Major depressive disorder (MDD) is the leading cause of disability worldwide and is associated with high rates of suicide and medical comorbidities. Current antidepressant medications are suboptimal, as most MDD patients fail to achieve complete remission from symptoms. At present, clinicians are unable to predict which antidepressant is most effective for a particular patient, exposing patients to multiple medication trials and side effects. Since MDD's etiology includes interactions between genes and environment, the epigenome is of interest for predictive utility and treatment monitoring. Epigenetic mechanisms of antidepressant medications are incompletely understood. Differences in epigenetic profiles may impact treatment response. A systematic literature search yielded 24 studies reporting the interaction between antidepressants and eight genes (BDNF, MAOA, SLC6A2, SLC6A4, HTR1A, HTR1B, IL6, IL11) and whole genome methylation. Methylation of certain sites within BDNF, SLC6A4, HTR1A, HTR1B, IL11, and the whole genome was predictive of antidepressant response. Comparing DNA methylation in patients during depressive episodes, during treatment, in remission, and after antidepressant cessation would help clarify the influence of antidepressant medications on DNA methylation. Individuals' unique methylation profiles may be used clinically for personalization of antidepressant choice in the future.

译文

重度抑郁症 (MDD) 是全球残疾的主要原因,与自杀和医疗合并症的高发生率有关。当前的抗抑郁药物是次优的,因为大多数MDD患者无法完全缓解症状。目前,临床医生无法预测哪种抗抑郁药对特定患者最有效,使患者暴露于多种药物试验和副作用。由于MDD的病因包括基因与环境之间的相互作用,因此表观基因组对于预测效用和治疗监测很有意义。抗抑郁药物的表观遗传机制尚不完全清楚。表观遗传谱的差异可能会影响治疗反应。系统的文献搜索产生了24项研究,报告了抗抑郁药与八个基因 (BDNF,MAOA,SLC6A2,SLC6A4,HTR1A,HTR1B,IL6,IL11) 和全基因组甲基化之间的相互作用。BDNF,SLC6A4,HTR1A,HTR1B,IL11和全基因组中某些位点的甲基化可预测抗抑郁反应。在抑郁发作期间,治疗期间,缓解期间以及抗抑郁药停止后比较患者的DNA甲基化将有助于阐明抗抑郁药物对DNA甲基化的影响。个人独特的甲基化谱可以在临床上用于抗抑郁药的个性化选择。

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