阿尔茨海默病的线粒体损伤机制

Mechanism of mitochondrial damage in Alzheimer’s disease

阿尔茨海默病(Alzheimer's disease, AD)是一种中枢神经系统的退行性疾病,发病机制复杂且尚未完全阐明。AD的主要病理特征为β淀粉样蛋白(Amyloid-β, Aβ)沉积、老年斑(Senile plaque, SP)形成、神经元纤维缠结(Neurofibrillary tangles, NFTs)、突触及神经元丢失,而线粒体损伤在这些病理机制中起着重要作用。线粒体是脑细胞中重要的细胞器,对维持脑细胞正常功能及能量代谢必不可少。由线粒体动力学、生物能量代谢及运输功能出现障碍引起的线粒体损伤被认为是引起AD发病和病情进展的重要因素之一。

Alzheimer's disease(AD)is a common neurodegenerative disease of the central nervous system, and its pathogenesis is complex and not fully elucidated. The main pathological characteristics of AD are deposition of amyloid-β(Aβ), formation of senile plaque(SP)and neurofibrillary tangles(NFTs), loss of synapse and neuron. Mitochondrial damage plays an important role in the pathogenesis of AD. Mitochondria are important organelles in brain cells and are essential for maintaining normal function and energy metabolism of brain cells. Mitochondrial damage caused by defects in mitochondrial dynamics, bioenergy metabolism, and axonal transport, is considered as one of the important contributing factors to AD pathogenesis and progression.