Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease
Identifieur interne : 001448 ( Main/Corpus ); précédent : 001447; suivant : 001449Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease
Auteurs : Yaroslau Compta ; María J. Martí ; Naroa Ibarretxe-Bilbao ; Carme Junqué ; Francesc Valldeoriola ; Esteban Mu Oz ; Mario Ezquerra ; Jose Ríos ; Eduardo TolosaSource :
- Movement Disorders [ 0885-3185 ] ; 2009-11-15.
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Abstract
Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (P < 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P < 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22594
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Martí</name><affiliation><mods:affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Ibarretxe Ilbao, Naroa" sort="Ibarretxe Ilbao, Naroa" uniqKey="Ibarretxe Ilbao N" first="Naroa" last="Ibarretxe-Bilbao">Naroa Ibarretxe-Bilbao</name><affiliation><mods:affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Junque, Carme" sort="Junque, Carme" uniqKey="Junque C" first="Carme" last="Junqué">Carme Junqué</name><affiliation><mods:affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Valldeoriola, Francesc" sort="Valldeoriola, Francesc" uniqKey="Valldeoriola F" first="Francesc" last="Valldeoriola">Francesc Valldeoriola</name><affiliation><mods:affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Mu Oz, Esteban" sort="Mu Oz, Esteban" uniqKey="Mu Oz E" first="Esteban" last="Mu Oz">Esteban Mu Oz</name><affiliation><mods:affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Ezquerra, Mario" sort="Ezquerra, Mario" uniqKey="Ezquerra M" first="Mario" last="Ezquerra">Mario Ezquerra</name><affiliation><mods:affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Rios, Jose" sort="Rios, Jose" uniqKey="Rios J" first="Jose" last="Ríos">Jose Ríos</name><affiliation><mods:affiliation>Statistics and Methodologic Support Unit, Unitat d'Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author><author><name sortKey="Tolosa, Eduardo" sort="Tolosa, Eduardo" uniqKey="Tolosa E" first="Eduardo" last="Tolosa">Eduardo Tolosa</name><affiliation><mods:affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="2009-11-15">2009-11-15</date><biblScope unit="volume">24</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2203">2203</biblScope><biblScope unit="page" to="2210">2210</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">D3532C6682933CC0328E0C7334A7EA83065A6165</idno><idno type="DOI">10.1002/mds.22594</idno><idno type="ArticleID">MDS22594</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>beta‐amyloid</term><term>cerebrospinal fluid</term><term>dementia</term><term>neuropsychological function</term><term>tau</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (P < 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P < 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yaroslau Compta MD</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>María J. Martí MD, PhD</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Naroa Ibarretxe‐Bilbao PhD</name><affiliations><json:string>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Carme Junqué PhD</name><affiliations><json:string>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Francesc Valldeoriola MD, PhD</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Esteban Muñoz MD, PhD</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Mario Ezquerra PhD</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Jose Ríos BSc</name><affiliations><json:string>Statistics and Methodologic Support Unit, Unitat d'Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</json:string></affiliations></json:item><json:item><name>Eduardo Tolosa MD, FRCP</name><affiliations><json:string>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</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>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cerebrospinal fluid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tau</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>beta‐amyloid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neuropsychological function</value></json:item></subject><articleId><json:string>MDS22594</json:string></articleId><language><json:string>eng</json:string></language><abstract>Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (P > 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P > 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 Movement Disorder Society</abstract><qualityIndicators><score>6.937</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 810 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>6</keywordCount><abstractCharCount>1404</abstractCharCount><pdfWordCount>4501</pdfWordCount><pdfCharCount>31789</pdfCharCount><pdfPageCount>8</pdfPageCount><abstractWordCount>203</abstractWordCount></qualityIndicators><title>Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>24</volume><publisherId><json:string>MDS</json:string></publisherId><pages><total>8</total><last>2210</last><first>2203</first></pages><issn><json:string>0885-3185</json:string></issn><issue>15</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>2009</publicationDate><copyrightDate>2009</copyrightDate><doi><json:string>10.1002/mds.22594</json:string></doi><id>D3532C6682933CC0328E0C7334A7EA83065A6165</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/D3532C6682933CC0328E0C7334A7EA83065A6165/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/D3532C6682933CC0328E0C7334A7EA83065A6165/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/D3532C6682933CC0328E0C7334A7EA83065A6165/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions 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>2009</date></publicationStmt><notesStmt><note type="content">*Potential conflict of interest: None reported.</note><note>Fundacio la Marato de TV3 2006 - No. N‐2006‐TV060510;</note><note>Spanish Neurology Society (SEN)</note><note>Naroa Ibarretxe‐Bilbao</note><note>Spanish Ministry of Education and Science - No. AP2005‐0191;</note><note>Laboratory of Experimental Neurology</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease</title><author><persName><forename type="first">Yaroslau</forename><surname>Compta</surname></persName><roleName type="degree">MD</roleName><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">María J.