Abstract:

Multiple sclerosis (MS) is progressive inflammatory, and chronic demyelinating, neurodegenerative disease of central nervous system (CNS). Autoimmune responses to myelin and other CNS antigens mediated by CD4+ T cells are critical for initiation and progression of disease.Migration of autoimmune T cells from the peripheral lymph organs into CNS parenchyma leads to inflammation, demyelination and damage of axonal cytoskeleton, which manifest indecreased impulse conduction velocity of motor and sensory nerves. Myelin and axonal pathology causes motor, sensory and autonomic nerve dysfunction, including paresis and paralysis of extremities, painful sensations, and bladder sphincter dysfunction, manifested as incontinence. Gray matter pathology in cortical and subcortical regions, including cerebellum and hippocampus underlies cognitive and behavioral dysfunctioncomprisingof among other, memory deficits, depression, and ataxic gait. Multifaceted cellular and molecular mechanisms involved in autoimmune – mediated inflammation, demyelination, and subsequent degeneration of axonal cytoskeleton as well asneuronal cell dysfunction and demise, have been researched in experimental autoimmune encephalomyelitis (EAE). With the development of new EAE models, significance of EAE in MS studies continues to be reexamined and the importance of similarity between two diseases to be highlighted. This autoimmune experimental model is regularly used in development and preclinical testing of MS therapy aimed at treating or ameliorating autoimmune responses observed in MS, with an ultimate goal to cure or diminish tissue damage and support axonal regeneration and repair.