Inflammation and neurodegeneration characterize the pathogenesis of multiple
sclerosis (MS). Slow axonal degeneration, rather than acute inflammation, is
considered the cause of chronic disability in MS. The signs of acute axonal damage
and loss have been shown to occur early in the lesion development of patients with
chronic MS and often correlate with demyelination and inflammation. While immune
activity in the central nervous system has traditionally been considered to be a
detrimental event in MS, recent studies have found that autoimmune T cells may play
an important role in protecting neurons from the ongoing spreading damage.
Neuroprotectio n in MS is a new and evolving concept, and many questions remain with
regard to potential targets for therapeutic intervention. Preliminary studies, both
in animals and in humans, have suggested that glatiramer acetate (GA) may confer
neuroprotective activity in addition to bystander suppression. Additional research
is needed to determine if these promising neuroprotective effects correlate with the
long-term effect of G A in MS.
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