Autoimmunity to Neuronal Antigens in Multiple Sclerosis

Multiple sclerosis (MS), first identified as a separate neurological disease by the French neurologist Jean-Martin Charcot (Charcot, 1868), is the most common disease of the central nervous system (CNS) in young adults. Affecting more than 2 million people worldwide, MS classically starts with visual problems and tingling sensations and in many patients develops into permanent disability frequently involving paralysis and spasticity (Matthews, 1985). Cognitive functions such as memory, attention and visuospacial abilities are frequently impaired, while language skills are preserved (Bobholz and Rao, 2003). Neuropathological or radiological examination of MS patients reveals the presence of sclerotic lesions or plaques, typically located in the periventricular white matter. Other preferential sites for lesions include the optic nerve, brainstem, cerebellum, and the (cervical) spinal cord. The grey matter may also be affected especially in secondary progressive disease (Vercellino et al., 2005). The lesions are sites of extensive demyelination, inflammation and axonal degeneration. The immunemediated removal of myelin sheaths results in an impaired or complete loss of axonal conduction, subsequently leading to neurological dysfunction. Adaptive mechanisms, like a redistribution of sodium channels (Waxman et al., 2004) or remyelination, may result in restoration of nerve conduction and resolution of clinical symptoms.

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