摘要
In the United States, approximately one-third of all injury-related deaths are due to traumatic brain injury (TBI). Anyone is at risk for TBI;however, the risk is higher for athletes in contact sports, military personnel, children, and the elderly. TBI is characterized by a mild, moderate, or severe mechanical force to the head which can be further classified as blast, blunt, or ballistic. The sheer mechanical force of the impact to the head results in the primary injury including diffuse axonal injury, internal bleeding, swelling, and neuronal cell death. Secondary injury occurs over time, often weeks to months post-TBI, and is characterized by neuroinflammation, blood-brain-barrier disruption, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, and other deleterious effects in the brain (Khatri et al., 2018). Recent research indicates that secondary injury from TBI may be considered a risk factor for neurodegenerative diseases occurring later in life, such as Alzheimer’s disease and chronic traumatic encephalopathy. A key molecular mechanism that contributes to secondary injury after TBI is free radical damage which is induced by the aberrant production of reactive oxygen species (ROS) and reactive nitrogen species (RNS).
