8.9: Presentation session: Keynote speaker and brain injuries and neuro-regeneration panel: “Pathogenic mechanisms induced by exposure to blast overpressure”

The increased incidence and severity of traumatic brain injury (TBI) induced by exposure to blast overpressure (BOP) observed in Operations Enduring Freedom and Iraqi Freedom (OEF/OIF) has significantly contributed to combat morbidity. The research efforts described here establish animal models to examine responses to BOP exposure and analyze the potential mechanisms of injury. The objective is to identify novel strategies for preventing or mitigating blast-related trauma. Overall, the biochemical and molecular mechanisms of BOP-induced TBI remain poorly understood but are believed to be shared by other forms of neurotrauma and involve excitotoxicity, inflammation, overproduction of reactive oxygen species (ROS) and apoptosis. Recently, is evidence suggests that ROS are a major component of the BOP-induced pathogenic responses and that treatment with antioxidants is associated with protection. In animal models, both genomic and proteomic responses associated with blast are investigated to enhance our understanding of the basic mechanisms of injury and identify prophylactic and treatment modalities.