IS INTERRUPTION OF OXIDATIVE DAMAGE ALONE ENOUGH TO ACHIEVE CLINICALLY MEANINGFUL NEUROPROTECTION?

Edward D. Hall, University of Kentucky Spinal Cord & Brain Injury Research Center; Lexington, KY 40536

Objectives: At the conclusion of this program, the participants will be able to:

•  Be knowledgeable about the spatial and temporal profile of reactive oxygen-induced oxidative damage after acute traumatic brain injury (TBI) and spinal cord injury (SCI);

•  Understand the relationship between oxidative damage and other secondary injury events, including mitochondrial dysfunction and the calcium-overload-induced, calpain-mediated proteolytic damage, after TBI or SCI;

•  Be familiar with the neuroprotective effects of individual neuroprotective strategies in models of acute TBI and SCI that target either oxidative damage, mitochondrial failure or calpain-mediated proteolysis;

•  Understand the rationale for combination, mechanistically complimentary, pharmacological therapies to achieve maximal neuroprotection after acute TBI or SCI.