脑铁代谢紊乱与阿尔茨海默病  

Disturbance of iron metabolism in brain and Alzheimer's disease

作　　者：符敬坦 王璞[2] 郭闯[2,3] 

机构地区：[1]衡水市妇幼保健院,河北衡水053000 [2]东北大学,辽宁沈阳110819 [3]河北联合大学秦皇岛分院,河北秦皇岛066001

出　　处：《解剖科学进展》2013年第1期79-82,共4页Progress of Anatomical Sciences

基　　金：国家自然科学基金资助项目(No.81071004)

摘　　要：脑内铁代谢的异常和其所致的氧化应激与阿尔茨海默病(Alzheimer'sdisease,AD)的发病有关。AD是常见于老年人的一种神经退行性疾病,其特征性的病理改变主要是脑内神经细胞外β-淀粉样蛋白(β-amyloid,Aβ)的沉积形成老年斑(senile plague,SP)、胞内神经原纤维缠结(neurofibrillary tangles,NFTs)和胆碱能神经元丢失。研究证实,在普通老年人和AD患者脑内有铁沉积增多的趋势,且铁等过渡金属离子与APP、Aβ和Tau蛋白密切相关,提示铁可能参与了AD的发病和进展等病理生理过程。因此,深入探讨铁在AD发病中可能的作用,有利于了解AD的发病机制,从而为AD疾病的治疗提供新的靶点。The dysregulation of iron homeostasis and consequential induction of oxidative stress in the brain were related to the pathogenesis of Alzheimer＇s disease（AD）. AD is a neurodegenerative disease often occurred in the old stage, with main pathologically features of the extraeellular β-amyloid （A β ） plaques, intracellular neurofibrillary tangles （NFTs） and selective eholinergic neuronal loss in the brain. Recent studies have shown that Tau, APP and its proteolytie product A β are associated with metal homeostasis in the AD brain, suggesting that exposure to metals may potentially modulate AD pathology, either triggering or ameliorating disease progression. Exploring the effect of iron on the pathogenesis of AD may provide a new target for the prevention and treatment of AD.

关 键 词：铁代谢紊乱 阿尔茨海默病 脑内神经 神经退行性疾病 Β-淀粉样蛋白 神经原纤维缠结 AD患者 发病机制 

分 类 号：R749.16[医药卫生—神经病学与精神病学]