Tadanori Hamano*, Kouji Hayashi, Norimichi Shirafuji and Yasunari Nakamoto Pages 1283 - 1296 ( 14 )
The pathogenic mechanisms of Alzheimer’s Disease (AD) involve the deposition of abnormally misfolded proteins, amyloid β protein (Aβ) and tau protein. Aβ comprises senile plaques, and tau aggregates form Neurofibrillary Tangles (NFTs), both of which are hallmarks of AD. Autophagy is the main conserved pathway for the degeneration of aggregated proteins, Aβ, tau and dysfunctional organelles in the cell. Many animal model studies have demonstrated that autophagy normally functions as the protective factor against AD progression associated with intracytoplasmic toxic Aβ and tau aggregates. The upregulation of autophagy can also be favorable in AD treatment. An improved understanding of the signaling pathways that regulate autophagy is critical to developing AD treatments. The cellular and molecular machineries of autophagy, their function in the pathogenesis of AD, and current drug discovery strategies will be discussed in this review.
Alzheimer's disease, autophagy, tau, amyloid β protein, autophagosome, therapy.
Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui