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Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases

Nature volume 443, pages 787–795 (2006)Cite this article

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.

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Figure 1: Role of mitochondria in apoptosis and ageing.
Figure 2: Role of mitochondria in reactive oxygen species metabolism.
Figure 3: The role of mitochondria in ageing-related neurodegenerative diseases.

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Acknowledgements

This work was supported by grants from the National Institutes of Health and the American Federation for Aging Research/Beeson Program. We apologize to our many colleagues whose work we were unable to cite due to space limitations.

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  1. Department of Neurology and Neuroscience, Weill Medical College of Cornell University, Room F-610, 525 East 68th Street, New York, 10021, USA

    Michael T. Lin & M. Flint Beal

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Lin, M., Beal, M. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 443, 787–795 (2006). https://doi.org/10.1038/nature05292

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