Epigenetic mechanisms in pathogenesis of multiple sclerosis

Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system with immune induced myelin destruction followed by multifocal demyelination of the nervous tissues.1 MS is the most widely spread among the human diseases characterized by myelin destruction .2 Until now both the etiology and pathogenesis of MS have to a large extent remained unclear. Substantial efforts have been made over the last decades to identify biomarkers for MS that can identify disease diagnosis, predict disease progression, and improve clinical outcomes. Degenerative and inflammatory changes in the nervous tissue in MS are characterized by a multiple fibrosis of neuron myelin sheath accompanied by the formation of sclerotic plaques and axon pathology resulting in progressive neurological dysfunction.3,4 Based on the pathomorphological aspects of the disease, French neurologist Dr. Jean-Martin Charcot was the first to recognize MS as a distinct disease in the end of the 19th century. He described the clusters of inflammatory cells in the perivascular space in the brain and spinal cord in patients with intermittent neurological disorders.5