| Literature DB >> 33546471 |
JunHyuk Woo1,2, Hyesun Cho1, YunHee Seol1, Soon Ho Kim1, Chanhyeok Park1, Ali Yousefian-Jazi1, Seung Jae Hyeon1, Junghee Lee3,4, Hoon Ryu1,3.
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.Entities:
Keywords: Alzheimer’s disease; Huntington’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; antioxidants; computational modeling; mitochondria; oxidative stress
Year: 2021 PMID: 33546471 PMCID: PMC7913624 DOI: 10.3390/antiox10020229
Source DB: PubMed Journal: Antioxidants (Basel) ISSN: 2076-3921