Power Failure of Mitochondria and Oxidative Stress in Neurodegeneration and Its Computational Models

Authors
Woo, JunHyukCho, HyesunSeol, YunHeeKim, Soon HoPark, ChanhyeokYousefian-Jazi, AliHyeon, Seung JaeLee, JungheeRyu, Hoon
Issue Date
2021-02
Publisher
MDPI
Citation
ANTIOXIDANTS, v.10, no.2
Abstract
The brain needs more energy than other organs in the body. Mitochondria are the generator of vital power in the living organism. Not only do mitochondria sense signals from the outside of a cell, but they also orchestrate the cascade of subcellular events by supplying adenosine-5 '-triphosphate (ATP), the biochemical energy. It is known that impaired mitochondrial function and oxidative stress contribute or lead to neuronal damage and degeneration of the brain. This mini-review focuses on addressing how mitochondrial dysfunction and oxidative stress are associated with the pathogenesis of neurodegenerative disorders including Alzheimer's disease, amyotrophic lateral sclerosis, Huntington's disease, and Parkinson's disease. In addition, we discuss state-of-the-art computational models of mitochondrial functions in relation to oxidative stress and neurodegeneration. Together, a better understanding of brain disease-specific mitochondrial dysfunction and oxidative stress can pave the way to developing antioxidant therapeutic strategies to ameliorate neuronal activity and prevent neurodegeneration.
Keywords
mitochondria; oxidative stress; antioxidants; Alzheimer’ s disease; amyotrophic lateral sclerosis; Huntington’ s disease; Parkinson’ s disease; computational modeling
ISSN
2076-3921
URI
https://pubs.kist.re.kr/handle/201004/117442
DOI
10.3390/antiox10020229
Appears in Collections:
KIST Article > 2021
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