Oxidative stress and cellular pathologies in Parkinson’s disease

Molecular Brain

Sun Young Chung¹  Jae-won Shim²  Lesly Puspita² 

[1] Center for Stem Cell Biology, Sloan-Kettering Institute;Soonchunhyang Institute of Medi-bio Science (SIMS), Soonchunhyang University;

关键词: Alpha-synuclein;    Dopamine neurons;    Mitochondria;    Oxidative stress;    Parkinson’s disease;    Reactive oxygen species;   

DOI  :  10.1186/s13041-017-0340-9

来源: DOAJ

【 摘 要 】

Abstract 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, α-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.

【 授权许可】

Unknown