Traumatic brain injury (TBI) is the leading cause of death and disability among children in the United States with an estimated incidence of 193-376 cases per 100,000. Clinical data have shown that children less than four years of age may be more susceptible than older children to motor deficits and cognitive impairment as a result of TBI, especially with severe injury. While this difference may be due in part to differences in injury mechanisms, this observation also suggests underlying biologic differences between the immature and mature brain that influence a young child's recovery from TBI. We have developed a murine model of TBI at postnatal day 21 that mimics many of the clinical features of brain injury in toddler-aged children. We have found that cognitive function declines during maturation of the brain. Recent studies suggest that this decline is modulated by oxidative stress and neurogenesis. Our central hypothesis is that oxidative stress, resulting from inadequate antioxidant reserves, reduces neurogenesis in the injured, immature brain and contributes to cognitive decline. We further hypothesize that therapeutic strategies to reduce oxidative stress will rescue neurogenesis and improve cognitive function.