Current Research Program
 
Traumatic brain and spinal cord injuries often result in permanent disabilities that can profoundly affect the quality of life. The extent of functional recovery after either traumatic brain or spinal cord injury is a consequence of the initial mechanical destruction of tissue and secondary factors that collectively contribute to additional tissue damage. Data from our laboratory as well as from others have demonstrated that these secondary pathogenic factors are delayed in onset and can significantly impair the extent of functional recovery. Thus, one of the more promising therapeutic approaches is to develop strategies that target these secondary factors that are characteristically delayed in onset. The challenge is to carefully define these factors, define the time course of their expression, and to develop therapeutic interventions that target their temporal 'window' of expression. Our laboratory has been committed to defining early mediators of secondary tissue damage after traumatic injury. To address complex objective, we developed and characterized reproducible models of traumatic brain and spinal cord injury in the rat and more recently in the mouse that accurately mimic the human condition. Using these models we have focused on early pathogenic events that contribute to secondary damage, including dysfunction of the blood-brain/spinal cord barrier, inflammation, and oxidative damage.