ArticleNeurotoxicity research2017
Treadmill Exercise Attenuates α-Synuclein Levels by Promoting Mitochondrial Function and Autophagy Possibly via SIRT1 in the Chronic MPTP/P-Induced Mouse Model of Parkinson's Disease.
Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers, 2 of them syntheses that pooled it.
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Who cites it
38 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- Effects of exercise on α-synuclein in rodent models of Parkinson's disease: a systematic review and meta-analysis.Experimental brain research · 2026Pooled it
- Dance movement therapy for neurodegenerative diseases: A systematic review.Frontiers in aging neuroscience · 2022Pooled it
- Targeting GPCR Signaling in Parkinson's Disease: From Molecular Pathology to Exercise-Based Therapeutics.Molecular neurobiology · 2026Review
- Exercise Intervention for REM Sleep Behavior Disorder in Parkinson's Disease: Mechanisms and Implications for Neurorehabilitation.CNS neuroscience & therapeutics · 2026Review
- Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Exercise suppresses apoptosis for alleviating Parkinson's disease: effects on pathophysiological molecular pathways.Frontiers in aging neuroscience · 2026Review
- Molecular mechanisms of exercise-induced neuroprotection against Parkinson's disease.Sports medicine and health science · 2026Review
- Identification of the mitochondria-related genePeerJ · 2026Article
- Therapeutic applications of exercise in neurodegenerative diseases: focusing on the mechanism of SIRT1.Molecular and cellular biochemistry · 2025Review
- Aerobic exercise-induced changes in fluid biomarkers in Parkinson's disease.NPJ Parkinson's disease · 2025Review
- Exercise Ameliorates Dysregulated Mitochondrial Fission, Mitochondrial Respiration, and Neuronal Apoptosis in Parkinson's Disease Mice via the Irisin/AMPK/SIRT1 Pathway.Molecular neurobiology · 2025Article
- Voluntary exercise alleviates neural functional deficits in Parkinson's disease mice by inhibiting microglial ferroptosis via SLC7A11/ALOX12 axis.NPJ Parkinson's disease · 2025Article
- Exercise regulates mitophagy to alleviate parkinsonian neurodegeneration.Frontiers in aging neuroscience · 2025Review
- Integrative effects of saffron and physical activity on endurance performance, quality of life, cognitive, emotional, and metabolic outcomes in age-related and neurodegenerative diseases.Frontiers in nutrition · 2025Review
- The interplay between physical exercise and autophagy signaling in brain health, neurodegenerative diseases and aging.Frontiers in aging neuroscience · 2025Review
- Atractylenolide-I Attenuates MPTP/MPPNeurochemical research · 2024Article
- Physical activity and sleep pattern in relation to incident Parkinson's disease: a cohort study.The international journal of behavioral nutrition and physical activity · 2024Article
- What Can Inflammation Tell Us about Therapeutic Strategies for Parkinson's Disease?International journal of molecular sciences · 2024Review
- Molecular mechanisms underlying the neuroprotection of environmental enrichment in Parkinson's disease.Neural regeneration research · 2023Review
- Sirtuins at the Crossroads between Mitochondrial Quality Control and Neurodegenerative Diseases: Structure, Regulation, Modifications, and Modulators.Aging and disease · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Accumulation of alpha-synuclein (α-Syn) is significantly correlated with the presence of progressive motor deficits, which is the main symptom of Parkinson's disease (PD). Although physical exercise reduces α-Syn levels, the molecular mechanisms by which physical exercise decreases α-Syn remain unclear. We hypothesized that treadmill exercise (TE) decreases α-Syn levels by improving mitochondrial function and promoting autophagy via the sirtuin-1 (SIRT1) signaling pathway in the chronic 1-methyl-1,2,3,6-tetrahydropyridine with probenecid (MPTP/P)-induced mouse model of PD. We found that TE reduces α-Syn levels, which subsequently ameliorates dopaminergic (DAergic) neuron loss and α-Syn-mediated apoptotic cell death. Most importantly, TE increases SIRT1 expression, which results in increased mitochondrial biogenesis and decreased oxidative stress by activating peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α). SIRT1 activation by TE also promotes autophagic clearance of α-Syn by inducing the activation of microtubule-associated protein 1 light chain 3 (LC3). Collectively, our results demonstrate that TE may reduce α-Syn levels by improving mitochondrial function and increasing autophagic flux, thereby ameliorating chronic MPTP/P-induced motor deficits in PD mice.
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