Regulation of oxygen radical formation as a treatment for cell death in a rodent model of pediatric traumatic brain injury

Over 1.7 million people suffer from traumatic brain injuries (TBI) each year in the United States, surpassing multiple sclerosis, HIV/AIDS, breast cancer, and spinal cord injuries combined. TBI is the number one cause of death and disability in the pediatric population. One of the many consequences of TBI is cell death which is correlated with deficits in motor and cognitive skills. Cell death can be caused through the formation of free radicals, more specifically reactive oxygen species (ROS). In this study our goal is to characterize the efficiency of selenium, a scavenger drug, in preventing ROS-mediated cell death in a rodent model of pediatric TBI. We hypothesize that administration of selenium after TBI will diminish neuronal cell death and improve behavioral deficits. In order to test whether selenium can decrease cell death we first developed a model of pediatric brain injury that would generate significant cortical and hippocampal cell death as well as cognitive deficits.  Using a closed skull cortical impactor we were able to generate a range of TBI severities in pediatric rats as determined by levels of cortical and hippocampal cell death. Subsequent studies will first focus on whether cell death is correlated with behavioral deficits followed by evaluation of selenium as a potential treatment for TBI. If we can demonstrate the efficacy of treatment with ROS scavengers in our rodent model then our ultimate goal is to translate selenium into a therapy to improve outcome in pediatric patients suffering from TBI.