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An integrative review of methylation at the serotonin transporter gene and its dialogue with environmental risk factors, psychopathology and 5-HITLPR

机译:血清素转运蛋白基因甲基化的整合综述及其与环境风险因素,精神病理学和5-HITLPR的对话

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Gene environment (G x E) interactions have largely been regarded as the root of many complex disorders, including several psychiatric disorders. In this regard, it has been hypothesized that epigenetic mechanisms may be the main mediators of such interactions. Of particular interest is the previously described interaction between psychosocial stress and genetic variability of the serotonin transporter gene (SLC6A4) in its polymorphic region 5-HTTLPR. Here we review the literature concerning SLC6A4 methylation in association with environmental, clinical or genetic variables. While SLC6A4 hypermethylation has typically been described to be independently associated with both early life stress and depressive disorders, only a few papers address whether methylation could mediate the interaction between stress and 5-HTTLPR in predicting psychopathological risk Nevertheless, research preliminarily indicates a methylation-driven increased vulnerability of carriers, of the short allele of 5-HTTLPR to psychiatric disorders when exposed to early stress or soon after exposure to stress. (C) 2016 Published by Elsevier Ltd.
机译:基因环境(G X E)相互作用在很大程度上被视为许多复杂障碍的根源,包括几种精神病疾病。在这方面,已经假设表观遗传机制可以是这种相互作用的主要介质。特别令人兴趣的是在其多态区域5-HTTLPR中的血清素转运蛋白基因(SLC6A4)的心理社会应激和遗传变异之间的先前描述的相互作用。在这里,我们审查了与环境,临床或遗传变量相关联的SLC6A4甲基化的文献。虽然通常描述了SLC6A4高甲基化与早期生命胁迫和抑郁症的独立相关,但只有几篇论文可以解决甲基化是否可以介导应力和5-HTTLPR之间的相互作用,以预测精神病理风险,研究初步表明甲基化驱动在暴露于早期压力或暴露于应激后,在暴露于早期压力时,载体的脆弱性增加了5-Httlpr的短暂的等位基因。 (c)2016由elestvier有限公司出版

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