Int J Dev Neurosci, 2007 · DOI: 10.1016/j.ijdevneu.2007.02.002 · Published: May 1, 2007
Demyelination, the loss of the myelin sheath around nerve fibers, is associated with neurological disorders like multiple sclerosis (MS), spinal cord injury, and nerve compression. MS lesions often involve axon loss, making remyelination and neuroprotection key therapeutic goals. Experimental cellular transplantation has shown promise in animal models by remyelinating axons and improving functional outcomes. This involves using different myelin-forming cell types to repair damaged areas. Understanding these models and cell-based strategies offers opportunities to develop clinical studies for remyelination and neuroprotection in humans suffering from demyelinating diseases.
Cell-based therapies hold promise for treating demyelinating diseases like MS and spinal cord injury, but further research is needed to optimize cell types, delivery methods, and long-term efficacy.
Understanding the mechanisms of endogenous myelin repair and how to stimulate endogenous progenitors could lead to new pharmacological approaches for promoting remyelination.
Since axonopathy is common in MS lesions, cellular transplantation strategies should also aim to protect axons from further damage and promote axonal regeneration.