Biomarkers for Cognitive Impairment in Parkinson Disease
Identifieur interne : 000303 ( Main/Corpus ); précédent : 000302; suivant : 000304Biomarkers for Cognitive Impairment in Parkinson Disease
Auteurs : Min Shi ; Bertrand R. Huber ; Jing ZhangSource :
- Brain Pathology [ 1015-6305 ] ; 2010-05.
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- KwdEn :
Abstract
Cognitive impairment, including dementia, is commonly seen in those afflicted with Parkinson disease (PD), particularly at advanced disease stages. Pathologically, PD with dementia (PD‐D) is most often associated with the presence of cortical Lewy bodies, as is the closely related dementia with Lewy bodies (DLB). Both PD‐D and DLB are also frequently complicated by the presence of neurofibrillary tangles and amyloid plaques, features most often attributed to Alzheimer disease. Biomarkers are urgently needed to differentiate among these disease processes and predict dementia in PD as well as monitor responses of patients to new therapies. A few clinical assessments, along with structural and functional neuroimaging, have been utilized in the last few years with some success in this area. Additionally, a number of other strategies have been employed to identify biochemical/molecular biomarkers associated with cognitive impairment and dementia in PD, e.g. targeted analysis of candidate proteins known to be important to PD pathogenesis and progression in cerebrospinal fluid or blood. Finally, interesting results are emerging from preliminary studies with unbiased and high throughput genomic, proteomic and metabolomic techniques. The current findings and perspectives of applying these strategies and techniques are reviewed in this article, together with potential areas of advancement.
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DOI: 10.1111/j.1750-3639.2009.00370.x
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Huber</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</json:string></affiliations></json:item><json:item><name>Jing Zhang</name><affiliations><json:string>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>biomarker</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>dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genomics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>metabolomics</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>mild cognitive impairment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>proteomics</value></json:item></subject><articleId><json:string>BPA370</json:string></articleId><language><json:string>eng</json:string></language><abstract>Cognitive impairment, including dementia, is commonly seen in those afflicted with Parkinson disease (PD), particularly at advanced disease stages. 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Pathologically, PD with dementia (PD‐D) is most often associated with the presence of cortical Lewy bodies, as is the closely related dementia with Lewy bodies (DLB). Both PD‐D and DLB are also frequently complicated by the presence of neurofibrillary tangles and amyloid plaques, features most often attributed to Alzheimer disease. Biomarkers are urgently needed to differentiate among these disease processes and predict dementia in PD as well as monitor responses of patients to new therapies. A few clinical assessments, along with structural and functional neuroimaging, have been utilized in the last few years with some success in this area. Additionally, a number of other strategies have been employed to identify biochemical/molecular biomarkers associated with cognitive impairment and dementia in PD, e.g. targeted analysis of candidate proteins known to be important to PD pathogenesis and progression in cerebrospinal fluid or blood. Finally, interesting results are emerging from preliminary studies with unbiased and high throughput genomic, proteomic and metabolomic techniques. The current findings and perspectives of applying these strategies and techniques are reviewed in this article, together with potential areas of advancement.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>biomarker</term></item><item><term>cerebrospinal fluid</term></item><item><term>dementia</term></item><item><term>genomics</term></item><item><term>metabolomics</term></item><item><term>mild cognitive impairment</term></item><item><term>Parkinson disease</term></item><item><term>proteomics</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-05">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/1886F176974A285C3BD65580B868B89BBD603582/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1750-3639</doi><issn type="print">1015-6305</issn><issn type="electronic">1750-3639</issn><idGroup><id type="product" value="BPA"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="BRAIN PATHOLOGY">Brain Pathology</title></titleGroup></publicationMeta><publicationMeta level="part" position="05003"><doi origin="wiley">10.1111/bpa.2010.20.issue-3</doi><numberingGroup><numbering type="journalVolume" number="20">20</numbering><numbering type="journalIssue" number="3">3</numbering></numberingGroup><coverDate startDate="2010-05">May 2010</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="18" status="forIssue"><doi origin="wiley">10.1111/j.1750-3639.2009.00370.x</doi><idGroup><id type="unit" value="BPA370"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">MINI‐SYMPOSIUM: Dementia in Parkinson's Disease</title></titleGroup><copyright>© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology</copyright><eventGroup><event type="firstOnline" date="2010-04-12"></event><event type="publishedOnlineFinalForm" date="2010-04-12"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:FullText result:FullText" date="2010-05-18"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-08"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-15"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="660">660</numbering><numbering type="pageLast" number="671">671</numbering></numberingGroup><correspondenceTo>Jing Zhang, MD, PhD, Department of Pathology, University of Washington School of Medicine, HMC Box 359635, 325 9th Ave, Seattle, WA 98104 (E‐mail: <email>zhangj@uw.edu</email>) </correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:BPA.BPA370.