التفاصيل البيبلوغرافية
| العنوان: |
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. |
| المؤلفون: |
Koo, Jung-Hoon, Cho, Joon-Yong1 chojy86@knsu.ac.kr |
| المصدر: |
Neurotoxicity Research. Oct2017, Vol. 32 Issue 3, p473-486. 14p. |
| مصطلحات موضوعية: |
*TREADMILL exercise, *PARKINSON'S disease diagnosis, *PARKINSON'S disease treatment, *ELLIPTICAL trainers, *PHYSICAL activity, *AUTOPHAGY, *LABORATORY mice, *MICE behavior |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
| قاعدة البيانات: |
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