Assessing the Effects of a Novel Ketone Ester in an Established Rodent Model of Blast Traumatic Brain Injury

Blast-induced traumatic brain injury (TBI) is a concern in the military population, with many personnel exposed to blast from improvised explosive devices. At the cellular level TBI has been shown to decrease energy production, create oxidative products that are associated with destructive processes and lead to cell death. Because of these findings, many researchers think TBI is at least partially a result of dysfunction of brain energy metabolism. In this study, animals were given a novel ketone ester after a blast exposure. In the hours and days following the exposure we expected this intervention to accelerate recovery and even prevent secondary injury processes. We have tested this hypothesis by monitoring blood glucose and ketone levels, body weight, behavioral responses, and oxidative stress for two weeks after exposure to blast in animals administered a ketone ester versus controlled conditions. Overall, while two weeks of ester administration resulted in a state of ketogenisis, most behavioral outcomes were unaffected. However, there was a trend suggesting that the ketone ester ameliorated blast-induced oxidative stress. The results are presented in detail in this report.