Physical exercise may exert its therapeutic influence on Alzheimer's disease through the reversal of mitochondrial dysfunction via SIRT1–FOXO1/3–PINK1–Parkin-mediated mitophagy
Authors:
Open Access
- 1 January 2021
- journal article
- editorial
- Published by Elsevier in Journal of Sport and Health Science
- Vol. 10 (1) , 1-3
Abstract
No abstract availableKeywords
Funding Information
- Fundamental Research Funds for the Central Universities (40500-20104-222290)
This publication has 29 references indexed in Scilit:
- Amyloid Beta and Phosphorylated Tau-Induced Defective Autophagy and Mitophagy in Alzheimer’s DiseaseCells, 2019
- Exercise activates lysosomal function in the brain through AMPK‐SIRT1‐TFEB pathwayCNS Neuroscience & Therapeutics, 2019
- Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s diseaseNature Neuroscience, 2019
- Mitochondria and Mitochondrial Cascades in Alzheimer’s DiseaseJournal of Alzheimer’s Disease, 2017
- Treadmill exercise decreases amyloid-β burden possibly via activation of SIRT-1 signaling in a mouse model of Alzheimer's diseaseExperimental Neurology, 2017
- Antiaging Properties of a Grape-Derived Antioxidant Are Regulated by Mitochondrial Balance of Fusion and Fission Leading to Mitophagy Triggered by a Signaling Network of Sirt1-Sirt3-Foxo3-PINK1-PARKINOxidative Medicine and Cellular Longevity, 2014
- SIRT1-mediated deacetylation of MeCP2 contributes to BDNF expressionEpigenetics, 2012
- Nicotinamide-induced MitophagyJournal of Biological Chemistry, 2012
- Autophagy failure in Alzheimer's disease—locating the primary defectNeurobiology of Disease, 2011
- Twenty Years of the Alzheimer’s Disease Amyloid Hypothesis: A Genetic PerspectiveCell, 2005