Journal
CURRENT ALZHEIMER RESEARCH
Volume 15, Issue 14, Pages 1283-1296Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1567205015666181004143432
Keywords
Alzheimer's disease; autophagy; tau; amyloid beta protein; autophagosome; therapy
Categories
Funding
- JSPS KAKEN [25460893, 15K08904, 16K09235]
- JST [AS242Z03676Q]
- University of Fukui
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The pathogenic mechanisms of Alzheimer's Disease (AD) involve the deposition of abnormally misfolded proteins, amyloid beta protein (A beta) and tau protein. A beta 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, A beta, tau and dysfunctional organ-elles in the cell. Many animal model studies have demonstrated that autophagy normally functions as the protective factor against AD progression associated with intracytoplasmic toxic A beta 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.
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