Abstract: Traumatic brain injury (TBI) is a leading cause of mortality and long-term disability world-wide, involving complex pathophysiological mechanisms such as coagulation dysfunction, neuroinflammation, and blood-brain barrier disruption. In recent years, fibrinogen (Fg), a core protein in the coagulation cascade, has attracted considerable attention for its role in TBI. In addition to participating in hemostasis and thrombosis, Fg can leak into the brain parenchyma, where it directly activates microglia and promotes patho-logical protein aggregation, thereby exacerbating neuroinflammation and neurodegenerative changes. Notably, Fg exhibits a dual role in TBI:on one hand, its excessive consumption can induce coagulation disorders and aggravate secondary brain injury; on the other hand, abnormal deposition of Fg in the brain parenchyma may enhance neurotoxicity through pro-inflammatory signaling pathways. Consequently, although fibrinogen supplementation may improve early coagulation parameters, its efficacy and safety remain controversial, with excessive administration potentially increasing the risk of thrombosis. This review summarizes the mechanisms of action of Fg in TBI and its clinical therapeutic implications, aiming to provide a theoretical basis for optimizing TBI treatment strategies.