Neuroprotection by Anti-Oxidative Stress Response After Severe Traumatic Brain Injury – Do Extracellular Vesicles Count?

Severe traumatic brain injury (sTBI) is a serious and potentially life-threatening brain injury typically caused by a severe blow or impact to the head. The clinical manifestation can vary greatly and include loss of consciousness, cognitive impairment, memory problems, and sensory, motor, and behavioural disturbances. sTBI requires emergent treatment because the initial injury can be further aggravated by hypoxia, hypotension, and raised intracranial pressure. Acute management is therefore focused on preventing and/or mitigating additional damage to the brain by relying on macrophysiological parameters. However, a deeper understanding of the cellular and molecular pathophysiology of sTBI might offer additional insight into underlying processes in the brain and contribute to medical decision-making. Here we provide an overview of the main TBI features, including treatment in the acute phase. We describe the molecular pathophysiology with emphasis on oxidative stress as one of the major detrimental events in acute sTBI. Furthermore, we discuss if the anti-oxidative response after sTBI might be mediated by extracellular vesicles, nano-sized particles secreted by cells into body fluids including cerebrospinal fluid (CSF). EVs were attributed different roles in oxidative stress, and as carriers of various macromolecules, CSF-EVs might further combat oxidative stress in sTBI. Taken together, sTBI has a complex and dynamic pathophysiology with oxidative stress playing a significant part. Newly discovered mediators of anti-oxidative response are EVs which are present in CSF and can reveal ongoing processes in the brain. Further studies are required to determine if and how CSF-EVs participate in anti-oxidative response in sTBI.