Title |
Neuroprotective effect of treadmill exercise possibly via regulation of lysosomal degradation molecules in mice with pharmacologically induced Parkinson’s disease
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Published in |
The Journal of Physiological Sciences, December 2017
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DOI | 10.1007/s12576-017-0586-0 |
Pubmed ID | |
Authors |
Dong-Joo Hwang, Jung-Hoon Koo, Ki-Cheon Kwon, Dong-Hoon Choi, Sung-Deuk Shin, Jae-Hoon Jeong, Hyun-Seob Um, Joon-Yong Cho |
Abstract |
Dysfunction of mitophagy, which is a selective degradation of defective mitochondria for quality control, is known to be implicated in the pathogenesis of Parkinson's disease (PD). However, how treadmill exercise (TE) regulates mitophagy-related molecules in PD remains to be elucidated. Therefore, we aimed to investigate how TE regulates α-synuclein (α-syn)-induced neurotoxicity and mitophagy-related molecules in the nigro-striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mice. Our data showed that TE exhibited a significant restoration of tyrosine hydroxylase and motor coordination with suppression of α-syn expression, hallmarks of PD, possibly via up-regulation of lysosomal degradation molecules, LAMP-2 and cathepsin L, with down-regulation of p62, LC3-II/LC3-I ratio, PINK1 and parkin in the substantia nigra of MPTP mice. Therefore, these results suggest that treadmill exercise can be used as a non-invasive intervention to improve the pathological features and maintain a healthier mitochondrial network through appropriate elimination of defective mitochondria in PD. |
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Demographic breakdown
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Members of the public | 1 | 50% |
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Student > Doctoral Student | 4 | 11% |
Student > Ph. D. Student | 4 | 11% |
Researcher | 3 | 8% |
Student > Postgraduate | 2 | 5% |
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Sports and Recreations | 2 | 5% |
Other | 5 | 14% |
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