β淀粉样蛋白导致的线粒体损伤研究进展

Recent Progress of Mitochondrial Dysfunction Induced by β-Amyloid Protein

阿尔茨海默病(Alzheimer disease,AD)是老年人中最常见的神经退行性疾病之一,但目前对于AD发病机制尚不清楚.越来越多的研究表明,β淀粉样蛋白(β-amyloid,Aβ)引起的线粒体结构异常和功能损伤在AD的发病过程中发挥重要作用.Aβ引发线粒体损伤的机制主要为诱导线粒体能量代谢中几种关键酶的活性下降、线粒体分裂/融合平衡的破坏以及线粒体通透性转换孔(mitochondrial permeability transitionpore,mPTP)开放.综述了Aβ引发线粒体损伤的以上几方面机制在近年来取得的进展.

Alzheimer′ s disease （AD） is one of the most prevalent neurodegenerative disorders. However, the mechanisms of the disease are still unclear. Increasing evidences demonstrated that mitochondrial dysfunction and structural abnormalities induced by Aβ play important roles in this disease. β-Amyloid （Aβ） induced mitochondrial damage can be attributed to reduced activities of several key enzymes of mitochondrial energy metabolism, impaired balance of mitochondrial fission and fusion as well as mitochondrial membrane permeability transition pore （mPTP） formation. The recent progress in the mechanisms of Aβ induced mitochondrial damage was summarized.