Following injury to the central nervous system, functional loss is exacerbated by spreading damage causing secondary degeneration of surrounding tissue. Using a model of secondary degeneration where the optic nerve is partially transected, has allowed demonstration of oxidative stress and myelin abnormalities in nerve vulnerable to spreading damage. Therapeutic strategies designed to reduce oxidative stress and dysmyelination, including combination of calcium channel inhibitors, prevent the functional loss of secondary degeneration in this model.
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