In multiple sclerosis, conduction block in demyelinated axons underlies early neurological symptoms, whereas
axonal transection is believed to be responsible for more permanent later deficits. Approved treatments for the disease are
immunoregulatory and reduce the rate of lesion formation and clinical exacerbation, but are only partially effective in
preventing the onset of disability. Remyelination is a term for the re-generation of the nerve's myelin sheath and is a
subject of active medical research. Remyelination capacity varies from patient to patient or even from lesion to lesion in
one and the same patient. Efforts to understand the causes for remyelination failure have prompted research into the
biology of remyelination and the complex molecular factors that regulate remyelination.
In the current review article we address challenges of remyelination research with a special focus on histo-pathological
studies using brain biopsy and autopsy material. We summarize our current knowledge about extent of remyelination in
multiple sclerosis patients and its relation to disease duration, lesion type, inflammation, affected brain region and gender.
Furthermore we will address which step(s) of the oligodendrocyte maturation program is impaired and, thus, could be a
feasible target for therapeutic interventions. Specifically mentioned will be the distribution of oligodendrocyte progenitor
cells in demyelinated multiple sclerosis plaques and therapeutic approaches which aim to boost intrinsic properties of
progenitor cells or to supply progenitors by cell transplantation approaches. This comprehensive overview is
complemented by recent findings suggesting that U.S. Food and Drug Administration-approved treatment options, such as
FTY720 (Gilenya®) or glatiramer acetate (Copaxone®) might boost myelin repair.