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TBI can be characterized by alterations in brain immune signaling, which are associated with physiologic and cognitive changes. We are interested in understanding the relationship between these immune changes and their role in driving poor outcomes.

 TBI is a brain dysfunction caused by an outside force to the head. It is among one of the most heterogenous neurological disorders due to the number of pathophysiological changes that occur (e.g. neuroinflammation, blood brain barrier disruption, and neuronal death). 80% of TBI are considered mild, and 15% of these patients have difficulty recovering. They experience chronic somatic, emotional, and behavioral changes that last for years. Studies have associated neuroinflammation with these long-term deficits identified in patients. Neuroinflammation is characterized by the activation of microglia cells (Iba1), release of pro-inflammation cytokines, and dysregulation of immune signaling pathways (MAPK, NF-κB). Researchers believe that understanding and targeting these immune changes can lead to fast recovery.

Lab for Systems Biology of Inflammation
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