CYP2D6 polymorphism, pesticide exposure, and Parkinson's disease.
Identifieur interne : 001029 ( PubMed/Corpus ); précédent : 001028; suivant : 001030CYP2D6 polymorphism, pesticide exposure, and Parkinson's disease.
Auteurs : Alexis Elbaz ; Clotilde Levecque ; Jacqueline Clavel ; Jean-Sébastien Vidal ; Florence Richard ; Philippe Amouyel ; Annick Alpérovitch ; Marie-Christine Chartier-Harlin ; Christophe TzourioSource :
- Annals of neurology [ 0364-5134 ] ; 2004.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Case-Control Studies, Cross-Sectional Studies, Cytochrome P-450 CYP2D6 (genetics), Environmental Exposure, Female, Gene Frequency, Genetic Predisposition to Disease (genetics), Humans, Male, Middle Aged, Occupational Exposure (statistics & numerical data), Parkinson Disease (epidemiology), Parkinson Disease (etiology), Parkinson Disease (genetics), Pesticides (poisoning), Polymerase Chain Reaction (methods), Polymorphism, Genetic, Prevalence.
- MESH :
- chemical , genetics : Cytochrome P-450 CYP2D6.
- epidemiology : Parkinson Disease.
- etiology : Parkinson Disease.
- genetics : Genetic Predisposition to Disease, Parkinson Disease.
- methods : Polymerase Chain Reaction.
- chemical , poisoning : Pesticides.
- statistics & numerical data : Occupational Exposure.
- Adolescent, Adult, Aged, Case-Control Studies, Cross-Sectional Studies, Environmental Exposure, Female, Gene Frequency, Humans, Male, Middle Aged, Polymorphism, Genetic, Prevalence.
Abstract
We performed a case-control study of Parkinson's disease (PD) in a population characterized by a high prevalence of pesticide exposure and studied the joint effect of pesticide exposure and CYP2D6. Although they are based on a small group of subjects with the joint exposure, our findings are consistent with a gene-environment interaction disease model according to which (1) pesticides have a modest effect in subjects who are not CYP2D6 poor metabolizers, (2) pesticides' effect is increased in poor metabolizers (approximately twofold), and (3) poor metabolizers are not at increased PD risk in the absence of pesticide exposure.
DOI: 10.1002/ana.20051
PubMed: 14991823
Links to Exploration step
pubmed:14991823Le document en format XML
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<author><name sortKey="Chartier Harlin, Marie Christine" sort="Chartier Harlin, Marie Christine" uniqKey="Chartier Harlin M" first="Marie-Christine" last="Chartier-Harlin">Marie-Christine Chartier-Harlin</name>
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<term>Cross-Sectional Studies</term>
<term>Cytochrome P-450 CYP2D6 (genetics)</term>
<term>Environmental Exposure</term>
<term>Female</term>
<term>Gene Frequency</term>
<term>Genetic Predisposition to Disease (genetics)</term>
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<term>Middle Aged</term>
<term>Occupational Exposure (statistics & numerical data)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Parkinson Disease (etiology)</term>
<term>Parkinson Disease (genetics)</term>
<term>Pesticides (poisoning)</term>
<term>Polymerase Chain Reaction (methods)</term>
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<term>Polymorphism, Genetic</term>
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<front><div type="abstract" xml:lang="en">We performed a case-control study of Parkinson's disease (PD) in a population characterized by a high prevalence of pesticide exposure and studied the joint effect of pesticide exposure and CYP2D6. Although they are based on a small group of subjects with the joint exposure, our findings are consistent with a gene-environment interaction disease model according to which (1) pesticides have a modest effect in subjects who are not CYP2D6 poor metabolizers, (2) pesticides' effect is increased in poor metabolizers (approximately twofold), and (3) poor metabolizers are not at increased PD risk in the absence of pesticide exposure.</div>
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