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2
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Arch Gen Psychiatry. 2012 Jan;69(1):89-97. doi: 10.1001/archgenpsychiatry.2011.109. Epub 2011 Sep 5.
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A critical review of the first 10 years of candidate gene-by-environment interaction research in psychiatry.精神医学中候选基因-环境交互作用研究的头 10 年的批判性回顾。
Am J Psychiatry. 2011 Oct;168(10):1041-9. doi: 10.1176/appi.ajp.2011.11020191. Epub 2011 Sep 2.
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Am J Psychiatry. 2011 Oct;168(10):1107-16. doi: 10.1176/appi.ajp.2011.10111577. Epub 2011 Aug 24.
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Proc Natl Acad Sci U S A. 2011 May 17;108(20):8189-93. doi: 10.1073/pnas.1014129108. Epub 2011 May 16.
6
The serotonin transporter promoter variant (5-HTTLPR), stress, and depression meta-analysis revisited: evidence of genetic moderation.血清素转运体启动子变体(5-HTTLPR)、压力与抑郁的元分析再探讨:基因调节的证据
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Looking on the bright side of serotonin transporter gene variation.从血清素转运体基因变异的积极面来看。
Biol Psychiatry. 2011 Mar 15;69(6):513-9. doi: 10.1016/j.biopsych.2010.09.024. Epub 2010 Nov 2.
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Association study of trauma load and SLC6A4 promoter polymorphism in posttraumatic stress disorder: evidence from survivors of the Rwandan genocide.创伤负荷与 SLC6A4 启动子多态性在创伤后应激障碍中的关联研究:来自卢旺达种族灭绝幸存者的证据。
J Clin Psychiatry. 2010 May;71(5):543-7. doi: 10.4088/JCP.08m04787blu. Epub 2010 Apr 6.

5-羟色胺转运体 5-HTTLPR 基因型调节童年逆境对创伤后应激障碍风险的影响:一项复制研究。

Serotonin transporter 5-HTTLPR genotype moderates the effects of childhood adversity on posttraumatic stress disorder risk: a replication study.

机构信息

Department of Genetics, Yale University School of Medicine, New Haven, CT, USA.

出版信息

Am J Med Genet B Neuropsychiatr Genet. 2012 Sep;159B(6):644-52. doi: 10.1002/ajmg.b.32068. Epub 2012 Jun 12.

DOI:10.1002/ajmg.b.32068
PMID:22693124
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3428016/
Abstract

We reported that the 5-HTTLPR polymorphism in the promoter region of the serotonin transporter gene (SLC6A4) moderates the effect of childhood adversity on posttraumatic stress disorder (PTSD) risk [Xie et al. (2009); Arch Gen Psychiatry 66 (11): 1201-1209]. In the present study, we considered 5,178 subjects (a group with generally high substance dependence comorbidity, as for our previous study) using similar methodology to replicate our previous results. We used logistic regression analyses to explore the interaction effect of 5-HTTLPR genotype and childhood adversity on PTSD risk. We found that, as reported in our previous study, in individuals with childhood adversity, the presence of one or two copies of the S allele of 5-HTTLPR increased the risk to develop PTSD. This gene-environment interaction effect was present in European Americans (EAs), but not in African Americans (AAs; EAs, OR = 1.49, 95% CI = 1.07-2.08, P = 0.019; AAs, OR = 0.90, 95% CI = 0.60-1.35, P = 0.62). The statistical power to detect this interaction effect was increased when data were combined with those from our previous study [Xie et al. (2009); Arch Gen Psychiatry 66 (11): 1201-1209]. The findings reported here replicate those from our previous work, adding to a growing body of research demonstrating that the 5-HTTLPR genotype moderates risk for anxiety and depression phenotypes in the context of stress and adverse events.

摘要

我们曾报道过,5-羟色胺转运体基因(SLC6A4)启动子区域的 5-HTTLPR 多态性调节了童年逆境对创伤后应激障碍(PTSD)风险的影响[Xie 等人,(2009);《美国精神病学杂志》66(11):1201-1209]。在本研究中,我们使用类似的方法考虑了 5178 名受试者(一组具有普遍较高的物质依赖共病,与我们之前的研究相同),以复制我们之前的结果。我们使用逻辑回归分析来探讨 5-HTTLPR 基因型和童年逆境对 PTSD 风险的交互作用。我们发现,正如我们之前的研究报告的那样,在有童年逆境的个体中,5-HTTLPR 的 S 等位基因的一个或两个拷贝的存在增加了发生 PTSD 的风险。这种基因-环境相互作用效应存在于欧洲裔美国人(EA)中,但不存在于非裔美国人(AA)中;EA,OR=1.49,95%CI=1.07-2.08,P=0.019;AA,OR=0.90,95%CI=0.60-1.35,P=0.62)。当将数据与我们之前的研究[Xie 等人,(2009);《美国精神病学杂志》66(11):1201-1209]合并时,检测这种相互作用效应的统计效力增加了。这里报道的发现与我们之前的工作相重复,增加了越来越多的研究表明,5-HTTLPR 基因型在应激和不良事件的背景下调节焦虑和抑郁表型的风险。