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Current Alzheimer Research


ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Review Article

The Implications of Autophagy in Alzheimer’s Disease

Author(s): Tadanori Hamano*, Kouji Hayashi, Norimichi Shirafuji and Yasunari Nakamoto

Volume 15, Issue 14, 2018

Page: [1283 - 1296] Pages: 14

DOI: 10.2174/1567205015666181004143432

Price: $65


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.

Keywords: Alzheimer's disease, autophagy, tau, amyloid β protein, autophagosome, therapy.

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