Multiple sclerosis: looking beyond autoimmunity

Bill Brayer of MS Helping Hands provided the following :

Intro:

The chronic incurable disorder multiple sclerosis (MS) is characterized by neurodegeneration, multifocal demyelination and astroglial proliferation (gliosis).² The prevalence of MS is influencedby geography and genetics. In the Western world it is a leading cause of neurological disability in the young. The cause and exact pathogenesis are still unknown. Some see MS as a T-cell-driven autoimmune inflammatory disease, targeting the myelin sheaths in the central nervous system,³ but there is no proof. Unlike autoimmune conditions such as rheumatoid arthritis, systemic lupus erythematosus or myasthenia gravis, MS has no specific immunological marker.^2,4

An animal model that has been used in MS research is experimental allergic encephalomyelitis (EAE), in which demyelination is induced by sensitization against myelin basic protein. Clinically and pathologically, however, EAE resembles acute disseminated encephalomyelitis (ADEM) rather than MS.² Nonetheless, the EAE model has been used to drive the autoimmune theory and to develop treatments. An inflammatory hypothesis of demyelination also fails to explain various salient features of the disease (Box 1).^5-7 Here, we explain our view that research and treatment strategy in MS need to change direction.

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