抑郁症发展成为应激与个体对应激易感性的相互作用的结果,早期的生活压力和基因–环境相互作用可能是抑郁症的危险因素,并在个体应激易感的进展中发挥重要作用。糖皮质激素受体基因启动子的表观调节被认为是应激易感性的分子基础。脑源性神经营养因子启动子的组蛋白修饰可能是抗抑郁药和电休克治疗的调节机制。临床遗传学研究表明基因组印记参与了双向障碍的发病,但还没有直接的分子证据的报道。通过组蛋白脱乙酰基酶抑制剂-丙戊酸盐及DNA甲基化供体-S-腺苷甲硫氨酸的抗躁狂作用的研究,认为DNA甲基化参与了情绪的调节。双向障碍患者的尸检发现,其脑组织膜结合儿茶酚胺-O-甲基转移酶的启动子区的DNA存在甲基化改变。一对患有双向障碍单卵双生的双胞胎的PPIEL被发现存在DNA甲基化状态。在一个双向障碍II型的对照病例中发现PPIEL低甲基化。这些研究结果表明表观遗传在情感障碍中可能发生作用。对情感障碍的表观遗传机制的进一步研究是必要的。Depression developed into a result of the interaction of stress and individual stress susceptibility, the possible risk factors were the early life pressure and gene-environment interaction, which played an important role in the development of individual stress susceptibility. The glucocorticoid receptor gene promoter apparent adjustment was considered to be the molecular basis of the susceptibility of stress. Brain-deried neurotrophic factor promoters of the protein modification may be antidepressants and electric shock treatment of adjustment mechanism. Clinical genetics research indicated that genomic imprinting involved in the biplor disorder come on, but had no direct evidence of the molecules of the report. Through the research resistance to manic function of group of protein deacelation base enzyme inhibitors-valproic acid salt and DNA methylation donor-S-adenosine armour sulfur
