Basile V S, Masellis M, Badri F, Paterson A D, Meltzer H Y, Lieberman J A, Potkin S G, Macciardi F, Kennedy J L
Neurogenetics Section, Clarke Institute of Psychiatry, University of Toronto, Canada.
Neuropsychopharmacology. 1999 Jul;21(1):17-27. doi: 10.1016/S0893-133X(98)00114-6.
In 112 schizophrenic patients previously treated with typical neuroleptics, we investigated the putative role of the dopamine D3 receptor gene (DRD3) in tardive dyskinesia (TD). Patients were assessed for TD severity using the Abnormal Involuntary Movement Scale (AIMS) and were subsequently genotyped for the MscI 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 neuroleptic-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.
在112例先前接受过传统抗精神病药物治疗的精神分裂症患者中，我们研究了多巴胺D3受体基因（DRD3）在迟发性运动障碍（TD）中的假定作用。使用异常不自主运动量表（AIMS）评估患者的TD严重程度，随后对DRD3中识别丝氨酸到甘氨酸替代的MscI多态性进行基因分型。采用纳入了TD多个临床风险因素的修正协方差分析模型，来检测不同基因型组之间TD严重程度的差异。发现DRD3的甘氨酸等位基因与传统抗精神病药物诱发的TD相关（F[2,95] = 8.25，p <.0005）。与杂合子和丝氨酸纯合子患者相比，DRD3基因甘氨酸变体纯合子患者的平均AIMS评分更高。尽管需要重复验证，但这一发现支持多巴胺D3受体在TD发病机制中起作用。
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