University of Delaware.
Dev Psychopathol. 2013 Nov;25(4 Pt 2):1279-91. doi: 10.1017/S0954579413000618.
In the past decade, there have been exciting advances in the field of behavioral epigenetics that have provided new insights into a biological basis of neural and behavioral effects of gene-environment interactions. It is now understood that changes in the activity of genes established through epigenetic alterations occur as a consequence of exposure to environmental adversity, social stress, and traumatic experiences. DNA methylation in particular has thus emerged as a leading candidate biological pathway linking gene-environment interactions to long-term and even multigenerational trajectories in behavioral development, including the vulnerability and resilience to psychopathology. This paper discusses what we have learned from research using animal models and from studies in which the translation of these findings has been made to humans. Studies concerning the significance of DNA methylation alterations in outcomes associated with stress exposure later in life and dysfunction in the form of neuropsychiatric disorders are highlighted, and several avenues of future research are suggested that promise to advance our understanding of epigenetics both as a mechanism by which the environment can contribute to the development of psychiatric disorders and as an avenue for more effective intervention and treatment strategies.
在过去的十年中，行为表观遗传学领域取得了令人兴奋的进展，为基因-环境相互作用对神经和行为影响的生物学基础提供了新的见解。现在人们已经明白，通过表观遗传改变而建立的基因活性的变化是暴露于环境逆境、社会压力和创伤经历的结果。特别是 DNA 甲基化已经成为将基因-环境相互作用与行为发展的长期甚至多代轨迹联系起来的主要候选生物途径，包括对精神病理学的易感性和弹性。本文讨论了我们从使用动物模型的研究和将这些发现转化为人类的研究中所学到的东西。强调了 DNA 甲基化改变在与生活后期应激暴露相关的结果以及神经精神障碍形式的功能障碍中的意义的研究，并提出了未来研究的几个途径，有望增进我们对表观遗传学的理解，既作为环境导致精神疾病发展的一种机制，也作为更有效干预和治疗策略的一种途径。
