老年阿尔兹海默症患者认知功能与氧化应激指标关系的研究进展  

Research progress on the relationship between cognitive function andoxidative stress indicators in elderly patients with Alzheimer′s disease

作　　者：陈绍敏 张亭亭 CHEN Shaomin;ZHANG Tingting(Center of Gerontology and Geriatrics,West China Hospital Sichuan University,Sichuan University,Chengdu,Sichuan 610000,China;Department of Gastroenterology,West China Hospital No.4,Sichuan University,Chengdu,Sichuan 610000,China)

机构地区：[1]四川大学华西医院老年医学中心/干部医疗科,四川成都610000 [2]四川大学华西第四医院消化内科,四川成都610000

出　　处：《公共卫生与预防医学》2024年第3期123-127,共5页Journal of Public Health and Preventive Medicine

基　　金：四川省卫生健康委员会医学科技项目(21PJ015)。

摘　　要：目的阿尔兹海默病(Alzheimer′s disease,AD)是一种随着年龄增长而不断进展的神经退行性疾病,患者临床常表现为认知障碍、记忆力衰退、精神症状以及行为障碍等。氧化应激反应是机体氧化与抗氧化能力失衡导致,其造成的氧化损伤与AD发生密切相关。氧化应激导致自由基大量产生,增加神经细胞大分子物质氧化、β淀粉样蛋白(βamyloid,Aβ)聚集以及tau蛋白过度磷酸化,形成神经纤维缠结,进而诱导神经组织细胞凋亡。此外大量自由基还可造成大脑炎症反应,加重神经组织的损伤。此文主要对AD发病过程及其与氧化应激反应之间关系进行综述,旨在为临床研究提供思路。Alzheimer′s disease(AD)is a neurodegenerative disease that progresses with age and is clinically characterized by cognitive impairment,memory decline,mental symptoms and behavioral disorders.Oxidative stress emerges when an imbalance exists between the generation of free radicals and the antioxidant capacity to scavenge them in the body,and the resulting oxidative injury is closely related to the occurrence of AD.Oxidative stress leads to the mass production of free radicals,which increases the oxidation of macromolecules of nerve cells,the aggregation ofβamyloid(Aβ)and the excessive phosphorylation of tau protein and forms the neurofibrillary tangles,thereby inducing apoptosis of nerve tissue cells.In addition,a large number of free radicals can also cause brain inflammatory response and aggravate nerve tissue injury.This paper mainly reviews the pathogenesis of AD and its relationship with oxidative stress,aiming to provide ideas for clinical research.

关 键 词：阿尔兹海默症 氧化应激 AΒ蛋白 TAU蛋白 自由基 

分 类 号：R181[医药卫生—流行病学]