脑组织胆固醇稳态失衡对阿尔茨海默病的影响及其分子机制研究  

Effects of brain cholesterol homeostasis imbalance on Alzheimer’s disease and its related molecular mechanisms

作　　者：王苏苏 吴美琴[1] 裴尚飞 颜崇淮[1] WANG Su-su;WU Mei-qin;PEI Shang-fei;YAN Chong-huai(Ministry of Education-Shanghai Key Laboratory of Children's Environmental Health,Xinhua Hospital Affiliated to Shanghai Jiaotong University School of Medicine,Shanghai 200092,China;Department of Nutrition,The Third Affiliated Hospital of Naval Medical University,Shanghai 200438,China)

机构地区：[1]上海交通大学医学院附属新华医院教育部和上海市环境与儿童健康重点实验室,200092 [2]海军军医大学第三附属医院营养科,上海200438

出　　处：《中国现代神经疾病杂志》2022年第3期200-204,共5页Chinese Journal of Contemporary Neurology and Neurosurgery

基　　金：国家自然科学基金资助项目(项目编号:81973062)。

摘　　要：阿尔茨海默病的发病机制主要包括神经元和突触减少、细胞外β-淀粉样蛋白(Aβ)沉积、神经炎性斑(NPs)形成和细胞内tau蛋白过磷酸化,导致神经原纤维缠结(NFTs)形成。其中,神经炎性斑和神经原纤维缠结形成与脑组织胆固醇稳态失衡密切相关,提示后者在阿尔茨海默病的发生发展中起决定作用。本文综述脑组织胆固醇稳态失衡对阿尔茨海默病的分子调控机制。The pathogenesis of Alzheimer’s disease(AD)mainly includes the decrease of neurons and synapses,the deposition of the extracellularβ-amyloid protein(Aβ),the formation of neuritic plaques(NPs)and neurofibrillary tangles(NFTs)caused by intracellular tau protein hyperphosphorylation.NPs and NFTs are closely related to the brain cholesterol homeostasis imbalance,suggesting that normal brain cholesterol homeostasis may play a decisive role in the development of AD.This paper reviews the molecular regulation mechanism of brain cholesterol homeostasis imbalance in AD.

关 键 词：阿尔茨海默病 胆固醇 分子生物学 综述 

分 类 号：R749.16[医药卫生—神经病学与精神病学]