Multiple Sclerosis 15 June 2004, vol. 10, no. Supplement 1, pp. 81-89(9)
Kreitman R.R.; Blanchette F.
 Teva Neuroscience, North Wales, PA, USA
 Teva Neuroscience, Montréal, Québec, Canada
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.
Neuroprotection 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 GA in MS.