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Traumatic brain injury (TBI), which results from an outside force causing mechanical disruption of brain tissue, is potentially life-threatening and therefore a critical public health problem throughout the world. In the USA, approximately 1.7 million individuals per year sustain a TBI, and about 43% of patients hospitalized because of TBI develop long-term physical disability as well as psychological disorders, such as neurocognitive deficits, epilepsy, and depression (Roozenbeek et al., 2013). The primary brain damage that occurs due to the mechanical disruption of brain tissue is usually irreversible and therapeutically inaccessible. In the sequel, secondary injury processes, including blood-brain barrier disturbances, excitotoxicity with following generation of reactive oxygen species, and inflammation, contribute to the exacerbation of traumatic brain damage. One major predictor of outcome is the development of cerebral edema in the acute phase after brain injury. In addition to acute TBI, it has become evident over recent years that some TBI patients develop progressive brain atrophy and dementia, which is referred to as “chronic TBI”. It is speculated that in these “chronic TBI” conditions, neuroinflammation plays a decisive role. The treatment options for traumatic brain damage are limited and no specific drug therapy approved for TBI is available so far. Considering the highly relevant socio-economic burden of TBI, there is a pressing clinical demand for new therapeutic options. As the pathophysiology of TBI involves multiple mechanisms of secondary brain damage, successful therapeutic strategies must target its key pathological hallmarks. In this respect and according to current scientific evidence, drugs targeting the kallikrein-kinin system show promise in improving the outcome of TBI.

The kallikrein-kinin system: a promising therapeutic target for traumatic brain injury