Centre for Addiction and Mental Health, University of Toronto, Toronto, Ontario, Canada.
Int Clin Psychopharmacol. 2010 Sep;25(5):264-9. doi: 10.1097/YIC.0b013e32833a5ff9.
Phosphodiesterase 4B (PDE4B) has been evaluated as a genetic risk factor for schizophrenia. Selective PDE4 inhibitor drugs have antipsychotic-like effects and reduce tardive dyskinesia-like movements in animal models. We investigated whether PDE4B genetic variants are associated with antipsychotic-induced tardive dyskinesia incidence and severity in schizophrenia patients. Our sample consisted of 169 Caucasian patients taking typical antipsychotic medication for at least 1 year. We found two PDE4B gene variants to be nominally associated with tardive dyskinesia (rs1338719 and rs7528545) in the overall population and two other variants nominally associated with the presence of tardive dyskinesia and severity in female patients (rs1890196 and rs783036). None of these results survived correction for multiple testing. Overall, our results do not support a genetic association between tardive dyskinesia and PDE4B.
磷酸二酯酶 4B（PDE4B）已被评估为精神分裂症的遗传风险因素。选择性 PDE4 抑制剂药物具有抗精神病样作用，并减少动物模型中的迟发性运动障碍样运动。我们研究了 PDE4B 遗传变异是否与精神分裂症患者抗精神病药引起的迟发性运动障碍的发生率和严重程度有关。我们的样本包括 169 名服用典型抗精神病药物至少 1 年的白种人患者。我们发现两个 PDE4B 基因变异在总体人群中与迟发性运动障碍呈名义相关（rs1338719 和 rs7528545），另外两个变异在女性患者中与迟发性运动障碍的存在和严重程度呈名义相关（rs1890196 和 rs783036）。这些结果均未通过多重检验校正。总体而言，我们的结果不支持迟发性运动障碍与 PDE4B 之间存在遗传关联。
