The role of calpains in traumatic brain injury

This article attempts to provide a framework that will help to illustrate the roles of calpains in the process of traumatic brain injury (TBI).

This review provides meaningful points about the essential role of calpains in the neuropathological changes that follow TBI, identifies useful biomarkers of calpain activation and states the important roles of calpain in the treatment of TBI.

Neuronal calpains can be activated within hours or even minutes following contusive or diffuse brain trauma in animals. It has been suggested that they are early mediators of neuronal damage. Trauma can produce sustained calpain activation. In turn, this may result in axonal degeneration and neuronal death in models of TBI. Calpains can cleave cytoskeletal proteins into stable proteolytic fragments that have been widely used as biomarkers of the activation of calpain. The inhibition of calpains can reduce the functional and behavioural deficits by ameliorating axonal pathology and reducing cell deaths in animal models of TBI.

This review concentrates on the current understanding of the role of calpains in neuropathology that has been induced by TBI and the significance of calpains as a therapeutic target for the treatment of primary and secondary injuries that are associated with brain trauma.