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Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases

Author

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  • Michael T. Lin

    (Weill Medical College of Cornell University)

  • M. Flint Beal

    (Weill Medical College of Cornell University)

Abstract

Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.

Suggested Citation

  • Michael T. Lin & M. Flint Beal, 2006. "Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases," Nature, Nature, vol. 443(7113), pages 787-795, October.
  • Handle: RePEc:nat:nature:v:443:y:2006:i:7113:d:10.1038_nature05292
    DOI: 10.1038/nature05292
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    13. Ying Shao & Zhongli Chen & Lingling Wu, 2019. "Oxidative Stress Effects of Soluble Sulfide on Human Hepatocyte Cell Line LO2," IJERPH, MDPI, vol. 16(9), pages 1-11, May.
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