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Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models

Title
Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models
Author(s)
Cho, BongkiKim, TaeyunHuh, Yu-JinLee, JaeminLee, Yun-Il
Issued Date
2019-10
Citation
International Journal of Molecular Sciences, v.20, no.20, pp.5208
Type
Article
Author Keywords
Parkinson's disease (PD)mitochondrial dysfunctiondynamicshormesisproteostasisubiquitin-proteasome system (UPS)autophagymitophagynatural compounds
Keywords
ALPHA-SYNUCLEIN AGGREGATIONPROTECTS DOPAMINERGIC-NEURONSUBIQUITIN-PROTEASOME SYSTEMNEUROBLASTOMA SH-SY5Y CELLSMPTP-INDUCED PARKINSONISMINDUCED OXIDATIVE STRESSMPP+-INDUCED APOPTOSISINDUCED RAT MODELSUBSTANTIA-NIGRAMOUSE MODEL
ISSN
1661-6596
Abstract
Parkinson’s disease (PD) is a well-known age-related neurodegenerative disorder associated with longer lifespans and rapidly aging populations. The pathophysiological mechanism is a complex progress involving cellular damage such as mitochondrial dysfunction and protein homeostasis. Age-mediated degenerative neurological disorders can reduce the quality of life and also impose economic burdens. Currently, the common treatment is replacement with levodopa to address low dopamine levels; however, this does not halt the progression of PD and is associated with adverse effects, including dyskinesis. In addition, elderly patients can react negatively to treatment with synthetic neuroprotection agents. Recently, natural compounds such as phytochemicals with fewer side effects have been reported as candidate treatments of age-related neurodegenerative diseases. This review focuses on mitochondrial dysfunction, oxidative stress, hormesis, proteostasis, the ubiquitin-proteasome system, and autophagy (mitophagy) to explain the neuroprotective effects of using natural products as a therapeutic strategy. We also summarize the efforts to use natural extracts to develop novel pharmacological candidates for treatment of age-related PD. © 2019 by the authors. Licensee MDPI, Basel, Switzerland.
URI
http://hdl.handle.net/20.500.11750/10883
DOI
10.3390/ijms20205208
Publisher
Multidisciplinary Digital Publishing Institute (MDPI)
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Appears in Collections:
Division of Biotechnology 1. Journal Articles
Department of New Biology Aging, Metabolism and Physiology Lab 1. Journal Articles

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