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

期刊

ANTIOXIDANTS
卷 10, 期 2, 页码 -

出版社

MDPI
DOI: 10.3390/antiox10020229

关键词

mitochondria; oxidative stress; antioxidants; Alzheimer’ s disease; amyotrophic lateral sclerosis; Huntington’ s disease; Parkinson’ s disease; computational modeling

资金

  1. National Research Foundation (NRF) [NRF-2016M3C7A1904233, NRF-2018M3C7A1056894, NRF-2020M3E5D9079742]
  2. National Research Council of Science & Technology (NST) grant from the Korea Ministry of Science, ICT and Future Planning (MSIP) [CRC-15-04-KIST]
  3. Korea Institute of Science and Technology of South Korea [2E30954, 2E30762]
  4. NIH [R01AG054156, R01NS109537]

向作者/读者索取更多资源

The brain requires a significant amount of energy, with mitochondria serving as the energy generator within cells and playing a crucial role in the pathogenesis of neurodegenerative disorders.
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.

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