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-beta protein in the pathogenesis of Alzheimer's disease (AD). Furthermore, a link between mitochondrial dysfunction, amyloid-beta 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.
Sheng Fong, Emelyne Teo, Li Fang Ng, Ce-Belle Chen, Lakshmi Narayanan Lakshmanan, Sau Yee Tsoi, Philip K. Moore, Takao Inoue, Barry Halliwell, Jan Gruber
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