Veterans are approximately 30% more likely than non-veterans to suffer from severe hearing impairment. Tinnitus, or ringing in the ears, which is increasingly common among military service men and women, has been linked to significant cognitive and psychological impairment and can be worsened by the same sounds that trigger post-traumatic stress disorder (PTSD). In fact, tinnitus and PTSD often present as comorbidities, and recent studies suggest these two disorders may share a common neurological pathway. Additional studies are required to better understand the connection between hearing loss and impaired cognitive function such as that observed in with PTSD. Here, we use the fruit fly, Drosophila melanogaster, to explore the relationship between hearing loss and cognitive function. Negative geotaxis climbing assays and courtship behavior analysis were used to examine neurobehavioral changes induced by prolonged, intense auditory stimulation. Preliminary results suggest that exposure to loud noise for an extended period of time significantly affected Drosophila behavior, with males being more sensitive than females. Based on our results, there appears to be a potential connection between noise exposure and behavior, further suggesting that Drosophila could be an effective model to study the link between hearing loss and PTSD.

Damage to the Central Nervous System (CNS), such as traumatic brain injury (TBI) can often lead to a systemic inflammatory response since inflammatory mediators can be carried through the cardiovascular system. Past studies indicate that this inflammatory response that started at the CNS can increase the risk of heart disease. This growing interest in the heart-brain axis led our lab to explore if there is any impact of TBI on cardiac function and remodeling. TBI has been shown to have short-term effects on the heart, but few studies evaluate the long-term impact of TBI on the heart. To analyze any long-term impacts, we extracted hearts from rats 6 months post TBI, or sham that had been treated with vehicle or lipopolysaccharide (LPS) injections. LPS was administered to assess how inflammation could impact protein expression in the heart. Reactive oxygen species (ROS) targets such as NOX2, NOX4, SOD1, SOD2, catalase, and osteopontin were measured as potential indicators of cardiac remodeling. Rats that received vehicle TBI and LPS TBI resulted in no statistically significant differences (p>0.05) when evaluated as fold-change over the vehicle. This trend was consistent when normalizing to LPS sham. Since there were no changes in ROS targets, the hypothesis that there is long-term cardiac remodeling in the heart post-TBI was rejected. Further investigation is warranted since the present design of this study may not be ideal for evaluating long-term impact as histology samples were not obtained nor cardiac function assessments.