On the horizon: possible neuroprotective role for glatiramer acetate.
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 correlated with the long-term effect of GA in MS.
Kreitman
Rivka Riven
RR
Teva Neuroscience, 1090 Horsham Road, North Wales, PA 19454-1090, USA. rivka.kreitman@tevaneuro.com
Blanchette
François
F
D000276:Adjuvants, Immunologic / Q000627:therapeutic use*; D000068717:Glatiramer Acetate; D006801:Humans; D020528:Multiple Sclerosis, Chronic Progressive / Q000188:drug therapy*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010455:Peptides / Q000627:therapeutic use*
D000276:Adjuvants, Immunologic; D018696:Neuroprotective Agents; D010455:Peptides; D000068717:Glatiramer Acetate