β淀粉样蛋白级联假说相关的阿尔茨海默病发病机制及防治策略研究进展  

β Amyloid Hypothesis in Alzheimer’s Disease:Pathogenesis, Prevention,and Management

作　　者：张赫 郑焱[1] ZHANG He;ZHENG Yan(Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Capital Medical University,Beijing 100069,China)

机构地区：[1]首都医科大学基础医学院生理学与病理生理学系

出　　处：《中国医学科学院学报》2019年第5期702-708,共7页Acta Academiae Medicinae Sinicae

摘　　要：阿尔茨海默病(AD)是一种以进行性认知功能障碍和记忆衰退为特点的中枢神经系统疾病。研究表明,β淀粉样蛋白(Aβ)是AD发生的关键环节,被认为是遗传因素和环境因素共同作用引发AD病程的上游分子。Aβ聚集及由此引发的细胞炎症反应等被认为是AD患者脑内提前于神经元变性的早期事件,但目前针对Aβ聚集这一环节的药物尚无一种通过临床3期试验,提示了AD发病过程的复杂性,也使Aβ级联假说面临挑战。本文总结了AD发病机制中的重要学说—Aβ级联假说及与其相关的AD病理、病理生理过程和治疗的研究进展。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.

关 键 词：阿尔茨海默病 Β淀粉样蛋白 炎症反应 TAU蛋白 

分 类 号：R741.02[医药卫生—神经病学与精神病学]