硒缺乏与阿尔茨海默症  

Selenium deficiency and Alzheimer’s disease

作　　者：刘琼[1] 田静[1] 陈平[1] 杨思林 宋云 

机构地区：[1]深圳大学生命科学学院,深圳518060 [2]安徽省华信生物药业股份有限公司,界首236500

出　　处：《生命科学》2012年第8期892-900,共9页Chinese Bulletin of Life Sciences

基　　金：国家自然科学基金项目(31070731;30901182);广东省自然科学基金项目(10151806001000023);深圳市科技项目(CXB201005240008A)

摘　　要：微量元素硒对维持中枢神经系统的生物功能具有重要作用。生物摄入硒后优先供给脑部。长期缺硒会引起包括阿尔茨海默症(AD)在内的脑疾病。AD的病理特征为β-淀粉样肽聚集形成老年斑和tau蛋白过度磷酸化造成神经纤维缠结。氧化应激和信号转导紊乱在AD形成过程中具有重要作用。硒缺乏会影响AD发生发展的各个环节,与认知功能降低和AD形成密切相关。对近年有关硒与AD关系的研究进展进行综述,着重总结了硒缺乏对氧化应激、信号转导以及AD病理特征形成的作用和机制,探讨补硒延缓AD形成的可能性。Trace element selenium plays an important role in maintaining the biological function of central nervous system. It is preferentially provided to brain after its intake. Long term selenium deficiency results in brain diseases including Alzheimer＇s disease （AD）. The pathological characteristics of AD are the aggregation of β-amyloid to form senile plaque and the hyperphosphorylation of tau protein to form intracellular neurofibrillary tangles. Oxidative stress and signal transduction disturbance are also closely linked to AD. Selenium deficiency has impacts on those key points of AD formation, resulting in cognitive dysfunction and AD pathology. This paper summarizes recent advances in selenium and AD relation, mainly focusing on the effect and mechanism of selenium deficiency toward oxidative stress, signal transduction, and AD pathology. The possibility for selenium to prevent ADformation is also discussed in this review.

关 键 词：硒 阿尔茨海默症 硒蛋白 氧化应激 β-淀粉样蛋白(Aβ) TAU蛋白 信号转导 认知功能 

分 类 号：O623.52[理学—有机化学] R749.1[理学—化学]