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Autophagy in Alzheimer's Disease Publisher Pubmed



Zareshahabadi A1 ; Masliah E2 ; Johnson GVW3 ; Rezaei N1, 4, 5
Authors
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Authors Affiliations
  1. 1. Molecular Immunology Research Center, Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, 14194, Iran
  2. 2. Department of Neurosciences, University of California at San Diego, San Diego, 92093-0662, CA, United States
  3. 3. Department of Anesthesiology, University of Rochester, Rochester, NY, United States
  4. 4. Universal Scientific Education and Research Network (USERN), Tehran, 14194, Iran
  5. 5. Research Center for Immunodeficiencies, Pediatrics Center of Excellence, Children's Medical Center, Tehran University of Medical Sciences, Tehran, 14194, Iran

Source: Reviews in the Neurosciences Published:2015


Abstract

Autophagy is a vesicle and lysosome-mediated degradative pathway that is essential for protein homeostasis and cell health. In particular, compared to nonneuronal cells, neurons are dependent on high basal autophagy for survival. There is emerging agreement that defects in autophagy are likely to contribute to the neurodegenerative processes in numerous diseases, including Alzheimer's disease (AD). Autophagy-lysosome defects occur early in the pathogenesis of AD and have been proposed to be a significant contributor to the disease process. Given the fact that autophagy deficits are likely major contributors to the etiology of AD, the focus of this review will be on recent studies that support a role for autophagy deficits in AD. © 2015 by De Gruyter 2015.