My research aims to evaluate the etiology of chronic neurological deficits caused by traumatic neurological injury (TBI) in order to identify mechanisms and optimal time frames for prophylactic and therapeutic treatment. Our translational experiments are carried out in a model of diffuse axonal injury (DAI) in male and female adolescent–young adult rats, where TBI induced DAI instigates late-onset or persisting sensory, affective, and cognitive deficits. These neurological deficits are mediated by specific networks of brain circuitry that are changed as the injured brain attempts to repair itself. Our research evaluates relevant brain circuits to identify mechanisms that modulate structural and functional reparative or maladaptive processes responsible for morbidity.
Ongoing research projects focus on the role of circuit-directed rehabilitation (to promote adaptive responses in healthy circuitry) and pharmacological inhibition of neuroplasticity (to prevent inappropriate connections) over the time it takes to develop and maintain chronic neurological deficits. Both functions are highly regulated by TBI-induced neuroendocrine responses (stress and sex hormones).
BS in Agricultural Biotechnology, University of Kentucky; PhD in Anatomy and Neuroscience, University of Kentucky; Postdoc at the Spinal Cord and Brain Injury Research Center, University of Kentucky
Assistant Professor, Dept of Child Health, UA College of Medicine-Phoenix