MicroRNAs在抑郁症中的潜在作用

Title:Prospective Role of MicroRNAs in Depression

Volume: 24 Issue: 32

关键词: 抑郁症，MicroRNA，突触可塑性，下丘脑 - 垂体 - 肾上腺，学习和记忆功能障碍，压力，认知障碍。

摘要: Background: Depression is a debilitating disease that is affecting a growing number of patients, both physically and mentally. In addition to mood changes, depression results in cognitive impairment. Although depression studies have been going on for decades, the underlying mechanism still remains unclear. MicroRNAs (miRNAs), a type of small non-coding RNAs, predominantly control the expression of their target mRNAs to exert their functions. Some evidences have revealed the importance of miRNAs in the mechanism of depression,however, these studies are still in their infancy. Alterations in brain regions, synaptic plasticity, hypothalamic-pituitary-adrenal (HPA) axis, changes in the levels of serotonin and glucocorticoids, together with stress response have been proven to be involved in depression. These alterations can influence cognition, learning and memory, with recent evidences demonstrating the involvement of miRNAs in several aspects of stress response, neural plasticity and neurogenesis as well as pathogenesis of depression.

Objective: In light of these theories of depression, this review was aimed at elucidating the role of miRNAs in the underlying mechanisms of depression resulting in cognitive, learning and memory impairments.

Method/Results: Both PubMed and Scopus databases were employed in scouring for research reports pertaining to this area of study. A total of 180 articles were obtained from these two databases.

Conclusion: With the probing of classical theories of depression as well as the connection between miRNAs and depression, more studies,nevertheless, are needed to ascertain the full mechanism of depression along with its resultant cognitive, learning and memory impediments.

Cite this article as:

Prospective Role of MicroRNAs in Depression, Current Medicinal Chemistry 2017; 24 (32) . https://dx.doi.org/10.2174/0929867324666170714112620