Mechanisms and Therapeutic Strategies for Central and Peripheral Remyelination

Myelin sheaths are produced by myelinating glia and provide metabolic support to neuronal axons while accelerating electrical signal conduction. Myelinating glia, which include oligodendrocytes in the central nervous system (CNS) and Schwann cells in the peripheral nervous system (PNS), have distinct developmental origins and biological characteristics that profoundly influence their capacity for myelin regeneration following demyelinating insults. In various demyelinating diseases, loss of myelin and myelinating glia resulting from autoimmune disorders, inflammation, or genetic defects causes neurological dysfunction. Beyond removing disease-causing factors, inducing and accelerating remyelination represents a critical therapeutic goal for demyelinating diseases. In this review, we first summarize and compare molecular mechanisms underlying CNS and PNS remyelination, including extracellular signaling pathways, transcriptional regulation, and intercellular communication. We then highlight current treatments and ongoing clinical trials for common demyelination disorders, including neonatal white matter injury, multiple sclerosis, and inherited peripheral neuropathies.