Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.
Identifieur interne : 001810 ( PubMed/Corpus ); précédent : 001809; suivant : 001811Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.
Auteurs : Susanne A. Schneider ; Leonora Wilkinson ; Kailash P. Bhatia ; Susie M D. Henley ; John C. Rothwell ; Sarah J. Tabrizi ; Marjan JahanshahiSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Age of Onset, Executive Function (physiology), Female, Humans, Huntington Disease (complications), Huntington Disease (genetics), Learning Disorders (classification), Learning Disorders (etiology), Male, Memory, Short-Term (physiology), Middle Aged, Neuropsychological Tests, Serial Learning (physiology), Statistics as Topic, Trinucleotide Repeat Expansion (genetics).
- MESH :
- classification : Learning Disorders.
- complications : Huntington Disease.
- etiology : Learning Disorders.
- genetics : Huntington Disease, Trinucleotide Repeat Expansion.
- physiology : Executive Function, Memory, Short-Term, Serial Learning.
- Adult, Age of Onset, Female, Humans, Male, Middle Aged, Neuropsychological Tests, Statistics as Topic.
Abstract
Learning may occur with or without awareness, as explicit (intentional) or implicit (incidental) learning. The caudate nucleus and the putamen, which are affected early in Huntington's disease (HD), are thought to be essential for motor sequence learning. However, the results of existing studies are inconsistent concerning presence/absence of deficits in implicit and explicit motor sequence learning in HD. We assessed implicit and explicit motor sequence learning using sequences of equivalent structure in 15 individuals with a positive HD genetic test (7 premanifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of normal implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and premanifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.
DOI: 10.1002/mds.22692
PubMed: 20544716
Links to Exploration step
pubmed:20544716Le document en format XML
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Henley</name></author><author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C" last="Rothwell">John C. Rothwell</name></author><author><name sortKey="Tabrizi, Sarah J" sort="Tabrizi, Sarah J" uniqKey="Tabrizi S" first="Sarah J" last="Tabrizi">Sarah J. Tabrizi</name></author><author><name sortKey="Jahanshahi, Marjan" sort="Jahanshahi, Marjan" uniqKey="Jahanshahi M" first="Marjan" last="Jahanshahi">Marjan Jahanshahi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.22692</idno><idno type="RBID">pubmed:20544716</idno><idno type="pmid">20544716</idno><idno type="wicri:Area/PubMed/Corpus">001810</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.</title><author><name sortKey="Schneider, Susanne A" sort="Schneider, Susanne A" uniqKey="Schneider S" first="Susanne A" last="Schneider">Susanne A. Schneider</name><affiliation><nlm:affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, UCL, Institute of Neurology, Queen Square,London, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Wilkinson, Leonora" sort="Wilkinson, Leonora" uniqKey="Wilkinson L" first="Leonora" last="Wilkinson">Leonora Wilkinson</name></author><author><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P" last="Bhatia">Kailash P. Bhatia</name></author><author><name sortKey="Henley, Susie M D" sort="Henley, Susie M D" uniqKey="Henley S" first="Susie M D" last="Henley">Susie M D. Henley</name></author><author><name sortKey="Rothwell, John C" sort="Rothwell, John C" uniqKey="Rothwell J" first="John C" last="Rothwell">John C. Rothwell</name></author><author><name sortKey="Tabrizi, Sarah J" sort="Tabrizi, Sarah J" uniqKey="Tabrizi S" first="Sarah J" last="Tabrizi">Sarah J. Tabrizi</name></author><author><name sortKey="Jahanshahi, Marjan" sort="Jahanshahi, Marjan" uniqKey="Jahanshahi M" first="Marjan" last="Jahanshahi">Marjan Jahanshahi</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Executive Function (physiology)</term><term>Female</term><term>Humans</term><term>Huntington Disease (complications)</term><term>Huntington Disease (genetics)</term><term>Learning Disorders (classification)</term><term>Learning Disorders (etiology)</term><term>Male</term><term>Memory, Short-Term (physiology)</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Serial Learning (physiology)</term><term>Statistics as Topic</term><term>Trinucleotide Repeat Expansion (genetics)</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Learning Disorders</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Learning Disorders</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term><term>Trinucleotide Repeat Expansion</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Executive Function</term><term>Memory, Short-Term</term><term>Serial Learning</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Neuropsychological Tests</term><term>Statistics as Topic</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Learning may occur with or without