线粒体功能障碍与阿尔茨海默病关系的研究进展  

Research progress of the relationship between mitochondrial dysfunction and Alzheimer's disease

作　　者：曹玉成[1] 宋炜熙[1] 王哲[2] 

机构地区：[1]湖南中医药大学中西医结合学院,长沙410208 [2]中南大学湘雅二医院中西医结合科,长沙410011

出　　处：《临床与病理杂志》2016年第3期308-313,共6页Journal of Clinical and Pathological Research

基　　金：国家自然科学基金资助项目(81373705);湖南省自然科学基金资助项目(13JJ3030)~~

摘　　要：阿尔茨海默病是老年痴呆症中最常见的类型,其发病机制十分复杂。线粒体是动态细胞器,参与能量代谢、氧化应激,细胞凋亡等调节过程。β淀粉样蛋白、Tau及氧化应激均能够导致线粒体功能损伤,引起线粒体功能障碍,并因此造成突触受损,神经细胞凋亡,促进阿尔茨海默病程的进展。Alzheimer＇s disease is the most common type of dementia,and its pathogenesis is very complex.Mitochondria are dynamic organelles that participate in the regulation of energy metabolism,oxidative stress,cell apoptosis and so on.Beta amyloid protein,Tau and oxidative stress can lead to mitochondrial dysfunction,which can result in synaptic damage,nerve cell apoptosis and promote the progress of Alzheimer＇s disease.

关 键 词：线粒体 阿尔茨海默病 氧化应激 Β淀粉样蛋白 TAU 

分 类 号：R749.16[医药卫生—神经病学与精神病学]