Virginia Research Day 2025

Graduate Student Research Biomedical

01 Investigating Regional Diffrences in Migroglia Phenotype Across Combined Repetative Blast Exposure and Delayed Closed Head Controlled Cortical Impact Induced Traumatic Brain Injury

Nora Ahmed; Jessica Wilkes; Susan Murphy; Pamela VandeVord Corresponding author: noraa23@vt.edu

Virginia Tech Wake Forest School of Biomedical Engineering & Sciences

Traumatic brain injury (TBI) continues to be a serious clinical challenge. When focusing on the military population, it is known that Service Members with TBIs are at higher risk of subsequent TBIs because of risk-taking behaviors. Veterans diagnosed with TBI had a substantially greater risk of being hospitalized for motor vehicle accidents than those without TBI diagnoses. Thus, one of the goals of this research was to optimize a preclinical model that simulates a delayed secondary impact in a solider that was exposed to blast. This study focuses on how microglia respond to this dual-TBI paradigm. Microglia

serve as the brain's active immune cells and exhibit various functional roles based on their morphological presentation and transcriptional profiles after a blast injury. Even though the molecular presentation of microglia have been shown to vary spatially and temporally across brain injuries, the phenotypic differences of microglia across a dual-injury model has yet to be explored. Here in this study, adult male Sprague Dawley rats were subjected to a repetitive blast injury and then to a single closed head cortical impact (cCCI) injury 2 weeks later. Brains were then collected 2 weeks following impact and microglial

activation was explored using immunohistochemistry. The results show that overall microglia exhibit shorter process length and less endpoints per cell in the dual repetitive blast exposure and delayed cCCI-induced injury compared to a single cCCI injury. Overall, the study shows that morphological changes in microglia continue to persist chronically following a Veteran relevant complex TBI model and could contribute to long-term neuropathology.

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