awareness, as explicit (intentional) or implicit (incidental) learning. The caudate nucleus and the putamen, which are affected early in Huntington's disease (HD), are thought to be essential for motor sequence learning. However, the results of existing studies are inconsistent concerning presence/absence of deficits in implicit and explicit motor sequence learning in HD. We assessed implicit and explicit motor sequence learning using sequences of equivalent structure in 15 individuals with a positive HD genetic test (7 premanifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of normal implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and premanifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">20544716</PMID><DateCreated><Year>2010</Year><Month>08</Month><Day>02</Day></DateCreated><DateCompleted><Year>2010</Year><Month>12</Month><Day>02</Day></DateCompleted><DateRevised><Year>2014</Year><Month>08</Month><Day>24</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>10</Issue><PubDate><Year>2010</Year><Month>Jul</Month><Day>30</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Abnormal explicit but normal implicit sequence learning in premanifest and early Huntington's disease.</ArticleTitle><Pagination><MedlinePgn>1343-9</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22692</ELocationID><Abstract><AbstractText>Learning may occur with or without awareness, as explicit (intentional) or implicit (incidental) learning. The caudate nucleus and the putamen, which are affected early in Huntington's disease (HD), are thought to be essential for motor sequence learning. However, the results of existing studies are inconsistent concerning presence/absence of deficits in implicit and explicit motor sequence learning in HD. We assessed implicit and explicit motor sequence learning using sequences of equivalent structure in 15 individuals with a positive HD genetic test (7 premanifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of normal implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and premanifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.</AbstractText><CopyrightInformation>(c) 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Schneider</LastName><ForeName>Susanne A</ForeName><Initials>SA</Initials><AffiliationInfo><Affiliation>Sobell Department of Motor Neuroscience and Movement Disorders, UCL, Institute of Neurology, Queen Square,London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wilkinson</LastName><ForeName>Leonora</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Bhatia</LastName><ForeName>Kailash P</ForeName><Initials>KP</Initials></Author><Author ValidYN="Y"><LastName>Henley</LastName><ForeName>Susie M D</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Rothwell</LastName><ForeName>John C</ForeName><Initials>JC</Initials></Author><Author ValidYN="Y"><LastName>Tabrizi</LastName><ForeName>Sarah J</ForeName><Initials>SJ</Initials></Author><Author ValidYN="Y"><LastName>Jahanshahi</LastName><ForeName>Marjan</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>F-0608</GrantID><Agency>Parkinson's UK</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>G0500258</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 2006 Jan;59(1):53-9</RefSource><PMID Version="1">16261565</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12566-71</RefSource><PMID Version="1">16107540</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain Res. 2007 Mar 16;1137(1):117-30</RefSource><PMID Version="1">17229409</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neuropsychologia. 2007 Apr 9;45(8):1767-76</RefSource><PMID Version="1">17303196</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Neurology. 2007 Mar 20;68(12):906-10</RefSource><PMID Version="1">17372125</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol 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Version="1">15772354</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Cereb Cortex. 2006 Nov;16(11):1546-55</RefSource><PMID Version="1">16373455</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D017668">Age of Onset</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D056344">Executive Function</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006816">Huntington Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000150">complications</QualifierName><QualifierName 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UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013223">Statistics as Topic</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019680">Trinucleotide Repeat Expansion</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC2997693</OtherID><OtherID Source="NLM">UKMS33573</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2010</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2010</Year><Month>6</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>12</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId 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