Rietschel M, Krauss H, Müller D J, Schulze T G, Knapp M, Marwinski K, Maroldt A O, Paus S, Grünhage F, Propping P, Maier W, Held T, Nöthen M M
Department of Psychiatry, University of Bonn, Germany.
Eur Arch Psychiatry Clin Neurosci. 2000;250(1):31-5. doi: 10.1007/pl00007536.
In the search for genetic factors contributing to tardive dyskinesia, dopamine receptor genes are considered major candidates. The dopamine D3 receptor is of primary interest as dopamine D3 receptor knock-out mice show locomotor hyperactivation resembling extrapyramidal side-effects of neuroleptic treatment. Furthermore, Steen and colleagues (1997) recently reported an association between tardive dyskinesia and a dopamine D3 receptor gene variant. In the present study we tried to replicate this finding. We investigated 157 patients with schizophrenia or schizoaffective disorder receiving long-term neuroleptic medication who never or persistently displayed tardive dyskinesia. As advanced age is a main risk factor for tardive dyskinesia, we also compared older patients with a long duration of schizophrenia not displaying tardive dyskinesia to younger patients with a shorter duration of the illness displaying tardive dyskinesia. However, we found no evidence that the dopamine D3 receptor gene is likely to confer susceptibility to the development of tardive dyskinesia.
在寻找导致迟发性运动障碍的遗传因素时，多巴胺受体基因被视为主要候选基因。多巴胺D3受体备受关注，因为多巴胺D3受体基因敲除小鼠表现出运动亢进，类似于抗精神病药物治疗的锥体外系副作用。此外，斯汀及其同事（1997年）最近报告了迟发性运动障碍与一种多巴胺D3受体基因变体之间的关联。在本研究中，我们试图重复这一发现。我们调查了157例接受长期抗精神病药物治疗的精神分裂症或分裂情感性障碍患者，这些患者从未或持续表现出迟发性运动障碍。由于高龄是迟发性运动障碍的主要危险因素，我们还将未表现出迟发性运动障碍的病程较长的老年精神分裂症患者与病程较短但表现出迟发性运动障碍的年轻患者进行了比较。然而，我们没有发现证据表明多巴胺D3受体基因可能会使人易患迟发性运动障碍。
