Oligodendrocytes are the myelinating cells of the central nervous system, functioning to accelerate neurotransmission and provide trophic support to the axon. In response to the pathological loss of oligodendrocytes, myelin sheaths can be replaced by oligodendrocyte progenitor cells (OPCs), in a process called remyelination. The failure of remyelination in demyelinating diseases is caused by the inability of OPCs to differentiate into mature oligodendrocytes. In the mouse embryonic forebrain OPCs are generated in spatiotemporal waves, with ventral OPCs emerging prior to dorsal OPCs. As ventral and dorsal OPCs possess differing potential to contribute to remyelination in the adult murine corpus callosum, identify the underlying molecular mechanisms of the different remyelination efficiencies of the developmentally heterogeneous OPC populations in disease may reveal general important mediators of remyelination as well as potential therapeutic targets for the enhancement of remyelination.
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