Citation

Khatri N, Thankur M, Pareek V, Kumar S, Sharma S, Datusalia AK. CNS Neurol. Disord. Drug Targets 2018; 17(9): 689-695.

Affiliation

National Brain Research Center, Manesar, Haryana. India.

Copyright

(Copyright © 2018, Bentham Science Publishers)

DOI

10.2174/1871527317666180627120501

PMID

29952272

Abstract

Traumatic Brain Injury, representing mild, moderate and severe effects of physical impact on the brain is the leading cause of mortality and morbidity worldwide. Traumatic injury causes sequential, primary and secondary injuries of brain where primary injury is due to the first physical impact, the blow or jolt to the brain compartment. Secondary injury follows primary injury temporally, involving the biochemical, cellular, and physiological responses like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and oxidative stress. Glutamate induced excitotoxicity is the major factor causing neuronal cell death in its vicinity, explained by higher levels of calcium levels intracellularly in neurons. Excessive glutamate at synaptic junction which in turn activates its NMDA and AMPA receptors that facilitates excessive calcium influx into the neuronal cells and promote oxidative stress and further leads to mitochondrial dysfunction, oxidation of lipids, proteins and DNA leads to the neuronal cell death. Present literature review is intended to give extensive view summarizing effects of reactive oxygen species (ROS) induced oxidative stress and its fatal effects on brain after traumatic brain injury.

Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.

Language: en

Keywords

Glutamate excitotoxicity; Mitochondrial dysfunction; Oxidative stress; Traumatic brain injury; secondary injury.