</forename><surname>Martí</surname></persName><roleName type="degree">MD, PhD</roleName><note type="correspondence"><p>Correspondence: Movement Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, c./Villarroel 170, 08036 Barcelona, Spain</p></note><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Naroa</forename><surname>Ibarretxe‐Bilbao</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Carme</forename><surname>Junqué</surname></persName><roleName type="degree">PhD</roleName><affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Francesc</forename><surname>Valldeoriola</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Esteban</forename><surname>Muñoz</surname></persName><roleName type="degree">MD, PhD</roleName><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Mario</forename><surname>Ezquerra</surname></persName><roleName type="degree">PhD</roleName><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Jose</forename><surname>Ríos</surname></persName><roleName type="degree">BSc</roleName><affiliation>Statistics and Methodologic Support Unit, Unitat d'Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</affiliation></author><author><persName><forename type="first">Eduardo</forename><surname>Tolosa</surname></persName><roleName type="degree">MD, FRCP</roleName><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="2009-11-15"></date><biblScope unit="volume">24</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2203">2203</biblScope><biblScope unit="page" to="2210">2210</biblScope></imprint></monogr><idno type="istex">D3532C6682933CC0328E0C7334A7EA83065A6165</idno><idno type="DOI">10.1002/mds.22594</idno><idno type="ArticleID">MDS22594</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2009</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (P < 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P < 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 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>dementia</term></item><item><term>cerebrospinal fluid</term></item><item><term>tau</term></item><item><term>beta‐amyloid</term></item><item><term>neuropsychological function</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="2009-01-12">Received</change><change when="2009-03-17">Registration</change><change when="2009-11-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/D3532C6682933CC0328E0C7334A7EA83065A6165/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="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="150"><doi origin="wiley" registered="yes">10.1002/mds.v24:15</doi><numberingGroup><numbering type="journalVolume" number="24">24</numbering><numbering type="journalIssue">15</numbering></numberingGroup><coverDate startDate="2009-11-15">15 November 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="40" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.22594</doi><idGroup><id type="unit" value="MDS22594"></id></idGroup><countGroup><count type="pageTotal" number="8"></count></countGroup><titleGroup><title type="articleCategory">Research Article</title><title type="tocHeading1">Research Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 2009 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="2009-01-12"></event><event type="manuscriptRevised" date="2009-03-11"></event><event type="manuscriptAccepted" date="2009-03-17"></event><event type="publishedOnlineEarlyUnpaginated" date="2009-09-30"></event><event type="firstOnline" date="2009-09-30"></event><event type="publishedOnlineFinalForm" date="2009-11-19"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-09"></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">2203</numbering><numbering type="pageLast">2210</numbering></numberingGroup><correspondenceTo>Movement Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, c./Villarroel 170, 08036 Barcelona, Spain</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS22594.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="45"></count><count type="wordTotal" number="6480"></count></countGroup><titleGroup><title type="main" xml:lang="en">Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease<link href="#fn6"></link></title><title type="short" xml:lang="en">CSF and Neuropsychological Markers in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Yaroslau</givenNames><familyName>Compta</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>María J.</givenNames><familyName>Martí</familyName><degrees>MD, PhD</degrees></personName><contactDetails><email>mjmarti@clinic.ub.es</email></contactDetails></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Naroa</givenNames><familyName>Ibarretxe‐Bilbao</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Carme</givenNames><familyName>Junqué</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Francesc</givenNames><familyName>Valldeoriola</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Esteban</givenNames><familyName>Muñoz</familyName><degrees>MD, PhD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Mario</givenNames><familyName>Ezquerra</familyName><degrees>PhD</degrees></personName></creator><creator xml:id="au8" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Jose</givenNames><familyName>Ríos</familyName><degrees>BSc</degrees></personName></creator><creator xml:id="au9" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Eduardo</givenNames><familyName>Tolosa</familyName><degrees>MD, FRCP</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="ES" type="organization"><unparsedAffiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="ES" type="organization"><unparsedAffiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="ES" type="organization"><unparsedAffiliation>Statistics and Methodologic Support Unit, Unitat d'Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">dementia</keyword><keyword xml:id="kwd3">cerebrospinal fluid</keyword><keyword xml:id="kwd4">tau</keyword><keyword xml:id="kwd5">beta‐amyloid</keyword><keyword xml:id="kwd6">neuropsychological function</keyword></keywordGroup><fundingInfo><fundingAgency>Fundacio la Marato de TV3 2006</fundingAgency><fundingNumber>N‐2006‐TV060510</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Spanish Neurology Society (SEN)</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Naroa Ibarretxe‐Bilbao</fundingAgency></fundingInfo><fundingInfo><fundingAgency>Spanish Ministry of Education and Science</fundingAgency><fundingNumber>AP2005‐0191</fundingNumber></fundingInfo><fundingInfo><fundingAgency>Laboratory of Experimental Neurology</fundingAgency></fundingInfo><supportingInformation><p> Additional Supporting Information may be found in the online version of this article. </p><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22594:MDS_22594_sm_SuppFig1"></mediaResource><caption>Supporting Information Figure 1. Correlation between CSF beta‐amyloid levels (expressed in pg/mL) and scores in Phonetic Fluency test in PDND patients (n= 20; r= 0.52; p= 0.04) with linear trend superimposed (linear regression: y=336.36+22.72*PhoneticFluencyScore; beta= 0.57; p= 0.08).