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A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease
Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclus...
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| Published in: | Journal of clinical and experimental neuropsychology 2010-07, Vol.32 (6), p.590-598 |
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| Main Authors: | , , , |
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| cites | cdi_FETCH-LOGICAL-c463t-f28aee8521a955fd6be7418f02062741321bb06e7c3fca951a725d08ecd8b05b3 |
| container_end_page | 598 |
| container_issue | 6 |
| container_start_page | 590 |
| container_title | Journal of clinical and experimental neuropsychology |
| container_volume | 32 |
| creator | van Walsem, Marleen R. Sundet, Kjetil Retterstøl, Lars Sundseth, Øyvind |
| description | Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclusion criteria for attaining a homogeneous sample. Results obtained by analyses of variance and effect size calculations indicate no clinical evidence of significant cognitive decline in asymptomatic HD carriers very far from onset of illness compared to noncarriers. Closeness to disease onset amongst gene carriers influenced cognition negatively whereas cytosine-adenine-guanine (CAG) repeat size did not. The findings call for longitudinal follow-up studies using a combination of clinical instruments and experimental paradigms to pinpoint when subtle cognitive deficits occur and within which of the cognitive domains. |
| doi_str_mv | 10.1080/13803390903337878 |
| format | article |
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The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclusion criteria for attaining a homogeneous sample. Results obtained by analyses of variance and effect size calculations indicate no clinical evidence of significant cognitive decline in asymptomatic HD carriers very far from onset of illness compared to noncarriers. Closeness to disease onset amongst gene carriers influenced cognition negatively whereas cytosine-adenine-guanine (CAG) repeat size did not. The findings call for longitudinal follow-up studies using a combination of clinical instruments and experimental paradigms to pinpoint when subtle cognitive deficits occur and within which of the cognitive domains.</description><identifier>ISSN: 1380-3395</identifier><identifier>EISSN: 1744-411X</identifier><identifier>DOI: 10.1080/13803390903337878</identifier><identifier>PMID: 19916101</identifier><language>eng</language><publisher>Hove: Taylor & Francis Group</publisher><subject>Adult ; Adult and adolescent clinical studies ; Analysis of Variance ; Asymptomatic ; Biological and medical sciences ; Cognition ; Cognition Disorders - diagnosis ; Cognition Disorders - etiology ; Cognition Disorders - genetics ; Cohort Studies ; Cytosine-adenine-guanine ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Double-Blind Method ; Female ; Humans ; Huntington Disease - complications ; Huntington Disease - genetics ; Huntington's disease ; Male ; Medical sciences ; Middle Aged ; Nervous system (semeiology, syndromes) ; Nervous system as a whole ; Neurology ; Neuropsychological Tests ; Norway - epidemiology ; Organic mental disorders. Neuropsychology ; Proximity to disease onset ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; Retrospective Studies ; Trinucleotide Repeats - genetics</subject><ispartof>Journal of clinical and experimental neuropsychology, 2010-07, Vol.32 (6), p.590-598</ispartof><rights>Copyright 2009 Psychology Press, an imprint of the Taylor & Francis Group, an Informa business 2010</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c463t-f28aee8521a955fd6be7418f02062741321bb06e7c3fca951a725d08ecd8b05b3</citedby><cites>FETCH-LOGICAL-c463t-f28aee8521a955fd6be7418f02062741321bb06e7c3fca951a725d08ecd8b05b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23090697$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19916101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Walsem, Marleen R.</creatorcontrib><creatorcontrib>Sundet, Kjetil</creatorcontrib><creatorcontrib>Retterstøl, Lars</creatorcontrib><creatorcontrib>Sundseth, Øyvind</creatorcontrib><title>A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease</title><title>Journal of clinical and experimental neuropsychology</title><addtitle>J Clin Exp Neuropsychol</addtitle><description>Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclusion criteria for attaining a homogeneous sample. Results obtained by analyses of variance and effect size calculations indicate no clinical evidence of significant cognitive decline in asymptomatic HD carriers very far from onset of illness compared to noncarriers. Closeness to disease onset amongst gene carriers influenced cognition negatively whereas cytosine-adenine-guanine (CAG) repeat size did not. The findings call for longitudinal follow-up studies using a combination of clinical instruments and experimental paradigms to pinpoint when subtle cognitive deficits occur and within which of the cognitive domains.