MovDisordV3, Main, Exploration, bibRecord, 001E78

A retrospective study of the impact of lifestyle on age at onset of Huntington disease

Identifieur interne : 001E78 ( Main/Exploration ); précédent : 001E77; suivant : 001E79

A 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.

RBID : ISTEX:E123B3CB8590D9B7A4133C930AEF8838D0C83AC2

Descripteurs français

Pascal (Inist)
- Age apparition, Chorée de Huntington, Pathologie du système nerveux, Rétrospective.
Wicri :
- geographic : Nouvelle-Zélande.

English descriptors

KwdEn :
- Adult, Age of Onset, 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), Nervous system diseases, New Zealand (epidemiology), Nuclear Proteins (genetics), Retrospective, 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:

https://api.istex.fr/document/E123B3CB8590D9B7A4133C930AEF8838D0C83AC2/fulltext/pdf

DOI: 10.1002/mds.23108

Affiliations:

Australie, Nouvelle-Zélande

Le document en format XML

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<term>Age of Onset</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>Huntington disease</term>
<term>Life Style</term>
<term>Linear Models</term>
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<term>Middle Aged</term>
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<term>Nervous system diseases</term>
<term>New Zealand (epidemiology)</term>
<term>Nuclear Proteins (genetics)</term>
<term>Retrospective</term>
<term>Retrospective Studies</term>
<term>Statistics as Topic</term>
<term>Trinucleotide Repeat Expansion (genetics)</term>
<term>Young Adult</term>
<term>age‐at‐onset</term>
<term>environmental modifiers</term>
<term>lifestyle</term>
<term>passivity</term>
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<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>
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<term>Chorée de Huntington</term>
<term>Pathologie du   système nerveux</term>
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<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>
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<name sortKey="Churchyard, Andrew" sort="Churchyard, Andrew" uniqKey="Churchyard A" first="Andrew" last="Churchyard">Andrew Churchyard</name>
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Movement Disorders (revue)

A retrospective study of the impact of lifestyle on age at onset of Huntington disease

A retrospective study of the impact of lifestyle on age at onset of Huntington disease

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

	Movement Disorders (revue)
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