Spontaneous remyelination and repair mechanisms in multiple sclerosis are mostly insufficient and contribute to clinical disability. Treatments improving these processes are not yet available but basic research in animal models has led to the proposal of several repair strategies. These include enhancement of the naturally occurring mechanisms, remyelination due to a change of the immune response, and transfer of myelinating cells. Despite the encouraging experimental findings and the constantly increasing knowledge of the molecular mechanisms of remyelination and remyelination failure, there remain many questions before this knowledge can be successfully translated into clinical trials.