</caption></supportingInfoItem><supportingInfoItem><mediaResource alt="supporting information" href="urn-x:wiley:08853185:media:mds22594:MDS_22594_sm_SuppTable1"></mediaResource><caption>Supporting Information Table 1. CSF tau and phospho‐tau levels relation with verbal recognition and naming in PDD.</caption></supportingInfoItem></supportingInformation><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (<i>P</i> < 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (<i>P</i> < 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn6"><p>Potential conflict of interest: None reported.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>CSF and Neuropsychological Markers in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Cerebrospinal tau, phospho‐tau, and beta‐amyloid and neuropsychological functions in Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Yaroslau</namePart><namePart type="family">Compta</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">María J.</namePart><namePart type="family">Martí</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation><description>Correspondence: Movement Disorders Unit, Neurology Service, Hospital Clínic de Barcelona, c./Villarroel 170, 08036 Barcelona, Spain</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Naroa</namePart><namePart type="family">Ibarretxe‐Bilbao</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Carme</namePart><namePart type="family">Junqué</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Psychiatry and Clinical Psychobiology IDIBAPS, CIBERNED, Faculty of Medicine, University of Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Francesc</namePart><namePart type="family">Valldeoriola</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Esteban</namePart><namePart type="family">Muñoz</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Mario</namePart><namePart type="family">Ezquerra</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose</namePart><namePart type="family">Ríos</namePart><namePart type="termsOfAddress">BSc</namePart><affiliation>Statistics and Methodologic Support Unit, Unitat d'Avaluació, Suport i Prevenció (UASP), Hospital Clínic, IDIBAPS, Barcelona, Catalonia, Spain</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Eduardo</namePart><namePart type="family">Tolosa</namePart><namePart type="termsOfAddress">MD, FRCP</namePart><affiliation>Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències (ICN), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación en Red de Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, Barcelona, Catalonia, Spain</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">2009-11-15</dateIssued><dateCaptured encoding="w3cdtf">2009-01-12</dateCaptured><dateValid encoding="w3cdtf">2009-03-17</dateValid><copyrightDate encoding="w3cdtf">2009</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">4</extent><extent unit="references">45</extent><extent unit="words">6480</extent></physicalDescription><abstract lang="en">Alzheimer's disease (AD)‐pathology may play a role in Parkinson's disease (PD)‐related dementia (PDD). The aim of this study was to assess cerebrospinal fluid (CSF) levels of tau, phospho‐tau, and beta‐amyloid, proposed AD biomarkers, and their relationship with cognitive function in PD. Forty PD patients [20 nondemented (PDND); 20 PDD] and 30 controls underwent CSF tau, phospho‐tau, and beta‐amyloid analysis using specific ELISA techniques. All PD patients and 15 controls underwent neuropsychological testing of fronto‐subcortical (attention, fluency) and neocortical (memory, naming, visuoperceptive) functions. CSF markers levels were compared between groups, and compared and correlated with neuropsychological measures in PDND and PDD separately and as a continuum (PD). CSF tau and phospho‐tau were higher in PDD than in PDND and controls (P < 0.05). CSF beta‐amyloid ranged from high (controls) to intermediate (PDND) and low (PDD) levels (P < 0.001). In all PD and PDD patients, high CSF tau and phospho‐tau were associated with impaired memory and naming. In PDND, CSF beta‐amyloid was related with phonetic fluency. These findings suggest underlying AD‐pathology in PDD in association with cortical cognitive dysfunction, and that low CSF beta‐amyloid in PDND patients with impaired phonetic fluency can constitute an early marker of cognitive dysfunction. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: None reported.</note><note type="funding">Fundacio la Marato de TV3 2006 - No. N‐2006‐TV060510; </note><note type="funding">Spanish Neurology Society (SEN)</note><note type="funding">Naroa Ibarretxe‐Bilbao</note><note type="funding">Spanish Ministry of Education and Science - No. AP2005‐0191; </note><note type="funding">Laboratory of Experimental Neurology</note><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>dementia</topic><topic>cerebrospinal fluid</topic><topic>tau</topic><topic>beta‐amyloid</topic><topic>neuropsychological function</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><note type="content"> Additional Supporting Information may be found in the online version of this article.Supporting Info Item: Supporting Information Figure 1. Correlation between CSF beta‐amyloid levels (expressed in pg/mL) and scores in Phonetic Fluency test in PDND patients (n= 20; r= 0.52; p= 0.04) with linear trend superimposed (linear regression: y=336.36+22.72*PhoneticFluencyScore; beta= 0.57; p= 0.08). - Supporting Information Table 1. CSF tau and phospho‐tau levels relation with verbal recognition and naming in PDD. - </note><subject><genre>article category</genre><topic>Research Article</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>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>15</number></detail><extent unit="pages"><start>2203</start><end>2210</end><total>8</total></extent></part></relatedItem><identifier type="istex">D3532C6682933CC0328E0C7334A7EA83065A6165</identifier><identifier type="DOI">10.1002/mds.22594</identifier><identifier type="ArticleID">MDS22594</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 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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