金属离子代谢平衡失调与阿尔茨海默病早期发病机制  

Metal Metabolic Homeostasis Disruption and Early Initiation of Mechanism for Alzheimer′s Disease

作　　者：赵保路[1] 万莉[1] 

机构地区：[1]脑与认知国家重点实验室 中国科学院生物物理研究所,北京100101

出　　处：《生物化学与生物物理进展》2012年第8期756-763,共8页Progress In Biochemistry and Biophysics

基　　金：国家自然科学基金资助项目(30930036,30870587)~~

摘　　要：研究表明,脑内金属离子代谢失衡与阿尔茨海默病(AD)有关,但其机理尚需深入探讨.结合本实验室研究结果,作者对金属离子代谢紊乱与氧化应激,金属离子代谢紊乱与β-淀粉样蛋白、转铁蛋白和转铁蛋白受体、铁调节蛋白、二价金属离子转运体以及天然抗氧化剂通过调节金属离子代谢平衡缓解β-淀粉样蛋白的毒性和保护细胞的作用进行探讨.提出:铁、铜等金属离子缺乏可能主要与AD早期关系密切,而铁、铜等金属离子过载可能主要与AD后期损伤关系密切的学术观点.Many studies have shown there is a close relationship between metal homeostasis disruption and Alzheimer＇s disease （AD）, but the mechanism needs to be discussed. Recent progresses about these studies are reviewed especially the results in author＇s laboratory are discussed. Iron and copper homeostasis disruption, oxidative stress, β-amyloid （Aβ）, amyloid precursor protein （APP）, iron regulatory protein （IRP） and divalent metal transporter 1 （DMT1） are discussed in detail. We suggested that the overload of iron and copper might have closer relationship with the oxidative stress damage in the later phase in AD and the deficiency of iron and copper might have closer relationship with the early initiation of AD. The protective effects of natural antioxidant against AD through regulating iron and copper homeostasis disruption and oxidative stress are also discussed. This review may be useful for further research and prevention and therapy of AD.

关 键 词：阿尔茨海默病 金属离子代谢失衡 氧化应激 β-淀粉样蛋白(Aβ) Β-淀粉样蛋白前体 转铁蛋白和转铁蛋白受体 铁调节蛋白 二价金属离子转运体 天然抗氧化剂 

分 类 号：R74[医药卫生—神经病学与精神病学]