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 brain’s 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.