Genetic factors in anxiety disorders.

Modern trends in pharmacopsychiatry Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI:10.1159/000351932
Katharina Domschke, Eduard Maron
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引用次数: 17

Abstract

Presently available clinical genetic studies point to a considerable heritability of anxiety disorders (30-67%), with multiple vulnerability genes such as 5-HT1A, 5-HTT, MAO-A, COMT, CCK-B, ADORA2A, CRHR1, FKBP5, ACE, RGS2/7 and NPSR1 suggested by molecular genetic association studies. These genes have been shown to partially interact with each other as well as with environmental factors to shape the overall disease risk in a complex genetic model. Additionally, recent studies have pointed out the crucial role of epigenetic signatures such as methylation patterns in modifying environmental influences as well as in driving the functional impact of anxiety disorder risk genes. On a systems level, vulnerability genes of anxiety disorders seem to confer some of the disease risk via intermediate phenotypes like behavioral inhibition, anxiety sensitivity or several neurobiological traits such as increased startle reactivity or dysfunctional corticolimbic activity during emotional processing. Finally, first pharmaco- and psychotherapy-genetic studies provide evidence for certain risk genes to confer interindividual variability in response to a pharmacological or psychotherapeutic intervention in anxiety disorders. Genetic research in anxiety disorders will be discussed regarding its potential to foster innovative and individually tailored therapeutic approaches for patients with anxiety disorders.

焦虑症的遗传因素。
在一个复杂的遗传模型中,这些基因部分地相互作用,并与环境因素相互作用,从而形成整体疾病风险。此外,最近的研究指出了表观遗传特征(如甲基化模式)在改变环境影响以及驱动焦虑障碍风险基因的功能影响方面的关键作用。在系统层面上,焦虑症的易感基因似乎通过中间表型(如行为抑制、焦虑敏感性)或一些神经生物学特征(如增加的惊吓反应性或情绪处理过程中的皮质边缘活动功能障碍)赋予了一些疾病风险。最后,第一项药物和心理治疗遗传学研究提供了证据,证明某些风险基因在对焦虑症的药物或心理治疗干预的反应中具有个体间变异性。焦虑症的基因研究将讨论其促进焦虑症患者创新和个性化治疗方法的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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