Understanding the Underlying Neuroprotective Role of Estrogen in TBI Neuropathophysiology

TBI is a type of CNS injury that results after a blunt force is applied to the head, and it affects about 1.7 million cases in the USA every year. The more common events that lead to a TBI are vehicle collisions, domestic violence, falls, sports, and war [1]. Depending on the severity, a TBI can result in permanent disabilities, and in extreme cases, it is fatal. Some of the symptoms seen after a TBI are lumped together in what is termed PTSD. Symptoms typically include behaviors such as depression, anti-social behavior, impulsivity, and fear/anxiety. Additionally, TBI injuries have shown symptoms that are closely related to Parkinson’s and Alzheimer’slike symptoms. TBI related symptoms do not occur in a short timeframe, on the contrary, these often arise months or years after the injury has occurred, making the initial assessment of injury difficult [1-3]. A TBI occurs in two phases; the first phase is known as the primary injury or the initial injury. The second phase, referred to as the secondary injury consists of cellular processes that are activated after the initial injury and can persist for hours, days, and months after the initial impact [1,4]. Cellular processes such as nitric oxide formation, inadequate blood flow, imbalance of ions, neurotoxicity, and excitotoxicity compose the secondary injury and lead to tissue death. As a consequence, secondary injury contributes to the damage by affecting a larger area than the primary injury [4,5]. There is currently no treatment for this type of injury; there are only preventive measures such as wearing helmets or wearing seatbelts while driving. Thus, this review paper focused on estrogens’ neuroprotection mechanism on traumatic brain injury.