β淀粉样蛋白损伤线粒体机制的研究进展

Research Advances in Mechanisms of Mitochondria Damaged by β-amyloid

阿尔茨海默病是一种神经退行性疾病,是痴呆中最常见的病因。其最重要的病理特征是β淀粉样蛋白的沉积及tau蛋白的过磷酸化。目前认为β淀粉样蛋白导致线粒体功能障碍的具体机制为产生过量的氧化应激产物损伤线粒体及其蛋白质、DNA,从而使线粒体结构异常导致功能异常,进而影响神经细胞的存活及正常功能;或者通过影响线粒体膜及其电位的稳定性,影响蛋白质的折叠,进而影响DNA的完整性而致病。

Alzheimer disease,which is the most common cause of dementia,is a neurodegenerative disease.β-amyloid deposition and over-phosphorylation of the tau protein are the most important pathological features.The review is mainly to introduce how β-amyloid protein causes mitochondrial dysfunction,and produces excessive oxidative stress product-ROS/RNS to damage mitochondria and its protein,DNA,which results in mitochondrial structural abnormalities leading to abnormal function,and further affecting the survival and normal function of nerve cells.β-amyloid protein also affects the stability of the mitochondrial membrane and its potential,the folding of protein,thereby affects the integrity of DNA and causes diseases.