Abnormal explicit but not implicit sequence learning in pre-manifest and early Huntington’s disease
Identifieur interne : 000223 ( Pmc/Curation ); précédent : 000222; suivant : 000224Abnormal explicit but not implicit sequence learning in pre-manifest and early Huntington’s disease
Auteurs : Susanne A. Schneider [Royaume-Uni] ; Leonora Wilkinson [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni] ; Susie Henley [Royaume-Uni] ; John C. Rothwell [Royaume-Uni] ; Sarah J. Tabrizi [Royaume-Uni] ; Marjan Jahanshahi [Royaume-Uni]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2010.
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 fifteen individuals with a positive HD genetic test (7 pre-manifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and pre-manifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.
Url:
DOI: 10.1002/mds.22692
PubMed: 20544716
PubMed Central: 2997693
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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 fifteen individuals with a positive HD genetic test (7 pre-manifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and pre-manifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">8610688</journal-id><journal-id journal-id-type="pubmed-jr-id">5937</journal-id><journal-id journal-id-type="nlm-ta">Mov Disord</journal-id><journal-id journal-id-type="iso-abbrev">Mov. Disord.</journal-id><journal-title-group><journal-title>Movement disorders : official journal of the Movement Disorder Society</journal-title></journal-title-group><issn pub-type="ppub">0885-3185</issn><issn pub-type="epub">1531-8257</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20544716</article-id><article-id pub-id-type="pmc">2997693</article-id><article-id pub-id-type="doi">10.1002/mds.22692</article-id><article-id pub-id-type="manuscript">UKMS33573</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Abnormal explicit but not implicit sequence learning in pre-manifest and early Huntington’s disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Schneider</surname><given-names>Susanne A.</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Wilkinson</surname><given-names>Leonora</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Bhatia</surname><given-names>Kailash P.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Henley</surname><given-names>Susie</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Rothwell</surname><given-names>John C.</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Tabrizi</surname><given-names>Sarah J.</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Jahanshahi</surname><given-names>Marjan</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label> Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square; London WC1N 3BG, United Kingdom.</aff><aff id="A2"><label>2</label> Department of Neurodegenerative Disease; Institute of Neurology, Queen Square; London WC1N 3BG, United Kingdom.</aff><author-notes><corresp id="CR1"><bold>Correspondence</bold> should be addressed to, Prof. M. Jahanshahi, Sobell Department of Motor Neuroscience and Movement Disorders, The National Hospital for Neurology and Neurosurgery, Institute of Neurology, 33 Queen Square, London, WC1N 3 BG. Telephone: 0203 108 0035 Fax: (44) 0207 278 9836 <email>m.jahanshahi@ion.ucl.ac.uk</email>.
</corresp><fn id="FN2"><p id="P1">Author roles Conception (MJ, LW, KB, JCR, SJT), Organization (SAS, LW, SH, SJT, KB, JCR), Execution (SAS, LW, SH); Statistical Analysis (LW, MJ); Manuscript Writing of the first draft (SAS, LW, MJ) and review and critique (KB, SH, JCR, SJT).</p></fn><fn id="FN3"><p id="P2">Author note We are grateful to all the participants and we would like to thank E. Wild for his help with patient recruitment and C. Baader for helpful comments.</p></fn><fn fn-type="equal" id="FN1"><label>*</label><p id="P3">These authors contributed equally to this study</p></fn></author-notes><pub-date pub-type="nihms-submitted"><day>26</day><month>11</month><year>2010</year></pub-date><pub-date pub-type="ppub"><day>30</day><month>7</month><year>2010</year></pub-date><pub-date pub-type="pmc-release"><day>06</day><month>12</month><year>2010</year></pub-date><volume>25</volume><issue>10</issue><fpage>1343</fpage><lpage>1349</lpage><abstract><p id="P4">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 fifteen individuals with a positive HD genetic test (7 pre-manifest; 8 early stage disease) and 11 matched controls. The HD group showed evidence of implicit motor sequence learning, whereas explicit motor sequence learning was impaired in manifest and pre-manifest HD gene carriers, with progressive decline with progressive disease. Explicit sequence learning may be a useful cognitive biomarker for HD progression.</p></abstract><kwd-group><kwd>Huntington’s disease</kwd><kwd>Manifesting</kwd><kwd>Pre-symptomatic</kwd><kwd>Explicit sequence learning</kwd><kwd>Implicit sequence learning</kwd><kwd>Serial reaction time task</kwd></kwd-group><funding-group><award-group><funding-source country="United Kingdom">Parkinson's UK : </funding-source><award-id>F-0608 || PUK_</award-id></award-group><award-group><funding-source country="United Kingdom">Medical Research Council : </funding-source><award-id>G0500258(74086) || MRC_</award-id></award-group></funding-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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