Genotype and smoking history affect risk of levodopa-induced dyskinesias in Parkinson's disease

被引:62
作者
Strong, Judith A.
Dalvi, Arif
Revilla, Fredy J.
Sahay, Alok
Samaha, Frederick J.
Welge, Jeffrey A.
Gong, Jianhua
Gartner, Maureen
Yue, Xia
Yu, Lei
机构
[1] Univ Cincinnati, Coll Med, Dept Cell Biol Neurobiol & Anat, Cincinnati, OH USA
[2] Univ Cincinnati, Coll Med, Dept Neurol, Cincinnati, OH USA
[3] Univ Cincinnati, Coll Med, Dept Psychiat, Cincinnati, OH USA
关键词
mu opioid receptor; dopamine D2 receptor; dyskinesia; levodopa; smoking; A118G;
D O I
10.1002/mds.20785
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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, l 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. (C) 2006 Movement Disorder Society.
引用
收藏
页码:654 / 659
页数:6
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