titleInfo><name type="personal"><namePart type="given">Thomas J.</namePart><namePart type="family">Montine</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><description>Thomas J. Montine and Min Shi contributed equally to this work.</description><description>Correspondence: Department of Pathology, University of Washington; 300 9th Ave, Room 713B; Seattle, WA 98104</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Min</namePart><namePart type="family">Shi</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><description>Thomas J. Montine and Min Shi contributed equally to this work.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph F.</namePart><namePart type="family">Quinn</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elaine R.</namePart><namePart type="family">Peskind</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Suzanne</namePart><namePart type="family">Craft</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carmen</namePart><namePart type="family">Ginghina</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kathryn A.</namePart><namePart type="family">Chung</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Oregon Health & Science University, Portland, Oregon, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hojoong</namePart><namePart type="family">Kim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Douglas R.</namePart><namePart type="family">Galasko</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurosciences, University of California at San Diego, San Diego, California, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Joseph</namePart><namePart type="family">Jankovic</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, 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, MS</namePart><affiliation>Geriatric Research, Education, and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James B.</namePart><namePart type="family">Leverenz</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>VA Northwest Network Mental Illness Research, Education and Clinical Center, VA Puget Sound Health Care System, Seattle, Washington, USA</affiliation><affiliation>Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jing</namePart><namePart type="family">Zhang</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Washington, USA</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">2010-11-15</dateIssued><dateCaptured encoding="w3cdtf">2010-03-12</dateCaptured><dateValid encoding="w3cdtf">2010-05-10</dateValid><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="figures">1</extent><extent unit="tables">1</extent><extent unit="references">19</extent><extent unit="words">3140</extent></physicalDescription><abstract lang="en">We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD‐D) or with PD and Cognitive Impairment, Not Dementia (PD‐CIND). We quantified CSF Aβ42, total tau (T‐tau), and phospho‐tau (P181‐tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD‐CIND (62), and PD‐D (11). We observed expected changes in AD or aMCI compared with age‐matched or younger controls. CSF Aβ42 was reduced in PD‐CIND (P < 0.05) and PD‐D (P < 0.01), whereas average CSF T‐tau and P181‐tau were unchanged or decreased. One‐third of PD‐CIND and one‐half of PD‐D patients had the biomarker signature of AD. Abnormal metabolism of Aβ42 may be a common feature of PD‐CIND and PD‐D. © 2010 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><note type="funding">NIH - No. ES004696; No. NS057567; No. AG025327; No. AG033398; No. NS060252; No. NS062684; No. AG05136; No. AG08017; </note><note type="funding">Michael J. Fox Foundation</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>cognitive impairment</topic><topic>CSF biomarkers</topic><topic>Aβ42</topic><topic>tau</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>25</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2682</start><end>2685</end><total>4</total></extent></part></relatedItem><identifier type="istex">E22F3584401FA8AF62FC70D3542C9D9107AC3FA8</identifier><identifier type="DOI">10.1002/mds.23287</identifier><identifier type="ArticleID">MDS23287</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2010 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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