Mission Connect Mild TBI Translational Research Consortium
Annual rept. 1 Aug 2008-31 Jul 2009
TEXAS UNIV MEDICAL BRANCH AT GALVESTON
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Brain injury, particularly mild blast type injuries due to improvised exploding devices are difficult to detect clinically, although there are long term cognitive and behavioral deficits. Key inflammatory cytokines are unregulated after traumatic insults that play a role in the development of long-term deficits. Early events are increased IL-1 and TNFalpha cytokine levels, that contribute to cell death and inflammation, and microglial and astrocytic activation, mediators dysfunction via persistent inflammation. Our central hypothesis is that blocking inflammatory cytokine signaling after mild traumatic brain injury MTBI will improve outcomes by ameliorating inflammation and the resultant neuronal dysfunction. Our goal is to develop, implement and assess interventions to ameliorate the long term neurological deficits caused by MTBI by ameliorating injury-induced brain inflammation. We used lateral fluid percussion model of MTBI in rat. The results are that we have an appropriate injury that provides detectable damage as early as 6h after injury. We showed by immunohistochemistry that TBI induced significant astrocytic and microglial activation and increased IL-1alpha and TNFalpha in brain 6 hours and 18 days. We saw corresponding behavioral deficits based on beam balance and footfall assays. Thus, we have biomarkers to assess therapeutic strategies designed to minimize outcomes associated with MTBI.
- Anatomy and Physiology
- Medicine and Medical Research