Molecular Mechanisms of Traumatic Brain Injury

Traumatic Brain Injury (TBI) is a frequent head injury, one of the leading causes of disability worldwide and a global health issue. TBI is defined as a direct physical impact to the head, and it elicits physical, cognitive, psychological, psychosocial and functional impairments. TBI can be associated with a fatal outcome. In addition, TBI is related to high healthcare costs, long term rehabilitations, prolonged sick-leaves, and social and functional disability. The conflicts around the globe have facilitated the development of complications after TBI, especially in combat veterans, but also in civilians affected by conflicts and combat situations. The severity of TBI might vary from mild to moderate and severe forms of TBI. The complications of TBI include cognitive dysfunctions, posttraumatic epilepsy, headaches and other motor and sensory neurological impairments. There are two phases of TBI: primary (a head injury) and secondary (a biological response to primary TBI). The understanding of the pathophysiology of the secondary TBI is still unclear. Biological processes that develop after TBI are the result of the organism response to the primary TBI, and they include activation of the inflammatory mediators and secretion of neurotransmitters, the development of apoptosis or necrosis, regenerative processes and altered synaptic plasticity. The main goal in TBI research is to improve the understanding of the underlying molecular mechanisms leading to the secondary TBI, to develop biomarkers that would be used to monitor the severity of injury, to find new targets (new molecules) for treatment and to have biomarkers that would follow the treatment response to reduce mortality and physical, cognitive, psychological, psychosocial and functional impairments after TBI, and to improve the clinical outcome.