Mitochondrial dysfunctioning and neuroinflammation: Recent highlights on the possible mechanisms involved in Traumatic Brain Injury.

Traumatic brain injury (TBI) is the injury to the vasculature of brain while trauma caused by physical, chemical and biological stimuli. TBI is the leading cause of mortality and morbidity around the world. In this, primary insult leads to secondary injury through the involvement and initiation of various pathological processes. The most citable includes excitotoxicity, Blood Brain Barrier (BBB) dysfunction, inflammation, mitochondrial dysfunction, oxidative stress, calcium efflux, microglial mediated release of proinflammatory mediators (cytokine, chemokines, interleukin, tissue necrosis factor etc.). The morphological changes in TBI are proportional to mitochondrial dysfunctioning and microglial activation, which play an assorted role in neurodegeneration following traumatic brain injury. It is also assumed that the release of nitric oxide, activation of microglial cells plays a diversive role in maintaining the physiological and pathological balance. This review cites different pathophysiological mechanisms that are involved in progenesis of secondary injury after primary insult. These targets further are useful to explore the deep molecular mechanisms and to analyse the effectiveness of available drugs. Moreover, the present review reflects the underlying inflammatory cascade responsible for neuronal loss and neurological deficit in TBI.