Redox Redux in Alzheimer's Disease

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Science  03 Apr 2009:
Vol. 324, Issue 5923, pp. 11
DOI: 10.1126/science.324.5923.11e

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. (p. 102) describe a critical nitrosylation event induced by nitrosative stress in the pathogenesis of sporadic cases of Alzheimer's disease. Dynamin-related protein 1 (Drp1), which is known to be important for mitochondrial fission, is activated by S-nitrosylation, a redox reaction of NO with a critical cysteine thiol. The nitrosylation event is triggered by oligomerized amyloid-β peptide and appears to mediate the synaptic damage known to occur early in Alzheimer's disease. Thus, the pathogenesis of Alzheimer's disease involves a redox component, which may help to explain why redox metals can contribute to neuronal damage in Alzheimer's disease.

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