Full metadata record
DC Field | Value | Language |
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dc.contributor.author | Cho, Bongki | - |
dc.contributor.author | Kim, Taeyun | - |
dc.contributor.author | Huh, Yu-Jin | - |
dc.contributor.author | Lee, Jaemin | - |
dc.contributor.author | Lee, Yun-Il | - |
dc.date.accessioned | 2019-11-07T13:16:07Z | - |
dc.date.available | 2019-11-07T13:16:07Z | - |
dc.date.created | 2019-11-06 | - |
dc.date.issued | 2019-10 | - |
dc.identifier.issn | 1661-6596 | - |
dc.identifier.uri | http://hdl.handle.net/20.500.11750/10883 | - |
dc.description.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. | - |
dc.language | English | - |
dc.publisher | Multidisciplinary Digital Publishing Institute (MDPI) | - |
dc.title | Amelioration of Mitochondrial Quality Control and Proteostasis by Natural Compounds in Parkinson’s Disease Models | - |
dc.type | Article | - |
dc.identifier.doi | 10.3390/ijms20205208 | - |
dc.identifier.scopusid | 2-s2.0-85073717654 | - |
dc.identifier.bibliographicCitation | International Journal of Molecular Sciences, v.20, no.20, pp.5208 | - |
dc.description.isOpenAccess | TRUE | - |
dc.subject.keywordAuthor | Parkinson's disease (PD) | - |
dc.subject.keywordAuthor | mitochondrial dysfunction | - |
dc.subject.keywordAuthor | dynamics | - |
dc.subject.keywordAuthor | hormesis | - |
dc.subject.keywordAuthor | proteostasis | - |
dc.subject.keywordAuthor | ubiquitin-proteasome system (UPS) | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordAuthor | mitophagy | - |
dc.subject.keywordAuthor | natural compounds | - |
dc.subject.keywordPlus | ALPHA-SYNUCLEIN AGGREGATION | - |
dc.subject.keywordPlus | PROTECTS DOPAMINERGIC-NEURONS | - |
dc.subject.keywordPlus | UBIQUITIN-PROTEASOME SYSTEM | - |
dc.subject.keywordPlus | NEUROBLASTOMA SH-SY5Y CELLS | - |
dc.subject.keywordPlus | MPTP-INDUCED PARKINSONISM | - |
dc.subject.keywordPlus | INDUCED OXIDATIVE STRESS | - |
dc.subject.keywordPlus | MPP+-INDUCED APOPTOSIS | - |
dc.subject.keywordPlus | INDUCED RAT MODEL | - |
dc.subject.keywordPlus | SUBSTANTIA-NIGRA | - |
dc.subject.keywordPlus | MOUSE MODEL | - |
dc.citation.number | 20 | - |
dc.citation.startPage | 5208 | - |
dc.citation.title | International Journal of Molecular Sciences | - |
dc.citation.volume | 20 | - |
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