A retrospective study of the impact of lifestyle on age at onset of Huntington disease
Identifieur interne : 002314 ( Main/Merge ); précédent : 002313; suivant : 002315A retrospective study of the impact of lifestyle on age at onset of Huntington disease
Auteurs : M. Kaye Trembath [Australie] ; Zoë A. Horton [Australie] ; Lynette Tippett [Nouvelle-Zélande] ; Virginia Hogg [Nouvelle-Zélande] ; Veronica R. Collins [Australie] ; Andrew Churchyard [Australie] ; Dennis Velakoulis [Australie] ; Richard Roxburgh [Nouvelle-Zélande] ; Martin B. Delatycki [Australie]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-07-30.
Descripteurs français
- Wicri :
- geographic : Nouvelle-Zélande.
English descriptors
- KwdEn :
- Adult, Age of Onset, Aged, Cohort Studies, Female, Humans, Huntington Disease (epidemiology), Huntington Disease (genetics), Huntington Disease (psychology), Huntington disease, Life Style, Linear Models, Male, Middle Aged, Nerve Tissue Proteins (genetics), New Zealand (epidemiology), Nuclear Proteins (genetics), Retrospective Studies, Statistics as Topic, Trinucleotide Repeat Expansion (genetics), Young Adult, age‐at‐onset, environmental modifiers, lifestyle, passivity.
- MESH :
- chemical , genetics : Nerve Tissue Proteins, Nuclear Proteins.
- geographic , epidemiology : New Zealand.
- epidemiology : Huntington Disease.
- genetics : Huntington Disease, Trinucleotide Repeat Expansion.
- psychology : Huntington Disease.
- Adult, Age of Onset, Aged, Cohort Studies, Female, Humans, Life Style, Linear Models, Male, Middle Aged, Retrospective Studies, Statistics as Topic, Young Adult.
Abstract
In transgenic mouse models of Huntington disease (HD) environmental enrichment significantly delays disease onset. A questionnaire‐based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age‐at‐onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = −0.72, P < 0.001), but also with a lifestyle that included higher levels of passive activity (r = −0.38, P < 0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R2 = 0.54, b = −0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3–7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R2 = 0.12, b = 1.08, P < 0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23108
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A questionnaire‐based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age‐at‐onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = −0.72, P < 0.001), but also with a lifestyle that included higher levels of passive activity (r = −0.38, P < 0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R2 = 0.54, b = −0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3–7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R2 = 0.12, b = 1.08, P < 0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. © 2010 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.23108"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">A retrospective study of the impact of lifestyle on age at onset of Huntington disease</title><author><name sortKey="Trembath, M Kaye" sort="Trembath, M Kaye" uniqKey="Trembath M" first="M. Kaye" last="Trembath">M. Kaye Trembath</name></author><author><name sortKey="Horton, Zoe A" sort="Horton, Zoe A" uniqKey="Horton Z" first="Zoë A." last="Horton">Zoë A. Horton</name></author><author><name sortKey="Tippett, Lynette" sort="Tippett, Lynette" uniqKey="Tippett L" first="Lynette" last="Tippett">Lynette Tippett</name></author><author><name sortKey="Hogg, Virginia" sort="Hogg, Virginia" uniqKey="Hogg V" first="Virginia" last="Hogg">Virginia Hogg</name></author><author><name sortKey="Collins, Veronica R" sort="Collins, Veronica R" uniqKey="Collins V" first="Veronica R." last="Collins">Veronica R. Collins</name></author><author><name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name></author><author><name sortKey="Velakoulis, Dennis" sort="Velakoulis, Dennis" uniqKey="Velakoulis D" first="Dennis" last="Velakoulis">Dennis Velakoulis</name></author><author><name sortKey="Roxburgh, Richard" sort="Roxburgh, Richard" uniqKey="Roxburgh R" first="Richard" last="Roxburgh">Richard Roxburgh</name></author><author><name sortKey="Delatycki, Martin B" sort="Delatycki, Martin B" uniqKey="Delatycki M" first="Martin B." last="Delatycki">Martin B. 