Functional and Celluar Assessment of Limited Remyelination in the Cuprizone Model

Abstract : The promotion of remyelination after chronic or prolonged episodes of demyelination is an important therapeutic goal for demyelinating diseases. The leading cause of demyelination in humans is multiple sclerosis (MS). This thesis work focused on a mouse model of MS to examine cellular and molecular mechanisms that may cause limited remyelination after chronic demyelination. Cuprizone, a neurotoxicant, was used to induce experimental demyelination. This model mimics the effects of acute and chronic time courses of demyelinating disease progression.