期刊
MOLECULAR BRAIN
卷 10, 期 -, 页码 -出版社
BMC
DOI: 10.1186/s13041-017-0340-9
关键词
Alpha-synuclein; Dopamine neurons; Mitochondria; Oxidative stress; Parkinson's disease; Reactive oxygen species; Unfolded protein response
资金
- National Research Foundation of Korea (NRF) [NRF-2017M3A9B4062415, NRF-2017R1A2B4003018, NRF-2016K1A4A3914725]
- International Science and Business Belt Program - Korea government (MSIP) [2015 K000278]
- National Research Foundation of Korea [2016K1A4A3914725, 2016K000293, 2017M3A9B4062415] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Parkinson's disease (PD) is a chronic and progressive neurodegeneration of dopamine neurons in the substantia nigra. The reason for the death of these neurons is unclear; however, studies have demonstrated the potential involvement of mitochondria, endoplasmic reticulum, alpha-synuclein or dopamine levels in contributing to cellular oxidative stress as well as PD symptoms. Even though those papers had separately described the individual roles of each element leading to neurodegeneration, recent publications suggest that neurodegeneration is the product of various cellular interactions. This review discusses the role of oxidative stress in mediating separate pathological events that together, ultimately result in cell death in PD. Understanding the multi-faceted relationships between these events, with oxidative stress as a common denominator underlying these processes, is needed for developing better therapeutic strategies.
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