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Anodal transcranial direct current stimulation prevents methyl-4phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurotoxicity by modulating autophagy in an in vivo mouse model of Parkinson's diseaseopen access

Authors
Lee, Sang-BinKim, Hee-TaeYang, Hyun OkJang, Wooyoung
Issue Date
Oct-2018
Publisher
NATURE PUBLISHING GROUP
Citation
SCIENTIFIC REPORTS, v.8, pp.1 - 9
Indexed
SCIE
SCOPUS
Journal Title
SCIENTIFIC REPORTS
Volume
8
Start Page
1
End Page
9
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/149285
DOI
10.1038/s41598-018-33515-7
ISSN
2045-2322
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the accumulation of protein inclusions and the loss of dopaminergic neurons. Transcranial direct current stimulation (tDCS) is a non-invasive brain-stimulating technique that has demonstrated promising results in clinical studies of PD. Despite accumulating evidence indicating that tDCS exerts a protective effect, the mechanism underlying its activity remains unknown. In the present study, we first investigated the neuroprotective effect of tDCS in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model and then evaluated the effect of tDCS on the autophagy pathway. tDCS improved behavioral alterations, increased tyrosine hydroxylase protein levels and suppressed alpha-synuclein protein levels in MPTP-treated mice. MPTP-treated mice subjected to tDCS also had lower levels of autophagy-related proteins, such as microtubule-associated protein 1 light chain 3 and AMP-activated protein kinase, and higher levels of mechanistic target of rapamycin and p62. In addition, the protein levels of phosphoinositide 3-kinase and brain-derived neurotrophic factor were higher, and the levels of unc51-like kinase 1 were lower in MPTP-treated mice subjected to tDCS. Our findings suggest that tDCS protected against MPTP-induced PD in a mouse model by modulating autophagy.
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