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Abstract #0922

The Role of SOD2 in a Mouse Model of Multiple Sclerosis

Taeko Inoue1, Tabassum Majid2, Ann Quick1, Christine Beeton1, 2, Robia G. Pautler1, 2

1Molecular Physiology & Biophysics, Baylor College of Medicine, Houston, TX, United States; 2Translational Biology & Molecular Medicine, Baylor College of Medicine, Houston, TX, United States

Multiple Sclerosis (MS) is a demyelinating disease of the Central Nervous System. It is slow progressing and ultimately results in debilitation of afflicted individuals. It is characterized by periods of relapse and remission of neurological symptoms that include decreased vision, muscle weakness and coordination loss. The etiology of MS is currently unknown, however, it is understood that autoimmune mechanisms involving elevations in reactive oxygen species are involved in the development of lesions. As a result, we hypothesized that lowering of ROS by overexpressing an antioxidant, superoxide dismutase-2 in an EAE model of MS would result in decreased EAE phenotype.