Genotype and smoking history affect risk of levodopa‐induced dyskinesias in Parkinson's disease
Identifieur interne : 001194 ( Istex/Curation ); précédent : 001193; suivant : 001195Genotype 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.
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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
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DOI: 10.1002/mds.20785
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Revilla</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Sahay, Alok" sort="Sahay, Alok" uniqKey="Sahay A" first="Alok" last="Sahay">Alok Sahay</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Samaha, Frederick J" sort="Samaha, Frederick J" uniqKey="Samaha F" first="Frederick J." last="Samaha">Frederick J. Samaha</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Welge, Jeffrey A" sort="Welge, Jeffrey A" uniqKey="Welge J" first="Jeffrey A." last="Welge">Jeffrey A. Welge</name><affiliation wicri:level="1"><mods:affiliation>Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Psychiatry, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Gong, Jianhua" sort="Gong, Jianhua" uniqKey="Gong J" first="Jianhua" last="Gong">Jianhua Gong</name><affiliation wicri:level="1"><mods:affiliation>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Current Address: Food Research Program, Agriculture and Agri‐Food Canada, Guelph, Ontario, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Current Address: Food Research Program, Agriculture and Agri‐Food Canada, Guelph, Ontario</wicri:regionArea></affiliation></author><author><name sortKey="Gartner, Maureen" sort="Gartner, Maureen" uniqKey="Gartner M" first="Maureen" last="Gartner">Maureen Gartner</name><affiliation wicri:level="1"><mods:affiliation>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Yue, Xia" sort="Yue, Xia" uniqKey="Yue X" first="Xia" last="Yue">Xia Yue</name><affiliation wicri:level="1"><mods:affiliation>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation></author><author><name sortKey="Yu, Lei" sort="Yu, Lei" uniqKey="Yu L" first="Lei" last="Yu">Lei Yu</name><affiliation wicri:level="1"><mods:affiliation>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA</mods:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Cell Biology, Neurobiology, and Anatomy, University of Cincinnati College of Medicine, Cincinnati, Ohio</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>Current Address: Department of Zoology, University of Guelph, Guelph, Ontario, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Current Address: Department of Zoology, University of Guelph, Guelph, Ontario</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</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="2006-05">2006-05</date><biblScope unit="vol">21</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="654">654</biblScope><biblScope unit="page" to="659">659</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">975D26BF86995D19483745B7CE4BD0C660AAF62A</idno><idno type="DOI">10.1002/mds.20785</idno><idno type="ArticleID">MDS20785</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>A118G</term><term>dopamine D2 receptor</term><term>dyskinesia</term><term>levodopa</term><term>mu opioid receptor</term><term>smoking</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><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></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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