Record Detail

Traumatic brain injury is among the most common causes of death and disability in youth and young adults. In
addition to the acute risk of morbidity with moderate to severe injuries, traumatic brain injury is associated with a
number of chronic neurological and neuropsychiatric sequelae including neurodegenerative diseases such as
Alzheimer’s disease and Parkinson’s disease. However, despite the high incidence of traumatic brain injuries and the
established clinical correlation with neurodegeneration, the causative factors linking these processes have not yet been
fully elucidated. Apart from removal from activity, few, if any prophylactic treatments against post-traumatic brain injury
neurodegeneration exist. Therefore, it is imperative to understand the pathophysiological mechanisms of traumatic
brain injury and neurodegeneration in order to identify potential factors that initiate neurodegenerative processes.
Oxidative stress, neuroinflammation, and glutamatergic excitotoxicity have previously been implicated in both
secondary brain injury and neurodegeneration. In particular, reactive oxygen species appear to be key in mediating
molecular insult in neuroinflammation and excitotoxicity. As such, it is likely that post injury oxidative stress is a key
mechanism which links traumatic brain injury to increased risk of neurodegeneration. Consequently, reactive oxygen
species and their subsequent byproducts may serve as novel fluid markers for identification and monitoring of cellular
damage. Furthermore, these reactive species may further serve as a suitable therapeutic target to reduce the risk of
post-injury neurodegeneration and provide long term quality of life improvements for those suffering from traumatic
brain injury.