DNA methylation in the pathology of Alzheimer's disease: from gene to cognition

被引:35
作者
Poon, Chi Him [1 ]
Tse, Long Sum Rachel [1 ]
Lim, Lee Wei [1 ]
机构
[1] Univ Hong Kong, Li Ka Shing Fac Med, Sch Biomed Sci, Neuromodulat Lab, L4 Lab Block,21 Sassoon Rd, Hong Kong, Peoples R China
关键词
Alzheimer's disease; neuroepigenetics; DNA methylation; amyloid beta; neuroplasticity; LONG-TERM POTENTIATION; IMMEDIATE-EARLY GENE; PRECURSOR PROTEIN GENE; SYNAPTIC PLASTICITY; NEUROTROPHIC-FACTOR; EPIGENETIC REGULATION; MOUSE MODEL; TRANSGENIC MICE; MEMORY CONSOLIDATION; S-ADENOSYLMETHIONINE;
D O I
10.1111/nyas.14373
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Alzheimer's disease (AD) is a debilitating disorder that manifests with amyloid beta plaque deposition, neurofibrillary tangles, neuronal loss, and severe cognitive impairment. Although much effort has been made to decipher the pathogenesis of this disease, the mechanisms causing these detrimental outcomes remain obscure. Over the past few decades, neuroepigenetics has emerged as an important field that, among other things, explores how reversible modifications can change gene expression to control behavior and cognitive abilities. Among epigenetic modifications, DNA methylation requires further elucidation for the conflicting observations from AD research and its pivotal role in learning and memory. In this review, we focus on the essential components of DNA methylation, the effects of aberrant methylation on gene expressions in the amyloidogenic pathway and neurochemical processes, as well as memory epigenetics in Alzheimer's disease.
引用
收藏
页码:15 / 33
页数:19
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