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Kaye Trembath</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Horton, Zoe A" sort="Horton, Zoe A" uniqKey="Horton Z" first="Zoë A." last="Horton">Zoë A. Horton</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Tippett, Lynette" sort="Tippett, Lynette" uniqKey="Tippett L" first="Lynette" last="Tippett">Lynette Tippett</name><affiliation wicri:level="1"><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Psychology, The University of Auckland, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="Hogg, Virginia" sort="Hogg, Virginia" uniqKey="Hogg V" first="Virginia" last="Hogg">Virginia Hogg</name><affiliation wicri:level="1"><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Psychology, The University of Auckland, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="Collins, Veronica R" sort="Collins, Veronica R" uniqKey="Collins V" first="Veronica R." last="Collins">Veronica R. Collins</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Huntington Service, Calvary Healthcare Bethlehem, Caulfield, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Velakoulis, Dennis" sort="Velakoulis, Dennis" uniqKey="Velakoulis D" first="Dennis" last="Velakoulis">Dennis Velakoulis</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Neuropsychiatry Unit, Royal Melbourne Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Roxburgh, Richard" sort="Roxburgh, Richard" uniqKey="Roxburgh R" first="Richard" last="Roxburgh">Richard Roxburgh</name><affiliation wicri:level="1"><country xml:lang="fr">Nouvelle-Zélande</country><wicri:regionArea>Department of Neurology, Auckland City Hospital, Auckland</wicri:regionArea><wicri:noRegion>Auckland</wicri:noRegion></affiliation></author><author><name sortKey="Delatycki, Martin B" sort="Delatycki, Martin B" uniqKey="Delatycki M" first="Martin B." last="Delatycki">Martin B. Delatycki</name><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Clinical Genetics, Austin Health, Heidelberg, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Paediatrics, University of Melbourne, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-07-30">2010-07-30</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">10</biblScope><biblScope unit="page" from="1444">1444</biblScope><biblScope unit="page" to="1450">1450</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">E123B3CB8590D9B7A4133C930AEF8838D0C83AC2</idno><idno type="DOI">10.1002/mds.23108</idno><idno type="ArticleID">MDS23108</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Huntington disease</term><term>age‐at‐onset</term><term>environmental modifiers</term><term>lifestyle</term><term>passivity</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In transgenic mouse models of Huntington disease (HD) environmental enrichment significantly delays disease onset. A questionnaire‐based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age‐at‐onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = −0.72, P < 0.001), but also with a lifestyle that included higher levels of passive activity (r = −0.38, P < 0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R2 = 0.54, b = −0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3–7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R2 = 0.12, b = 1.08, P < 0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. © 2010 Movement Disorder Society</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A retrospective study of the impact of lifestyle on age at onset of Huntington disease.</title><author><name sortKey="Trembath, M Kaye" sort="Trembath, M Kaye" uniqKey="Trembath M" first="M Kaye" last="Trembath">M Kaye Trembath</name><affiliation wicri:level="1"><nlm:affiliation>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Horton, Zoe A" sort="Horton, Zoe A" uniqKey="Horton Z" first="Zoë A" last="Horton">Zoë A. Horton</name></author><author><name sortKey="Tippett, Lynette" sort="Tippett, Lynette" uniqKey="Tippett L" first="Lynette" last="Tippett">Lynette Tippett</name></author><author><name sortKey="Hogg, Virginia" sort="Hogg, Virginia" uniqKey="Hogg V" first="Virginia" last="Hogg">Virginia Hogg</name></author><author><name sortKey="Collins, Veronica R" sort="Collins, Veronica R" uniqKey="Collins V" first="Veronica R" last="Collins">Veronica R. Collins</name></author><author><name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name></author><author><name sortKey="Velakoulis, Dennis" sort="Velakoulis, Dennis" uniqKey="Velakoulis D" first="Dennis" last="Velakoulis">Dennis Velakoulis</name></author><author><name sortKey="Roxburgh, Richard" sort="Roxburgh, Richard" uniqKey="Roxburgh R" first="Richard" last="Roxburgh">Richard Roxburgh</name></author><author><name sortKey="Delatycki, Martin B" sort="Delatycki, Martin B" uniqKey="Delatycki M" first="Martin B" last="Delatycki">Martin B. Delatycki</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.23108</idno><idno type="RBID">pubmed:20629137</idno><idno type="pmid">20629137</idno><idno type="wicri:Area/PubMed/Corpus">001742</idno><idno type="wicri:Area/PubMed/Curation">001742</idno><idno type="wicri:Area/PubMed/Checkpoint">001A69</idno><idno type="wicri:Area/Ncbi/Merge">002C75</idno><idno type="wicri:Area/Ncbi/Curation">002C75</idno><idno type="wicri:Area/Ncbi/Checkpoint">002C75</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">A retrospective study of the impact of lifestyle on age at onset of Huntington disease.