Association of the MscI polymorphism of the dopamine D3 receptor gene with tardive dyskinesia in schizophrenia

被引:132
作者
Basile, VS
Masellis, M
Badri, F
Paterson, AD
Meltzer, HY
Lieberman, JA
Potkin, SG
Macciardi, F
Kennedy, JL
机构
[1] Univ Toronto, Clarke Inst Psychiat, Neurogenet Sect, Toronto, ON M5T 1R8, Canada
[2] Vanderbilt Univ, Dept Psychiat, Nashville, TN USA
[3] Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA
[4] Univ Calif Irvine, Dept Psychiat, Irvine, CA 92717 USA
[5] Osped San Raffaele, Inst Sci, Dept Neuropsychiat, Milan, Italy
基金
英国医学研究理事会;
关键词
tardive dyskinesia; pharmacogenetics; neuroleptics; receptor binding; dopamine; genetic association; extrapyramidal side effects; risk factor; DRD3;
D O I
10.1016/S0893-133X(98)00114-6
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In 112 schizophrenic patients previously treated with typical neuroleptics, we investigated the putative role of the dopamine D3 receptor gene (DADS) in tardive dyskinesia (TD). Patients were assessed for TD severity using the Abnormal Involuntary Movement Scale (AIMS) and were subsequently genotyped the Mscl polymorphism that identifies a serine to glycine substitution in DRD3. A modified analysis of covariance model, which incorporated several clinical risk factors for TD, was utilized to detect differences in TD severity among the various genotypic groups. The glycine allele of DRD3 was found to be associated with typical neuroeleptic-induced TD (F[2,95] = 8.25, p < .0005). Higher mean AIMS scores were found in patients homozygous for the glycine variant of the DRD3 gene, as compared to both heterozygous and serine homozygous patients. Although replication is necessary, this finding supports a role for the dopamine D3 receptor in the pathogenesis of TD. (C) 1999 American College of Neuropsychopharmacology. Published by Elsevier Science Inc.
引用
收藏
页码:17 / 27
页数:11
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