Power failure of mitochondria and oxidative stress in neurodegeneration and its computational models

Junhyuk Woo, Hyesun Cho, Yunhee Seol, Soon Ho Kim, Chanhyeok Park, Ali Yousefian-Jazi, Seung Jae Hyeon, Junghee Lee, Hoon Ryu

Research output: Contribution to journalReview articlepeer-review

17 Scopus citations

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 neurodegen-eration. 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.

Original languageEnglish
Article number229
Pages (from-to)1-19
Number of pages19
JournalAntioxidants
Volume10
Issue number2
DOIs
StatePublished - Feb 2021
Externally publishedYes

Bibliographical note

Funding Information:
Funding: This study was supported by the National Research Foundation (NRF) grant (NRF-2016M3C7A1904233, NRF-2018M3C7A1056894, and NRF-2020M3E5D9079742), the National Research Council of Science & Technology (NST) grant (No. CRC-15-04-KIST) from the Korea Ministry of Science, ICT and Future Planning (MSIP), and the grant (2E30954 and 2E30762) from Korea Institute of Science and Technology of South Korea. This study was also supported by NIH Grants (R01AG054156 to H.R. and R01NS109537 to J.L.).

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.

Keywords

  • Alzheimer’s disease
  • Amyotrophic lateral sclerosis
  • Antioxidants
  • Computational modeling
  • Huntington’s disease
  • Mitochondria
  • Oxidative stress
  • Parkinson’s disease

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