Role of neuroinflammation in the pathophysiology of traumatic brain injury

[[abstract]]Traumatic brain injury (TBI) is a serious public health problem causing morbidity and mortality worldwide yearly. Neuroinflammation is a hallmark symptom following TBI to induce delayed secondary injury. The excessive activation of microglia, astrocytes, and other immunological mediators release pro-inflammatory cytokines causing neuronal cell death leading to neurological deficits. Currently there are no FDA-approved medications to improve cognitive function after TBI, however, the use of fatty acids has gained notoriety in recent years with the use of ω-3 polyunsaturated fatty acids (ω-3 PUFAs, i.e., DHA) providing neuroprotection against TBI-induced neuroinflammation. DHA has been extensively studied in the context of anti-inflammation, but there is a poor understanding of cerebral autoregulation in the presence of TBI. In addition, the current treatments and other potential neuroprotective compounds for TBI such as resveratrol and palmitic acid methyl ester (PAME) are discussed