</description><subject>Adult</subject><subject>Adult and adolescent clinical studies</subject><subject>Analysis of Variance</subject><subject>Asymptomatic</subject><subject>Biological and medical sciences</subject><subject>Cognition</subject><subject>Cognition Disorders - diagnosis</subject><subject>Cognition Disorders - etiology</subject><subject>Cognition Disorders - genetics</subject><subject>Cohort Studies</subject><subject>Cytosine-adenine-guanine</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Double-Blind Method</subject><subject>Female</subject><subject>Humans</subject><subject>Huntington Disease - complications</subject><subject>Huntington Disease - genetics</subject><subject>Huntington's disease</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Nervous system as a whole</subject><subject>Neurology</subject><subject>Neuropsychological Tests</subject><subject>Norway - epidemiology</subject><subject>Organic mental disorders. Neuropsychology</subject><subject>Proximity to disease onset</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>Retrospective Studies</subject><subject>Trinucleotide Repeats - genetics</subject><issn>1380-3395</issn><issn>1744-411X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqFkUFrFTEUhYMotlZ_gBvJRroazZ3MTDLgphS1QtGNgrshk9w8I5nkmWTavn9vHu-piyLdJBfOd84lOYS8BPYGmGRvgUvG-cjGenIhhXxETkF0XdMBfH9c56o3FehPyLOcfzLGuBzbp-QExhEGYHBK1gtq4jp7pLN3wVC8UX5VxcVAo6U6boIr7gapQV11pC5QRT_HdIsbp0IFfsRU9qjKu2Vb4lK9mmqVksOU98LVGooLmxLDeabGZVQZn5MnVvmML473Gfn24f3Xy6vm-svHT5cX143uBl4a20qFKPsW1Nj31gwzig6kZS0b2jrxFuaZDSg0t7oioETbGyZRGzmzfuZn5PyQu03x14q5TIvLGr1XAeOaJyklAAcpHyQF50P94qGvJBxInWLOCe20TW5RaTcBm_a1TPdqqZ5Xx_R1XtD8cxx7qMDrI6CyVt4mFbTLf7mW17BhFJUTB84FG9OibmPyZipq52P6Y7q3fip3pTrfPejk_3_Bb4j2uvQ</recordid><startdate>20100707</startdate><enddate>20100707</enddate><creator>van Walsem, Marleen R.</creator><creator>Sundet, Kjetil</creator><creator>Retterstøl, Lars</creator><creator>Sundseth, Øyvind</creator><general>Taylor & Francis Group</general><general>Psychology Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100707</creationdate><title>A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease</title><author>van Walsem, Marleen R. ; Sundet, Kjetil ; Retterstøl, Lars ; Sundseth, Øyvind</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c463t-f28aee8521a955fd6be7418f02062741321bb06e7c3fca951a725d08ecd8b05b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Adult</topic><topic>Adult and adolescent clinical studies</topic><topic>Analysis of Variance</topic><topic>Asymptomatic</topic><topic>Biological and medical sciences</topic><topic>Cognition</topic><topic>Cognition Disorders - diagnosis</topic><topic>Cognition Disorders - etiology</topic><topic>Cognition Disorders - genetics</topic><topic>Cohort Studies</topic><topic>Cytosine-adenine-guanine</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</topic><topic>Double-Blind Method</topic><topic>Female</topic><topic>Humans</topic><topic>Huntington Disease - complications</topic><topic>Huntington Disease - genetics</topic><topic>Huntington's disease</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Nervous system as a whole</topic><topic>Neurology</topic><topic>Neuropsychological Tests</topic><topic>Norway - epidemiology</topic><topic>Organic mental disorders. Neuropsychology</topic><topic>Proximity to disease onset</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>Retrospective Studies</topic><topic>Trinucleotide Repeats - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Walsem, Marleen R.</creatorcontrib><creatorcontrib>Sundet, Kjetil</creatorcontrib><creatorcontrib>Retterstøl, Lars</creatorcontrib><creatorcontrib>Sundseth, Øyvind</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of clinical and experimental neuropsychology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Walsem, Marleen R.</au><au>Sundet, Kjetil</au><au>Retterstøl, Lars</au><au>Sundseth, Øyvind</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease</atitle><jtitle>Journal of clinical and experimental neuropsychology</jtitle><addtitle>J Clin Exp Neuropsychol</addtitle><date>2010-07-07</date><risdate>2010</risdate><volume>32</volume><issue>6</issue><spage>590</spage><epage>598</epage><pages>590-598</pages><issn>1380-3395</issn><eissn>1744-411X</eissn><abstract>Previous studies investigating subclinical signs of cognitive decline in presymptomatic carriers of Huntington's disease (HD) have shown conflicting results. The current study examines cognition in 105 at-risk individuals, using a broad neuropsychological test battery and adopting strict inclusion criteria for attaining a homogeneous sample. Results obtained by analyses of variance and effect size calculations indicate no clinical evidence of significant cognitive decline in asymptomatic HD carriers very far from onset of illness compared to noncarriers. Closeness to disease onset amongst gene carriers influenced cognition negatively whereas cytosine-adenine-guanine (CAG) repeat size did not. The findings call for longitudinal follow-up studies using a combination of clinical instruments and experimental paradigms to pinpoint when subtle cognitive deficits occur and within which of the cognitive domains.</abstract><cop>Hove</cop><pub>Taylor & Francis Group</pub><pmid>19916101</pmid><doi>10.1080/13803390903337878</doi><tpages>9</tpages></addata></record> |
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| ispartof | Journal of clinical and experimental neuropsychology, 2010-07, Vol.32 (6), p.590-598 |
| issn | 1380-3395 1744-411X |
| language | eng |
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| source | Taylor & Francis |
| subjects | Adult Adult and adolescent clinical studies Analysis of Variance Asymptomatic Biological and medical sciences Cognition Cognition Disorders - diagnosis Cognition Disorders - etiology Cognition Disorders - genetics Cohort Studies Cytosine-adenine-guanine Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Double-Blind Method Female Humans Huntington Disease - complications Huntington Disease - genetics Huntington's disease Male Medical sciences Middle Aged Nervous system (semeiology, syndromes) Nervous system as a whole Neurology Neuropsychological Tests Norway - epidemiology Organic mental disorders. Neuropsychology Proximity to disease onset Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry Retrospective Studies Trinucleotide Repeats - genetics |
| title | A double blind evaluation of cognitive decline in a Norwegian cohort of asymptomatic carriers of Huntington's disease |
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