Kenneth I. Strauss, PhD
Associate Professor, Translational Science & Molecular Medicine
Ph.D., 1990, Hahnemann University
The MSU Neurotrauma Research Lab studies the function and regulation of inflammatory genes after traumatic brain injury (TBI). After a head injury, medical professionals can stabilize a victim's life signs but there are no effective treatments for ameliorating the damage. Brain inflammation after TBI causes secondary, progressive damage resulting in worsened neurologic deficits. Our studies of the inflammatory mediator cyclooxygenase-2 (COX2) aim to better control inflammation and improve functional recovery after TBI. Currently, we are investigating brain metabolism of arachidonic acid (ArA), e.g., by COX2. ArA can be converted into over 50 biologically active eicosanoids that act locally where produced in the normal and injured brain. Eicosanoids mediate both pathophysiology and recovery after brain injuries.Investigations are ongoing to elucidate brain region-specific regulation and function of these eicosanoids and the enzymes that produce them. We use animal models to investigate molecular, biochemical, cellular, and behavioral outcomes. This knowledge will promote the development of new therapies to minimize harmful eicosanoid production, yet maximize potentially beneficial eicosanoid effects in the brain after injury. We are initiating studies on the relationship between inflammatory genes in the aging brain and changes in cognitive ability, i.e., premature cognitive decline. This has implications for natural and pathologic aging of the brain, for example, in early-onset dementia, Parkinson's and Alzheimer's diseases.