自噬
疾病
发病机制
神经退行性变
淀粉样蛋白(真菌学)
线粒体
神经科学
机制(生物学)
阿尔茨海默病
生物
变性(医学)
医学
细胞生物学
免疫学
病理
细胞凋亡
遗传学
哲学
认识论
作者
Paula I. Moreira,Renato X. Santos,Xiongwei Zhu,Hyoung Gon Lee,Mark A. Smith,Gemma Casadesús,George Perry
摘要
Autophagy is a degradation pathway for the turnover of dysfunctional organelles or aggregated proteins in cells. Extensive literature exists supporting a causative role of mitochondrial dysfunction and amyloid-β protein in the pathogenesis of Alzheimer’s disease (AD). Furthermore, a link between mitochondrial dysfunction, amyloid-β levels and autophagy has been reported to occur in AD. However, it is not yet clear if autophagy plays a causative role, a protective role or is a consequence of the disease process itself. Understanding the exact role of autophagy in different stages of AD progression may help to design more effective therapeutic strategies. A central issue in developing therapies for neurodegenerative diseases involves understanding why and when responses to stress or injury can help prevent neuronal degeneration and death.
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