ABSTRACT
Multiple sclerosis (MS) is a disease of the central nervous system (CNS) characterized by multifocal inflammation, demyelination, and axonal injury. The exact etiological factors or agents causing MS remain a mystery, although polygenic determinants and exposure to an unknown environmental trigger are likely. One class of potential environmental triggers is an antigen of viral or bacterial origin. Small peptide fragments of microbial components, with amino acid sequences similar to antigenic segments of myelin proteins, could induce a cross-reactive immune attack on the self by a process of molecular mimicry.[1]
Important insights into the mechanisms of immune-mediated myelin damage have come from animal models. For example, immunizing an animal to antigenic myelin components or peptide fragments can trigger experimental allergic encephalomyelitis (EAE), a form of CNS demyelination. Effective antigens in EAE induction include the major myelin proteins, myelin basic protein (MBP), proteolipid protein (PLP), and myelin oligodendrocyte glycoprotein (MOG). It is known that patients with MS and normal subjects have potentially autoreactive T cells that are specific to these myelin antigens in their peripheral circulation.[2-7]
The possibility that MS at certain stages is driven by similar immune mechanisms has led to extensive studies of antigen specific immune-modulating strategies. Recent recognition that axonal injury and axonal transection occurs early in MS and may correlate with permanent neurological deficits has provided additional motivation to find more effective treatments to slow or halt the disease process.[8]
When the Food and Drug Administration (FDA) in the USA approved copolymer 1 for relapsing-remitting MS in 1997, the generic name, glatiramer acetate (GA), was created. The trademark name of the drug is Copaxone®. This unique, synthetic copolymer drug has a long and interesting history leading to its use as a therapeutic agent for MS.
