profile was also found in MS lesions190. These studies suggest that therapeutic targeting of OL survival would need to also take into account the potential for ensuing poor quality remyelination. Revealing the mechanisms underpinning surviving OL-mediated remyelination, and how this can be improved, is key in harnessing the regenerative potential of these cells. This may be particularly important if drugs promoting OPC differentiation lead to eventual depletion of the progenitor pool, and considering that aged OPCs have decreased capacity to mature and remyelinate, and are less responsive to pro-remyelinating drugs101.
