Limiting and repairing the damage in multiple sclerosis.
Inflammation of the brain depends upon migration of activated lymphocytes across the blood brain barrier bringing to the abluminal surface of cerebral blood vessels a variety of cellular and soluble immune mediators. Treatments which reduce the availability of circulating lymphocytes or limit their entry into the nervous system influence human and experimental inflammatory brain disease. The knowledge that inflammatory processes in the brain culminate in contact between microglia and the oligodendrocyte-myelin unit, which is damaged by local release of tumour necrosis factor, provides additional opportunities for treatment. In these diseases, disability results both from the inflammatory process and the failure of precursor cells to enter the lesions, differentiate and remyelinate the naked axons. The probability for the future is that a combination of manoeuvres involving limitation of the inflammatory process, increased availability of glial progenitors and re-establishment of their developmental growth factor environment will be needed to repair demyelinated lesions.
Compston
A
A
University of Cambridge Clinical School, United Kingdom.
D001369:Axons / Q000378:metabolism; D001812:Blood-Brain Barrier; D001921:Brain / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000378:metabolism; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000628:therapy*; D009416:Nerve Regeneration; D009457:Neuroglia / Q000378:metabolism; D009836:Oligodendroglia / Q000378:metabolism; D013234:Stem Cells / Q000378:metabolism