Monoamine oxidase B polymorphism, cigarette smoking and risk of Parkinson's disease: A study in an Asian population
Identifieur interne : 000B80 ( Istex/Curation ); précédent : 000B79; suivant : 000B81Monoamine oxidase B polymorphism, cigarette smoking and risk of Parkinson's disease: A study in an Asian population
Auteurs : E Tan [Singapour] ; A Chai [Singapour] ; S Lum [Singapour] ; H Shen [Singapour] ; C Tan [Singapour] ; M Teoh [Singapour] ; Y Yih [Singapour] ; M Wong [Singapour] ; Y Zhao [Singapour]Source :
- American Journal of Medical Genetics Part B: Neuropsychiatric Genetics [ 1552-4841 ] ; 2003-07-01.
English descriptors
Abstract
Cigarette smoking is associated with reduced monoamine oxidase B (MAO B) activity. Polymorphisms of the MAO B gene may modify the relationship between smoking and Parkinson's Disease (PD). We examined the association of MAO B intron 13 G/A polymorphism and risk of PD, and the modulation of the polymorphism on smoking and PD in an Asian study population in Singapore. Two hundred and thirty PD patients (mean age 66.0 ± 9.4 years, 63% men) and 241 age, gender, and race matched controls (mean age 64 ± 9.2 years, 58.9% males) were studied. The frequency of G and A alleles in PD and controls was; 66/315 (21.0%) vs. 73/340 (21.5%) and 249/315 (79.0%) vs. 267/340 (78.5%). For women, the genotype frequency in PD and controls was; GG: 7/85 (8.2%) vs. 8/99 (8.1%); GA: 25/85 (29.4%) vs. 27/99 (27.3%); AA: 53/85 (62.4%) vs. 64/99 (64.6%). For men, allele frequency in PD and controls was; A: 118/145 (81.4%) vs. 112/142 (78.9%) and G: 27/145 (18.6%) vs. 30/142 (21.1%). The allele and genotype frequencies were not significantly different between young and late onset PD. The frequency of “ever” smokers in PD and controls was 31/230 (13.5%) vs. 52/241 (21.6%), P = 0.02. A stepwise logistic regression analysis did not reveal any interaction of smoking and the G allele and risk of PD. The MAO B G/A genotype frequency in our Asian population was quite different from Caucasians suggesting that ethnicity specific effects need to be considered in evaluating gene‐environmental interaction. © 2003 Wiley‐Liss, Inc.
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DOI: 10.1002/ajmg.b.20035
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oxidase B polymorphism, cigarette smoking and risk of Parkinson's disease: A study in an Asian population</title><author><name sortKey="Tan, E K" sort="Tan, E K" uniqKey="Tan E" first="E" last="Tan">E Tan</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, Singapore General Hospital, Singapore</mods:affiliation><country xml:lang="fr">Singapour</country><wicri:regionArea>Department of Neurology, Singapore General Hospital</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>National Neuroscience Institute, Singapore</mods:affiliation><country xml:lang="fr">Singapour</country><wicri:regionArea>National Neuroscience Institute</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>SingHealth, Singapore</mods:affiliation><country xml:lang="fr">Singapour</country><wicri:regionArea>SingHealth</wicri:regionArea></affiliation></author><author><name sortKey="Chai, A" sort="Chai, A" uniqKey="Chai A" first="A" 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Polymorphisms of the MAO B gene may modify the relationship between smoking and Parkinson's Disease (PD). We examined the association of MAO B intron 13 G/A polymorphism and risk of PD, and the modulation of the polymorphism on smoking and PD in an Asian study population in Singapore. Two hundred and thirty PD patients (mean age 66.0 ± 9.4 years, 63% men) and 241 age, gender, and race matched controls (mean age 64 ± 9.2 years, 58.9% males) were studied. The frequency of G and A alleles in PD and controls was; 66/315 (21.0%) vs. 73/340 (21.5%) and 249/315 (79.0%) vs. 267/340 (78.5%). For women, the genotype frequency in PD and controls was; GG: 7/85 (8.2%) vs. 8/99 (8.1%); GA: 25/85 (29.4%) vs. 27/99 (27.3%); AA: 53/85 (62.4%) vs. 64/99 (64.6%). For men, allele frequency in PD and controls was; A: 118/145 (81.4%) vs. 112/142 (78.9%) and G: 27/145 (18.6%) vs. 30/142 (21.1%). The allele and genotype frequencies were not significantly different between young and late onset PD. The frequency of “ever” smokers in PD and controls was 31/230 (13.5%) vs. 52/241 (21.6%), P = 0.02. A stepwise logistic regression analysis did not reveal any interaction of smoking and the G allele and risk of PD. The MAO B G/A genotype frequency in our Asian population was quite different from Caucasians suggesting that ethnicity specific effects need to be considered in evaluating gene‐environmental interaction. © 2003 Wiley‐Liss, Inc.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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