Epigenetic Regulation of Amyloid-beta Metabolism in Alzheimer's Disease

被引:8
作者
He, Chuan [1 ]
Huang, Zhong-sheng [1 ]
Yu, Chao-chao [2 ,3 ]
Wang, Hai-hua [4 ]
Zhou, Hua [1 ]
Kong, Li-hong [1 ]
机构
[1] Hubei Univ Chinese Med, Wuhan 430060, Peoples R China
[2] Shenzhen Tradit Chinese Med Hosp, Dept Tuina, Shenzhen 518000, Peoples R China
[3] Guangzhou Univ Chinese Med, Clin Coll 4, Shenzhen 518000, Peoples R China
[4] Hosp Tradit Chinese Med Fengrun Dist, Tangshan 064000, Peoples R China
来源
CURRENT MEDICAL SCIENCE | 2020年 / 40卷 / 06期
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; amyloid-beta; epigenetics; DNA methylation; microRNAs; histone modifications; GENE-PROMOTER METHYLATION; PRECURSOR PROTEIN GENE; NON-CODING RNA; DNA METHYLATION; MOUSE MODEL; CEREBROSPINAL-FLUID; COGNITIVE DEFICITS; NONCODING RNA; UP-REGULATION; IN-VITRO;
D O I
10.1007/s11596-020-2283-0
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Senile plaques (SPs) are one of the pathological features of Alzheimer's disease (AD) and they are formed by the overproduction and aggregation of amyloid-beta (A beta) peptides derived from the abnormal cleavage of amyloid precursor protein (APP). Thus, understanding the regulatory mechanisms during A beta metabolism is of great importance to elucidate AD pathogenesis. Recent studies have shown that epigenetic modulation-including DNA methylation, non-coding RNA alterations, and histone modifications-is of great significance in regulating A beta metabolism. In this article, we review the aberrant epigenetic regulation of A beta metabolism.
引用
收藏
页码:1022 / 1030
页数:9
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