Drug- and cell-based therapies for targeting neuroinflammation in traumatic brain injury.

Abstract

TBI pathology: Traumatic brain injury (TBI) is caused by an external force to the head, resulting in trauma to the brain. Approximately 1.7 million Americans suffer from TBI every year. Out of the 1.7 million suffering from TBI, an estimated 52,000 injuries result in death, leaving a mass amount of people with symptoms that could last a few days, a few years, or their entire life (Faul et al., 2010). TBI can be classified as mild, moderate and severe. Depending on the classification and the extent of the injury, TBI can cause both physical symptoms and cognitive disorders (Lozano et al., 2015). The most common physical symptoms include headaches, dizziness, nausea, fatigue, sleep disruption, hearing problems and visual disturbances. Cognitive disorders include attention deficit, memory and executive functioning problems. Brain damage occurs following TBI as a result of direct neural cell loss. Within minutes following the initial injury, secondary cell death occurs, exacerbating the damage and worsening the symptoms (Campolo et al., 2013). Neuroinflammation is one of many factors that can lead to neurodegeneration and cause secondary cell death, indicating that TBI presents with equally debilitating symptoms as a chronic disease in addition to the widely accepted pathological manifestations acutely after injury (DelaPena et al., 2014).