Biomarkers in Huntington's and Parkinson's Disease
Identifieur interne : 000695 ( Main/Corpus ); précédent : 000694; suivant : 000696Biomarkers in Huntington's and Parkinson's Disease
Auteurs : Gráinne C. O Eeffe ; Andrew W. Michell ; Roger A. BarkerSource :
- Annals of the New York Academy of SciencesBiomarkers in Brain Disease [ 0077-8923 ] ; 2009-10.
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- KwdEn :
Abstract
Parkinson's (PD) and Huntington's disease (HD) are chronic neurodegenerative conditions of the brain with a variety of clinical presentations including a disorder of movement and a range of nonmotor deficits. HD is genetic in origin and the causative gene and protein known, namely mutant Huntingtin, which leads to widespread early neuronal dysfunction and death throughout the brain. In contrast, the etiology of sporadic PD is unknown, and the pathology targets the nigrostriatal dopaminergic neurons with the formation of α‐synuclein positive Lewy bodies. In both diseases, the ability to accurately diagnose the disease in the early stages and monitor progression over time remains a major challenge given the majority of the pathology is sited deep within the CNS. This challenge has gained extra significance as the development of disease‐modifying drugs starts to emerge into the clinic. To this end, there is a need to find biomarkers that will help in the accurate diagnosis of the disease and/or prediction of its clinical onset as well as biomarkers that are able to faithfully track disease progression independent of any symptomatic effects of any therapies. In addition, these same markers may also help stratify each of these heterogeneous disorders into specific subtypes that share particular clinical and pathological characteristics.
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DOI: 10.1111/j.1749-6632.2009.04943.x
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ISTEX:7A3E7D44B7CB0D6368EE5B248E62A5AE16044A2ELe document en format XML
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O Eeffe</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, Department of Clinical Neuroscience, University of Cambridge, Cambridge, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Michell, Andrew W" sort="Michell, Andrew W" uniqKey="Michell A" first="Andrew W." last="Michell">Andrew W. Michell</name><affiliation><mods:affiliation>Cambridge Centre for Brain Repair, Department of Clinical Neuroscience, University of Cambridge, Cambridge, United Kingdom</mods:affiliation></affiliation></author><author><name sortKey="Barker, Roger A" sort="Barker, Roger A" uniqKey="Barker R" first="Roger A." last="Barker">Roger A. 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HD is genetic in origin and the causative gene and protein known, namely mutant Huntingtin, which leads to widespread early neuronal dysfunction and death throughout the brain. In contrast, the etiology of sporadic PD is unknown, and the pathology targets the nigrostriatal dopaminergic neurons with the formation of α‐synuclein positive Lewy bodies. In both diseases, the ability to accurately diagnose the disease in the early stages and monitor progression over time remains a major challenge given the majority of the pathology is sited deep within the CNS. This challenge has gained extra significance as the development of disease‐modifying drugs starts to emerge into the clinic. To this end, there is a need to find biomarkers that will help in the accurate diagnosis of the disease and/or prediction of its clinical onset as well as biomarkers that are able to faithfully track disease progression independent of any symptomatic effects of any therapies. In addition, these same markers may also help stratify each of these heterogeneous disorders into specific subtypes that share particular clinical and pathological characteristics.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>Huntington's disease</term></item><item><term>biomarker</term></item><item><term>imaging</term></item><item><term>motor measures</term></item><item><term>“wet” biomarker</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2009-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/7A3E7D44B7CB0D6368EE5B248E62A5AE16044A2E/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 Inc</publisherName><publisherLoc>Malden, USA</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1749-6632</doi><issn type="print">0077-8923</issn><issn type="electronic">1749-6632</issn><idGroup><id type="product" value="NYAS"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ANNALS OF NEW YORK ACADEMY SCIENCES">Annals of the New York Academy of Sciences</title></titleGroup></publicationMeta><publicationMeta level="part" position="11801"><doi origin="wiley">10.1111/nyas.2009.1180.issue-1</doi><titleGroup><title type="main">Biomarkers in Brain Disease</title></titleGroup><numberingGroup><numbering type="journalVolume" number="11801">1180</numbering><numbering type="journalIssue">1</numbering></numberingGroup><coverDate startDate="2009-10">October 2009</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="11" status="forIssue"><doi origin="wiley">10.1111/j.1749-6632.2009.04943.x</doi><idGroup><id type="unit" value="NYAS4943"></id></idGroup><countGroup><count type="pageTotal" number="14"></count></countGroup><titleGroup><title type="tocHeading1">Original Articles</title></titleGroup><copyright>© 2009 New York Academy of Sciences</copyright><eventGroup><event type="firstOnline" date="2009-11-03"></event><event type="publishedOnlineFinalForm" date="2009-11-03"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.4 mode:FullText" date="2011-01-31"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-19"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="97">97</numbering><numbering type="pageLast" number="110">110</numbering></numberingGroup><correspondenceTo>Address for correspondence: Dr. Roger A. Barker, Cambridge Centre for Brain Repair, Forvie Site, Robinson Way, Cambridge CB2 0PY, UK. Voice: 0044 1223 331160; fax: 0044 1223 331174. <email>rab46@cam.ac.uk</email> Gráinne O'Keeffe, Ph.D., Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, CB2 2PY, Cambridge, UK. Voice: +44 1223 331160; fax: +44 1223 331174. <email>go215@cam.ac.uk</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NYAS.NYAS4943.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="98"></count><count type="linksCrossRef" number="93"></count></countGroup><titleGroup><title type="main">Biomarkers in Huntington's and Parkinson's Disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>Gráinne C.</givenNames><familyName>O’Keeffe</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>Andrew W.</givenNames><familyName>Michell</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Roger A.</givenNames><familyName>Barker</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="GB"><unparsedAffiliation>Cambridge Centre for Brain Repair, Department of Clinical Neuroscience, University of Cambridge, Cambridge, United Kingdom</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">Huntington's disease</keyword><keyword xml:id="k3">biomarker</keyword><keyword xml:id="k4">imaging</keyword><keyword xml:id="k5">motor measures</keyword><keyword xml:id="k6">“wet” biomarker</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinson's (PD) and Huntington's disease (HD) are chronic neurodegenerative conditions of the brain with a variety of clinical presentations including a disorder of movement and a range of nonmotor deficits. 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In addition, these same markers may also help stratify each of these heterogeneous disorders into specific subtypes that share particular clinical and pathological characteristics.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>Huntington's disease</topic><topic>biomarker</topic><topic>imaging</topic><topic>motor measures</topic><topic>“wet” biomarker</topic></subject><relatedItem type="host"><titleInfo><title>Annals of the New York Academy of SciencesBiomarkers in Brain Disease</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0077-8923</identifier><identifier type="eISSN">1749-6632</identifier><identifier type="DOI">10.1111/(ISSN)1749-6632</identifier><identifier type="PublisherID">NYAS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>1180</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>97</start><end>110</end><total>14</total></extent></part></relatedItem><identifier type="istex">7A3E7D44B7CB0D6368EE5B248E62A5AE16044A2E</identifier><identifier type="DOI">10.1111/j.1749-6632.2009.04943.x</identifier><identifier type="ArticleID">NYAS4943</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 New York Academy of Sciences</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Inc</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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