The Zucker Hillside Hospital, Psychiatry Research, North Shore - Long Island Jewish Health System, Glen Oaks, NY, USA; Department of Neuropsychiatry, Fukushima Medical University School of Medicine, Fukushima, Japan.
The Zucker Hillside Hospital, Psychiatry Research, North Shore - Long Island Jewish Health System, Glen Oaks, NY, USA; Hofstra North Shore LIJ School of Medicine, Hempstead, NY, USA; The Feinstein Institute for Medical Research, Manhasset, NY, USA.
Schizophr Res. 2014 Feb;152(2-3):365-72. doi: 10.1016/j.schres.2013.12.011. Epub 2014 Jan 7.
Tardive dyskinesia (TD) is a serious long-term consequence of antipsychotic treatment. Since brain-derived neurotrophic factor (BDNF) has potent neurotrophic activity, genetic alterations in the BDNF gene may affect antipsychotic-induced TD.
Searching PubMed and Web of Science until 05/31/13, we conducted a systematic review and a meta-analysis of the effects of BDNF Val66Met polymorphism on antipsychotic-induced TD. Pooled odds ratio was calculated to assess the effects of BDNF Val66Met polymorphism on TD occurrence. Additionally, pooled standardized mean differences (Hedges' g) were calculated to assess the effects on Abnormal Involuntary Movement Scale (AIMS) total score.
Out of 699 potentially eligible hits, 6 studies (N=1740, mean age=46.0±10.4years; males=73.1%; Asians=80.5%, Caucasians=19.5%; schizophrenia=96.2%) were included in this meta-analysis. Pooling data from all studies, no significant associations were found between BDNF Val66Met polymorphism and TD (p=0.82) or AIMS total scores (p=0.11). However, in studies including only Caucasians (n=339), Met allele carriers had significantly higher AIMS total scores (Hedges' g=0.253, 95% confidence interval=0.030 to 0.476, p=0.026) and non-significantly higher TD occurrence (p=0.127). Conversely, there was no association between BDNF and AIMS scores (p=0.57) or TD (p=0.65) in Asians.
Although there was no significant association between BDNF Val66Met polymorphism and TD or AIMS scores across all patients, our results suggest that BDNF Val66Met polymorphism affects severity and, possibly, TD development in Caucasians. Since the number of studies and patients was still small, additional data are needed to confirm genotype-racial interactions. Furthermore, BDNF enhancing treatments for TD may require further study, especially in Caucasians.
迟发性运动障碍(TD)是抗精神病药物治疗的一种严重的长期后果。由于脑源性神经营养因子(BDNF)具有强大的神经营养活性,BDNF 基因的遗传改变可能会影响抗精神病药物引起的 TD。
我们在 PubMed 和 Web of Science 上进行了检索,检索时间截至 2013 年 5 月 31 日,对 BDNF Val66Met 多态性对抗精神病药物引起的 TD 的影响进行了系统评价和荟萃分析。计算汇总优势比来评估 BDNF Val66Met 多态性对 TD 发生的影响。此外,还计算了汇总标准化均数差(Hedges'g)来评估对异常不自主运动量表(AIMS)总分的影响。
在 699 项潜在的合格研究中,有 6 项研究(N=1740 例,平均年龄 46.0±10.4 岁;男性占 73.1%;亚洲人占 80.5%,白种人占 19.5%;精神分裂症占 96.2%)纳入了这项荟萃分析。对所有研究的数据进行汇总,BDNF Val66Met 多态性与 TD(p=0.82)或 AIMS 总分(p=0.11)之间无显著相关性。然而,在仅包括白种人的研究中(n=339),Met 等位基因携带者的 AIMS 总分显著升高(Hedges'g=0.253,95%置信区间为 0.030 至 0.476,p=0.026),TD 发生率非显著升高(p=0.127)。相反,BDNF 与亚洲人的 AIMS 评分(p=0.57)或 TD(p=0.65)之间无关联。
尽管在所有患者中,BDNF Val66Met 多态性与 TD 或 AIMS 评分之间无显著相关性,但我们的结果表明,BDNF Val66Met 多态性影响白种人的 TD 严重程度,可能影响 TD 的发展。由于研究和患者的数量仍然较少,需要更多的数据来确认基因型与种族的相互作用。此外,针对 TD 的 BDNF 增强治疗可能需要进一步研究,尤其是在白种人中。