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 18 November 2009; accepted 7 December 2009.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="2"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="149"></count><count type="wordTotal" number="10822"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Biomarkers for Cognitive Impairment in Parkinson Disease</title><title type="shortAuthors">Shi <i>et al</i></title><title type="short">Biomarkers for PD Cognitive Impairment</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>Min</givenNames><familyName>Shi</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#aff-1-1"><personName><givenNames>Bertrand R.</givenNames><familyName>Huber</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#aff-1-1"><personName><givenNames>Jing</givenNames><familyName>Zhang</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="US"><unparsedAffiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">biomarker</keyword><keyword xml:id="k2">cerebrospinal fluid</keyword><keyword xml:id="k3">dementia</keyword><keyword xml:id="k4">genomics</keyword><keyword xml:id="k5">metabolomics</keyword><keyword xml:id="k6">mild cognitive impairment</keyword><keyword xml:id="k7">Parkinson disease</keyword><keyword xml:id="k8">proteomics</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>Cognitive impairment, including dementia, is commonly seen in those afflicted with Parkinson disease (PD), particularly at advanced disease stages. Pathologically, PD with dementia (PD‐D) is most often associated with the presence of cortical Lewy bodies, as is the closely related dementia with Lewy bodies (DLB). Both PD‐D and DLB are also frequently complicated by the presence of neurofibrillary tangles and amyloid plaques, features most often attributed to Alzheimer disease. Biomarkers are urgently needed to differentiate among these disease processes and predict dementia in PD as well as monitor responses of patients to new therapies. A few clinical assessments, along with structural and functional neuroimaging, have been utilized in the last few years with some success in this area. Additionally, a number of other strategies have been employed to identify biochemical/molecular biomarkers associated with cognitive impairment and dementia in PD, e.g. targeted analysis of candidate proteins known to be important to PD pathogenesis and progression in cerebrospinal fluid or blood. Finally, interesting results are emerging from preliminary studies with unbiased and high throughput genomic, proteomic and metabolomic techniques. The current findings and perspectives of applying these strategies and techniques are reviewed in this article, together with potential areas of advancement.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Biomarkers for Cognitive Impairment in Parkinson Disease</title></titleInfo><titleInfo type="abbreviated"><title>Biomarkers for PD Cognitive Impairment</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Biomarkers for Cognitive Impairment in Parkinson Disease</title></titleInfo><name type="personal"><namePart type="given">Min</namePart><namePart type="family">Shi</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Bertrand R.</namePart><namePart type="family">Huber</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jing</namePart><namePart type="family">Zhang</namePart><affiliation>Department of Pathology, University of Washington School of Medicine, Seattle, Wa.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-05</dateIssued><edition>Received 18 November 2009; accepted 7 December 2009.</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">2</extent><extent unit="references">149</extent><extent unit="words">10822</extent></physicalDescription><abstract lang="en">Cognitive impairment, including dementia, is commonly seen in those afflicted with Parkinson disease (PD), particularly at advanced disease stages. Pathologically, PD with dementia (PD‐D) is most often associated with the presence of cortical Lewy bodies, as is the closely related dementia with Lewy bodies (DLB). Both PD‐D and DLB are also frequently complicated by the presence of neurofibrillary tangles and amyloid plaques, features most often attributed to Alzheimer disease. Biomarkers are urgently needed to differentiate among these disease processes and predict dementia in PD as well as monitor responses of patients to new therapies. A few clinical assessments, along with structural and functional neuroimaging, have been utilized in the last few years with some success in this area. Additionally, a number of other strategies have been employed to identify biochemical/molecular biomarkers associated with cognitive impairment and dementia in PD, e.g. targeted analysis of candidate proteins known to be important to PD pathogenesis and progression in cerebrospinal fluid or blood. Finally, interesting results are emerging from preliminary studies with unbiased and high throughput genomic, proteomic and metabolomic techniques. The current findings and perspectives of applying these strategies and techniques are reviewed in this article, together with potential areas of advancement.</abstract><subject lang="en"><genre>Keywords</genre><topic>biomarker</topic><topic>cerebrospinal fluid</topic><topic>dementia</topic><topic>genomics</topic><topic>metabolomics</topic><topic>mild cognitive impairment</topic><topic>Parkinson disease</topic><topic>proteomics</topic></subject><relatedItem type="host"><titleInfo><title>Brain Pathology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1015-6305</identifier><identifier type="eISSN">1750-3639</identifier><identifier type="DOI">10.1111/(ISSN)1750-3639</identifier><identifier type="PublisherID">BPA</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>3</number></detail><extent unit="pages"><start>660</start><end>671</end><total>12</total></extent></part></relatedItem><identifier type="istex">1886F176974A285C3BD65580B868B89BBD603582</identifier><identifier type="DOI">10.1111/j.1750-3639.2009.00370.x</identifier><identifier type="ArticleID">BPA370</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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