This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Multiple Sclerosis (MS) is a chronic and potentially highly disabling disorder with considerable social impact and economic consequences. It is the major cause of non-traumatic disability in young adults. The social costs associated with MS are high because of its long duration, the early loss of productivity, the need for assistance in activities of daily living and the use of immunomodulatory treatments and multidisciplinary health care. Increasing evidence suggests that oxidative stress plays a major role in the pathogenesis of MS. Reactive oxygen species (ROS), leading to oxidative stress, generated in excess primarily by macrophages, have been implicated as mediators of demyelination and axonal damage in both MS and experimental autoimmune encephalomyelitis (EAE), its animal model. Recently, we found that the mitochondrial targeted antioxidant, MitoQ has a neuroprotection role through its antioxidative property. We hypothesize that MitoQ may have a protection or curative role in MS. We are using a cell culture system (in vitro) and animal model (in vivo) to examine this new idea. This proposal may open a new window for treatment of MS.
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