Sci. Signal., 7 April 2009
Neuroscience Redox Redux in Alzheimers Disease
Stella M. Hurtley
Science, AAAS, Cambridge CB2 1LQ, UK
Neurodegenerative disorders involve a series of pathophysiological changes. Oxidative or nitrosative stress can induce a profound and abnormal degree of mitochondrial fission, leading to bioenergetic compromise, which may contribute to neurodegenerative disorders. Cho et al. describe a critical nitrosylation event induced by nitrosative stress in the pathogenesis of sporadic cases of Alzheimers disease. Dynamin-related protein 1 (Drp1), which is known to be important for mitochondrial fission, is activated by S-nitrosylation, a redox reaction of nitric oxide with a critical cysteine thiol. The nitrosylation event is triggered by oligomerized β-amyloid; peptide and appears to mediate the synaptic damage known to occur early in Alzheimers disease. Thus, the pathogenesis of Alzheimers disease involves a redox component, which may help to explain why redox metals can contribute to neuronal damage in Alzheimers disease.
D.-H. Cho, T. Nakamura, J. Fang, P. Cieplak, A. Godzik, Z. Gu, S. A. Lipton, S-nitrosylation of Drp1 mediates β-amyloid–related mitochondrial fission and neuronal injury. Science 324, 102–105 (2009). [Abstract] [Full Text]
Citation: S. M. Hurtley, Redox Redux in Alzheimers Disease. Sci. Signal. 2, ec124 (2009).
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