Assessing the Effects of a Novel Ketone Ester in an Established Rodent Model of Blast Traumatic Brain Injury
Abstract
Blast-induced traumatic brain injury (TBI) is an increasingly prevalent health 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 (Giza, 2014). Because of these findings, many researchers think TBI is at least partially a result of dysfunction of brain mitochondria, the structures in cells which are responsible for a large proportion of energy produced in the cell. In this study, animals will be given ketone ester after a blast exposure. In the hours and days following, we expect that that this intervention will accelerate recovery and even prevent secondary injury processes. We will test the first part of our hypothesis by administering ketone ester immediately after blast, allowing mitochondrial processes to function for several hours, then collecting tissue and testing for mitochondrial function. We will test the second part of our hypothesis by continuing to administer the ketone ester for two weeks following the blast, then collecting tissue and testing for pathology and repair in the brain. Assessments will involve examination of behavior, blood biochemistry, and brain tissue biochemistry.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 01, 2021
- Accession Number
- AD1133946
Entities
People
- Stephen T. Ahlers
- Usmah Kawoos
Organizations
- Naval Medical Research Center