Abstract
In this study we examined the role of fumaric acid esters (FAE) in a spontaneous and chronic animal model, the opticospinal EAE (OSE). Preventive treatment of dimethylfumarate (DMF) promotes onset of disease in animals treated with high dose DMF. This group also exhibited a significantly exacerbated disease course in a therapeutic treatment as compared to the low dose DMF approach, where less demyelination, macrophage infiltration, and increased Nrf2 expression in the spinal cord were observed. We conclude that low dose DMF treatment is effective in the therapy of the spontaneous opticospinal EAE model and mediates neuroprotective effects via the oxidative stress response pathway.
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