The Early Events That Initiate β-Amyloid Aggregation in Alzheimer's Disease

被引:83
|
作者
Zhang, Xingyu [1 ]
Fu, Zhihui [1 ]
Meng, Lanxia [1 ]
He, Mingyang [1 ]
Zhang, Zhentao [1 ]
机构
[1] Wuhan Univ, Renmin Hosp, Dept Neurol, Wuhan, Hubei, Peoples R China
来源
FRONTIERS IN AGING NEUROSCIENCE | 2018年 / 10卷
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; beta-amyloid; aggregation; age; diabetes; TRAUMATIC BRAIN-INJURY; APOLIPOPROTEIN APO E4; A-BETA; OXIDATIVE STRESS; HEAD-INJURY; DIABETES-MELLITUS; PRECURSOR PROTEIN; MOUSE MODEL; INFLAMMATORY S100A9; MICROGLIAL RESPONSE;
D O I
10.3389/fnagi.2018.00359
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Alzheimer's disease (AD) is characterized by the development of amyloid plaques and neurofibrillary tangles (NFTs) consisting of aggregated beta-amyloid (A beta) and tau, respectively. The amyloid hypothesis has been the predominant framework for research in AD for over two decades. According to this hypothesis, the accumulation of A beta in the brain is the primary factor initiating the pathogenesis of AD. However, it remains elusive what factors initiate A beta aggregation. Studies demonstrate that AD has multiple causes, including genetic and environmental factors. Furthermore, genetic factors, many age-related events and pathological conditions such as diabetes, traumatic brain injury (TBI) and aberrant microbiota also affect the aggregation of A beta. Here we provide an overview of the age-related early events and other pathological processes that precede A beta aggregation.
引用
收藏
页数:13
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