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.