J Neuroimmunol. 2003 Jun;139(1-2):9-16
Halfpenny CA, Scolding NJ.
Institute of Clinical Neurosciences, University of Bristol, Bristol, UK
Limited intrinsic myelin repair occurs in multiple sclerosis (MS), mediated by oligodendrocyte progenitors that divide and migrate into demyelinated lesions.
Experimental remyelination suggests that this repair restores function and may protect axons from subsequent degeneration.Immunomodulatory drugs such as corticosteroids, interferon-beta and azathioprine are widely used in MS.
However, their influence on disease progression is modest, for reasons that are not fully explained.
The direct effects of these drugs on remyelination biology remain relatively unexplored.We have investigated the effect of these MS therapies on oligodendrocyte progenitors to identify whether drug treatment might directly compromise repair, either therapeutic or spontaneous.
None of these drugs affected CG-4 survival, migration or proliferation.