Coordinate-Dependent Neuroinflammation and Metabolic Disruption Following Experimental Traumatic Brain Injury

Traumatic brain injury (TBI) is a leading cause of long-term neurological dysfunction, with secondary neuroinflammation playing a pivotal role in disease progression. Microglia, the brains resident immune cells, respond to injury in a spectrum of activation states, influencing neuronal survival and cognitive recovery. While past studies have broadly examined neuroinflammatory responses following TBI, the influence of injury approach--specifically, anterior vs. posterior impact--on microglial activation and neuronal damage remains unexplored. This study investigated how the site of controlled cortical impact (CCI) in a moderate TBI model alters neuroinflammatory responses and neuronal vulnerability, providing key insights into coordinate-specific mechanisms of injury.