羰基应激与衰老机理及阿尔茨海默病早期分子病因  

Carbonyl Stress,Aging Mechanisms,and The Up-stream Molecular Etiology of Alzheimer′s Disease

作　　者：印大中[1,2] 刘文锋[1,2] 

机构地区：[1]蛋白质化学与发育生物学教育部重点实验室 湖南师范大学生命科学学院,长沙410081 [2]体适能与运动康复湖南省重点实验室 湖南师范大学,长沙410012

出　　处：《生物化学与生物物理进展》2012年第8期747-755,共9页Progress In Biochemistry and Biophysics

基　　金：国家高技术研究发展计划(863)资助项目(2008AA02Z411)~~

摘　　要：本文从人体衰老过程中重要的共性生化过程——羰基应激——的角度出发,探讨老年性痴呆,主要指阿尔茨海默病(AD),发生发展的早期分子病因.首先,讨论与脂类、碳水化合物和蛋白质自由基氧化(氧应激)和非酶糖基化(糖应激)产生的羰基毒化作用相关的化学反应.接着,列举活性羰基在AD患者体内存在的证据并探究这些羰基毒素对细胞结构与功能的影响.最后,分析和归纳脑组织中针对羰基毒化的解毒机理,进而探讨寻找基于该机理防治AD以至抵御衰老、疲劳、亚健康的方法与途径.The up-stream molecular causes of Alzheimer＇s disease （AD） have been discussed from the aspect of carbonyl stress, which represents an important common biochemical process of human aging. Firstly, chemical reactions of carbonyl toxification, induced by free radical oxidative stress and glycation stress, on lipids, carbonhydrates and proteins are elaborated. Secondly, evidences of reactive carbonyls and their effects on cellular structure and functions in AD patients are provided. Finally, detoxification mechanisms against carbonyl stress in brain are analysed and summarized, and strategies based on the mechanism for treating AD, as well as for preventing aging, fatigue and sub-health are also introduced and discussed.

关 键 词：阿尔茨海默病(AD) 衰老 羰基应激 氧应激 糖应激 

分 类 号：R592[医药卫生—老年医学] R34[医药卫生—内科学]