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

页码：1022 / 1030

页数：9

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