Dear Colleagues,

Traumatic brain injury (TBI) is one of the most common causes of permanent physical and cognitive impairment. Mitochondrial dysfunction and oxidative stress (OS) have been implicated as important contributory factors to the secondary injury and long-term neurological damage associated with TBI. The brain uses approximately 20% of the body’s total amount of oxygen and has the highest oxygen supply in the body. Higher oxygen consumption post-injury suggests an increased likelihood of reactive oxygen species production and subsequent OS given the brain’s limited antioxidant defenses. OS results in the structural and functional impairment of cellular and subcellular components such as mitochondria. The resulting impairment of mitochondrial function can trigger a cascade of detrimental effects, including a cellular energy deficit, impaired calcium regulation, inflammation, OS, and loss of blood–brain barrier integrity, ultimately resulting in neural cell damage and impaired brain function. Therefore, in light of the pivotal role of OS and mitochondrial dysfunction in the pathophysiology of TBI, therapeutic strategies that target these parameters may contribute to cognitive and functional recovery post-TBI.

The purpose of this special edition of Frontiers in Bioscience-Landmark is to highlight appropriate therapeutic strategies that have the potential to ameliorate OS in TBI and target mitochondrial dysfunction. This Special Issue will also focus on suitable minimally invasive methods to assess evidence of OS and mitochondrial dysfunction in patients and their application to disease monitoring.

Iain Hargreaves
Guest Editor