The enduring cognitive deficits and histopathology associated with traumatic brain injury
(TBI) may arise from damage to mitochondrial populations, which initiates the metabolic
dysfunction observed in clinical and experimental TBI. The anecdotal evidence for in vivo
structural damage to mitochondria corroborates metabolic and physiologic dysfunction,
which depletes substrates and promotes free radical generation. Excessive calcium
pathology differentially disrupts the heterogeneous mitochondrial population, such that …