The wars in Iraq and Afghanistan have caused numerous injuries and deaths due to blast-induced traumatic brain injury (TBI). Non-blast closed impact injuries (nbTBI) are identified by pathophysiological mechanisms like direct tissue damage, bleeding, and diffuse axonal injury; and accumulation of proteins-like β-amyloid (Aβ)-linked to neurodegenerative diseases such as Alzheimer's disease. A comparison between the markers for non-blast TBI and blast-induced TBI begin to describe a methodology for treating victims of acute blast injury.
In a recent animal study, adult rats and mice were exposed to blast overpressures in a cylindrical steel shock tube. Animals received overpressures of 36.6, 74.5, or 116.7 kilopascals (kPa), with exposures corresponding to mild to severe blast-induced TBI. Following this brain injury, Aβ levels in the blast-induced TBI rodents decreased, suggesting that effective treatments to be developed for blast-induced TBI may differ from treatments for non-blast TBI.
De Gasperi R, Gama Sosa M, et al. Acute blast injury reduces brain abeta in two rodent species. Frontiers in Neurology. (December 2012).