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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