Work in the Courtney Robertson Lab is focused on identifying interventions that could minimize the neurological deficits that can persist after pediatric traumatic brain injury (TBI). One study used a preclinical model to examine potential disruption of mitochondrial function and alterations in cerebral metabolism. It was found that a substantial amount of mitochondrial dysfunction is present in the first six hours after TBI. In addition, we are using nuclear magnetic resonance spectroscopy to evaluate global and regional alterations in brain metabolism after TBI. We're also collaborating with researchers at the University of Pennsylvania to compare mitochondrial function after head injury in different clinically relevant models.

Founded in the late 1980s, our Lab explores the fundamental mechanisms of neural responses to traumatic and degenerative signals and works to identify targets for treating injury/degeneration with small molecules, peptides and cells. We currently focus on traumatic and degenerative axonopathies as they occur in traumatic brain injury (diffuse axonal injury), neurodegenerative diseases i.e. Alzheimer's disease and other white matter conditions, e.g. hypoxic ischemic encephalopathy, demyelination. We are especially interested in the role of the MAPK cascade of injury, NAD metabolism and SARM1 signaling and their convergence on Wallerian degeneration.