《生命科学》 2014, 26(4): 340-348
摘 要:自噬是真核细胞中降解易聚集蛋白质的重要途径,以应激和损伤时更为显著。自噬与阿尔茨海默病(Alzheimer’s disease, AD) 密切相关,在AD 中起到“双刃剑”的作用,与致病性β 淀粉样肽(Aβ) 和细胞骨架相关tau 蛋白的生成和代谢都有密切的关系。随着对自噬机制的深入了解,人们发现了自噬在AD 病理过程中的调节作用。综述了自噬的基本机制、自噬与AD 发病的互作关系以及如何从自噬的信号转导途径入手,调整AD 自噬稳态及重平衡,从而探索新的AD 治疗性药物靶标。
Abstract: Autophagy is a vital degradation process responsible for the clearance of aggregate-prone proteins,especially under stress and injury conditions. Autophagy is closely related with the neurodegenerative diseases, such as Alzheimer’s disease (AD). It has dual lives in AD pathogenesis, which is involved in generation and metabalism of β-amyloid peptid (Aβ) and microtubule-associated protein tau. People are getting to know the contribution of autophagy to AD with the development of neuroscience. Here, the basics of autophagy, interaction with AD and how to obtain autophagic balance are reviewed, so as to provide clues to AD therapeutic targets.