Although Charcot and others described many of the clinical and histopathologic features of multiple sclerosis (MS) as early as the 1860s, it was not until the end of the 20th century that immunomodulators emerged as potential disease-modifying therapies for MS. Recent research has increasingly demonstrated the importance of neurodegeneration at even the earliest stages of MS, which has prompted the focus on developing new neuroprotective therapies. Considerable evidence suggests that the clinical signs and symptoms of MS are the result of interactions between 2 distinct physiologic processes. Transient relapses are thought to reflect periods of acute central nervous system (CNS) inflammation, which become less frequent over time. Progressive disability is believed to reflect the gradual loss of CNS axons, which may begin even at the earliest stages of the disease. Studies of patients with MS have used magnetic resonance spectroscopy to reveal subtle and progressing abnormalities of CNS axons over time, even in patients without new T2 lesions or clinical relapses. These observations imply that neuroprotective therapies should be instituted as soon as possible after the diagnosis of MS in order to produce the greatest possible reduction in longterm disability. Some research suggests that glatiramer acetate may produce neuroprotective effects within the CNS, possibly by stimulating the release of neurotrophic factors from T lymphocytes or other cell populations. Interferon ß may also produce neuroprotective effects in patients with MS, possibly as a result of suppressing inflammation. Several new neuroprotective therapies are now in development for the treatment of MS, and these agents are likely to significantly expand the number of options for MS care during the next few years.
|Original language||English (US)|
|Number of pages||6|
|Journal||Johns Hopkins Advanced Studies in Medicine|
|State||Published - Jul 1 2009|
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