</title><author><name sortKey="Trembath, M Kaye" sort="Trembath, M Kaye" uniqKey="Trembath M" first="M Kaye" last="Trembath">M Kaye Trembath</name><affiliation wicri:level="1"><nlm:affiliation>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Bruce Lefroy Centre for Genetic Health Research, Murdoch Childrens Research Institute, Royal Children's Hospital, Parkville, Victoria</wicri:regionArea><wicri:noRegion>Victoria</wicri:noRegion></affiliation></author><author><name sortKey="Horton, Zoe A" sort="Horton, Zoe A" uniqKey="Horton Z" first="Zoë A" last="Horton">Zoë A. Horton</name></author><author><name sortKey="Tippett, Lynette" sort="Tippett, Lynette" uniqKey="Tippett L" first="Lynette" last="Tippett">Lynette Tippett</name></author><author><name sortKey="Hogg, Virginia" sort="Hogg, Virginia" uniqKey="Hogg V" first="Virginia" last="Hogg">Virginia Hogg</name></author><author><name sortKey="Collins, Veronica R" sort="Collins, Veronica R" uniqKey="Collins V" first="Veronica R" last="Collins">Veronica R. Collins</name></author><author><name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name></author><author><name sortKey="Velakoulis, Dennis" sort="Velakoulis, Dennis" uniqKey="Velakoulis D" first="Dennis" last="Velakoulis">Dennis Velakoulis</name></author><author><name sortKey="Roxburgh, Richard" sort="Roxburgh, Richard" uniqKey="Roxburgh R" first="Richard" last="Roxburgh">Richard Roxburgh</name></author><author><name sortKey="Delatycki, Martin B" sort="Delatycki, Martin B" uniqKey="Delatycki M" first="Martin B" last="Delatycki">Martin B. Delatycki</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>Aged</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Huntington Disease (epidemiology)</term><term>Huntington Disease (genetics)</term><term>Huntington Disease (psychology)</term><term>Life Style</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Nerve Tissue Proteins (genetics)</term><term>New Zealand (epidemiology)</term><term>Nuclear Proteins (genetics)</term><term>Retrospective Studies</term><term>Statistics as Topic</term><term>Trinucleotide Repeat Expansion (genetics)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Nerve Tissue Proteins</term><term>Nuclear Proteins</term></keywords><keywords scheme="MESH" type="geographic" qualifier="epidemiology" xml:lang="en"><term>New Zealand</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Huntington Disease</term><term>Trinucleotide Repeat Expansion</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Huntington Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Age of Onset</term><term>Aged</term><term>Cohort Studies</term><term>Female</term><term>Humans</term><term>Life Style</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Retrospective Studies</term><term>Statistics as Topic</term><term>Young Adult</term></keywords><keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>Nouvelle-Zélande</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In transgenic mouse models of Huntington disease (HD) environmental enrichment significantly delays disease onset. A questionnaire-based survey of 154 adults with diagnosed HD (mean 4.2 years postdiagnosis) and a known IT15 CAG repeat length, explored whether premorbid lifestyle may relate to age-at-onset (AO). Participants were drawn from HD outpatient clinics in Australia and New Zealand. Premorbid physical, intellectual, and passive activity levels were used to generate scores in the categories of leisure, nonleisure (education, occupation and domestic duties) and total lifestyle. AO was associated with increased CAG repeat length as expected (r = -0.72, P < 0.001), but also with a lifestyle that included higher levels of passive activity (r = -0.38, P < 0.001). Multiple linear regression modeling showed lifestyle passivity to be a variable independent of CAG repeat length in predicting AO (R(2) = 0.54, b = -0.22, P = 0.005). Comparison of the mean AO across tertiles of lifestyle passivity scores showed onset 4.6 years (95% CI = 1.3-7.9) later in the least compared with the most passive tertile. CAG repeat length was also shown to predict lifestyle passivity (R(2) = 0.12, b = 1.08, P < 0.0005). Neither intellectual nor physical activity showed significant relationships to AO or CAG repeat length in this cohort. Our study leads to two conclusions: that a passive lifestyle may be a preclinical expression of HD, and that it actually contributes to the earlier onset of symptoms. Overcoming the tendency to be passive may substantially delay onset of HD. (c) 2010 Movement Disorder Society.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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