Abstract
A comprehensive strategy for the future management of multiple sclerosis will involve limiting the inflammatory process and repairing the damage. Monoclonal antibody therapy offers one means for achieving very rapid and substantial antiinflammatory effects, but the presently available reagents will almost certainly not prove to be definitive. Other candidates in the cascade of events that leads to myelin destruction will need to be considered, including TNF-alpha and other cytokines. But for the large number of individuals who are currently disabled, the more ambitious but realizable approach of glial repair holds the best hope for reversing persistent disabilities, transferring the technology and discoveries of contemporary experimental cellular neurobiology to the clinic.