β Amyloid Hypothesis in Alzheimer's Disease:Pathogenesis,Prevention,and Management.
10.3881/j.issn.1000-503X.10875
- Author:
He ZHANG
1
;
Yan ZHENG
1
Author Information
1. Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China.
- Publication Type:Journal Article
- Keywords:
Alzheimer’s disease;
Tau protein;
inflammation;
β amyloid
- MeSH:
Alzheimer Disease;
pathology;
prevention & control;
therapy;
Amyloid beta-Peptides;
Brain;
physiopathology;
Humans
- From:
Acta Academiae Medicinae Sinicae
2019;41(5):702-708
- CountryChina
- Language:Chinese
-
Abstract:
Alzheimer's disease(AD)is a central nervous system disease characterized by progressive cognitive dysfunction and memory loss.Increasing evidences suggest that β amyloid(Aβ)plays a critical role and may be a upstream molecule in AD pathogenesis involving both genetic and environmental factors.Aβ accumulation and its related inflammation are considered early events preceding neurodegeneration and neuronal loss in AD brain.However,all strategies and compounds targeting Aβ deposition have failed in clinical trials,implying complexity of AD pathogenesis.This article reviews Aβ hypothesis and its related mechanisms,pathophysiological process,and therapeutics of AD.
