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Under neuroinflammatory conditions, dysfunctional mitochondria release ROS and damage-associated molecular patterns (DAMPs) (53), activating microglia and astrocytes, and triggering the release of pro-inflammatory cytokines and chemokines (54), thereby exacerbating the damage

Therefore, the problem that the agents successful in pre-clinical experimental autoimmune encephalitis trials, were either less effective in patients, worsened disease or caused unexpected, severe adverse events (60), may be at least partly solved with the more suited cuprizone model that reflects a toxic experimental model (12)

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Reducing severe disability from disease is key to minimizing health and social costs as the population increases