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• W1983644479 abstract "The mechanisms of axonal and neuronal degeneration causing disability in optic neuritis and multiple sclerosis are poorly understood. Here we describe the role of mitochondria, oxidative stress and the effects of modulating antioxidant gene expression in the optic nerves of mice induced with experimental autoimmune encephalomyelitis, with a focus on long-term neuroprotection. Oxidative injury to the mitochondrion began prior to inflammatory cell infiltration and continued. It affected subunits of the respiratory chain, glycolysis and a chaperone critical to the stabilization and import of proteins. Oxidative products were associated with loss of membrane potential, mitochondrial degeneration and severe axonal loss. Reductions in ATP synthesis were even greater than those associated with mitochondrial diseases. Increasing SOD2 levels by viral mediated gene transfer rescued ATP synthesis, suppressed myelin fiber injury and increased retinal ganglion cell survival 1 year later." @default.
• W1983644479 created "2016-06-24" @default.
• W1983644479 creator A5086342594 @default.
• W1983644479 date "2008-01-01" @default.
• W1983644479 modified "2023-09-26" @default.
• W1983644479 title "Optic Nerve Degeneration in Experimental Autoimmune Encephalomyelitis" @default.
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• W1983644479 doi "https://doi.org/10.1159/000119879" @default.
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