AbstractPurpose of review
The development of successful myelin repair strategies depends on the detailed knowledge of the cellular and molecular processes underlying demyelination and remyelination in the central nervous system of animal models and in patients with multiple sclerosis (MS). Based on the complexity of the demyelination and remyelination processes, it should be expected that effective therapeutic approaches will require a combination of strategies for immunomodulation, neuroprotection, and myelin replacement. This brief review highlights recent cellular and molecular findings and indicates that future therapeutic strategies to enhance remyelination may also require combinatorial treatment to accomplish.Recent findings
The relapsing–remitting course of some forms of multiple sclerosis has typically fueled hope for effective repair of multiple sclerosis lesions, if demyelinating activity could be attenuated. Recent findings support the potential of endogenous neural stem cells and progenitor cells to generate remyelinating oligodendrocytes. Importantly, interactions with viable axons and supportive astrocytic responses are required for endogenous immature cells to fulfill their potential remyelinating capacity.Summary
The research described here will help in identifying the major obstacles to effective remyelination and potential therapeutic targets to guide development of comprehensive approaches for testing in animal models and eventual treatment of patients with multiple sclerosis.