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Proteomics of a conundrum: Thoughts on addressing the aetiology versus progression of multiple sclerosis
Author(s) -
Partridge Melissa A.,
Myers Simon J.,
Gopinath Sumana,
Coorssen Jens R.
Publication year - 2015
Publication title -
proteomics – clinical applications
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.948
H-Index - 54
eISSN - 1862-8354
pISSN - 1862-8346
DOI - 10.1002/prca.201400141
Subject(s) - multiple sclerosis , disease , oligodendrocyte , neuroscience , degeneration (medical) , autoimmune disease , etiology , autoimmunity , experimental autoimmune encephalomyelitis , medicine , immune system , immunology , bioinformatics , biology , pathology , central nervous system , myelin
Currently in the field of multiple sclerosis (MS) research there is an ongoing debate concerning the cause of the disease. MS is widely considered to begin with an autoimmune dysregulation. The disease does have a prominent autoimmune component however this may be representative of a secondary effect. There is growing evidence that the disease may be initiated by an underlying degeneration of oligodendrocytes. In our viewpoint, we discuss the potential differences between the aetiology and progression of MS. For the most part, proteomic analysis has focused on the autoimmune component of the disease. We suggest that proteomic analysis should be applied to investigating oligodendrocyte degeneration. We discuss the potential of the cuprizone animal model of demyelination and its usefulness in understanding oligodendrocyte degeneration. Immune suppressive therapies are effective at reducing clinical symptoms and improving quality of life. However, a cure is still lacking and as such the disease does still progress. We suggest that if the initiating cause is poorly understood, then curing MS is unlikely.