Genotype and smoking history affect risk of levodopa‐induced dyskinesias in Parkinson's disease
Identifieur interne : 003422 ( Main/Exploration ); précédent : 003421; suivant : 003423Genotype and smoking history affect risk of levodopa‐induced dyskinesias in Parkinson's disease
Auteurs : Judith A. Strong [États-Unis] ; Arif Dalvi [États-Unis] ; Fredy J. Revilla [États-Unis] ; Alok Sahay [États-Unis] ; Frederick J. Samaha [États-Unis] ; Jeffrey A. Welge [États-Unis] ; Jianhua Gong [États-Unis, Canada] ; Maureen Gartner [États-Unis] ; Xia Yue [États-Unis] ; Lei Yu [États-Unis, Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-05.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Tabagisme.
English descriptors
- KwdEn :
- A118G, Adult, Aged, Aged, 80 and over, Antiparkinson Agents (adverse effects), D2 Dopamine receptor, Dyskinesia, Dyskinesia, Drug-Induced (etiology), Dyskinesia, Drug-Induced (genetics), Female, Follow-Up Studies, Genotype, Humans, Levodopa, Levodopa (adverse effects), Male, Middle Aged, Nervous system diseases, Opioid receptor, Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson disease, Polymorphism, Genetic, Receptors, Dopamine (genetics), Receptors, Opioid, mu (genetics), Risk, Risk factor, Smoking, Tobacco smoking, dopamine D2 receptor, dyskinesia, levodopa, mu opioid receptor, smoking.
- MESH :
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- drug therapy : Parkinson Disease.
- etiology : Dyskinesia, Drug-Induced.
- genetics : Dyskinesia, Drug-Induced, Parkinson Disease, Receptors, Dopamine, Receptors, Opioid, mu.
- Adult, Aged, Aged, 80 and over, Female, Follow-Up Studies, Genotype, Humans, Male, Middle Aged, Polymorphism, Genetic, Risk, Smoking.
Abstract
Parkinson's disease (PD) patients vary widely in their response to levodopa treatment, and this variation may be partially genetic in origin. We determined whether particular dopamine and opioid receptor polymorphisms were associated with risk of earlier onset of dyskinesia side effects during levodopa therapy. Smoking status was also examined. The 92 subjects were recruited from the movement disorders clinic of a neurology practice associated with a medical school. All were adult‐onset PD patients who had been taking levodopa at least 5 years and/or had developed levodopa‐induced dyskinesia. Carrying the G‐allele of the A118G single nucleotide coding region polymorphism of the mu opioid receptor, as well as a history of never smoking, were independently associated with increased risk of earlier onset of dyskinesia (P = 0.05 and 0.02, respectively). One genotype of the D2 dopamine receptor intronic dinucleotide repeat polymorphism (14 repeats/15 repeats, with frequency of 6%) was also associated with earlier dyskinesia (P = 0.003). History of smoking has previously been associated with reduced risk of developing PD. Our results suggest that smoking history may also influence the response to levodopa, with contribution comparable to those of individual genes including the mu opioid receptor and D2 dopamine receptor. © 2006 Movement Disorder Society
Url:
DOI: 10.1002/mds.20785
Affiliations:
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Le document en format XML
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<wicri:regionArea>Current Address: Department of Zoology, University of Guelph, Guelph, Ontario</wicri:regionArea>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A118G</term>
<term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Antiparkinson Agents (adverse effects)</term>
<term>D2 Dopamine receptor</term>
<term>Dyskinesia</term>
<term>Dyskinesia, Drug-Induced (etiology)</term>
<term>Dyskinesia, Drug-Induced (genetics)</term>
<term>Female</term>
<term>Follow-Up Studies</term>
<term>Genotype</term>
<term>Humans</term>
<term>Levodopa</term>
<term>Levodopa (adverse effects)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Nervous system diseases</term>
<term>Opioid receptor</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson disease</term>
<term>Polymorphism, Genetic</term>
<term>Receptors, Dopamine (genetics)</term>
<term>Receptors, Opioid, mu (genetics)</term>
<term>Risk</term>
<term>Risk factor</term>
<term>Smoking</term>
<term>Tobacco smoking</term>
<term>dopamine D2 receptor</term>
<term>dyskinesia</term>
<term>levodopa</term>
<term>mu opioid receptor</term>
<term>smoking</term>
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<keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Dyskinesia, Drug-Induced</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dyskinesia, Drug-Induced</term>
<term>Parkinson Disease</term>
<term>Receptors, Dopamine</term>
<term>Receptors, Opioid, mu</term>
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<keywords scheme="MESH" xml:lang="en"><term>Adult</term>
<term>Aged</term>
<term>Aged, 80 and over</term>
<term>Female</term>
<term>Follow-Up Studies</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Polymorphism, Genetic</term>
<term>Risk</term>
<term>Smoking</term>
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<term>Facteur risque</term>
<term>Génotype</term>
<term>Lévodopa</term>
<term>Parkinson maladie</term>
<term>Récepteur dopaminergique D2</term>
<term>Récepteur opiacé</term>
<term>Système nerveux pathologie</term>
<term>Tabagisme</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) patients vary widely in their response to levodopa treatment, and this variation may be partially genetic in origin. We determined whether particular dopamine and opioid receptor polymorphisms were associated with risk of earlier onset of dyskinesia side effects during levodopa therapy. Smoking status was also examined. The 92 subjects were recruited from the movement disorders clinic of a neurology practice associated with a medical school. All were adult‐onset PD patients who had been taking levodopa at least 5 years and/or had developed levodopa‐induced dyskinesia. Carrying the G‐allele of the A118G single nucleotide coding region polymorphism of the mu opioid receptor, as well as a history of never smoking, were independently associated with increased risk of earlier onset of dyskinesia (P = 0.05 and 0.02, respectively). One genotype of the D2 dopamine receptor intronic dinucleotide repeat polymorphism (14 repeats/15 repeats, with frequency of 6%) was also associated with earlier dyskinesia (P = 0.003). History of smoking has previously been associated with reduced risk of developing PD. Our results suggest that smoking history may also influence the response to levodopa, with contribution comparable to those of individual genes including the mu opioid receptor and D2 dopamine receptor. © 2006 Movement Disorder Society</div>
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