表观遗传学
DNA甲基化
后生
组蛋白
发病机制
生物
疾病
表观遗传疗法
神经科学
神经发生的表观遗传调控
阿尔茨海默病
生物信息学
遗传学
基因表达
医学
基因
免疫学
组蛋白甲基转移酶
病理
作者
Jun Wang,Jin‐Tai Yu,Meng‐Shan Tan,Teng Jiang,Lan Tan
标识
DOI:10.1016/j.arr.2013.05.003
摘要
The vast majority of Alzheimer's disease (AD) are late-onset forms (LOAD) likely due to the interplay of environmental influences and individual genetic susceptibility. Epigenetic mechanisms, including DNA methylation, histone modifications and non-coding RNAs, constitute dynamic intracellular processes for translating environmental stimuli into modifications in gene expression. Over the past decade it has become increasingly clear that epigenetic mechanisms play a pivotal role in aging the pathogenesis of AD. Here, we provide a review of the major mechanisms for epigenetic modification and how they are reportedly altered in aging and AD. Moreover, we also consider how aberrant epigenetic modifications may lead to AD pathogenesis, and we review the therapeutic potential of epigenetic treatments for AD.
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