Faculty Bibliography

Pre-deployment identification of risk and resilience factors is crucial in developing targets to reduce or prevent posttraumatic stress symptoms in military personnel. The Fort Campbell Cohort study was designed to assess pre-deployment biological and behavioral markers and build predictive models to identify risk and resistance for posttraumatic stress disorder (PTSD) following deployment. The aim of the current study was to use high-resolution metabolomics profiling to identify metabolic pathways and networks associated with PTSD checklist score differences and changes across multiple pre and post-deployment time points. In addition, we have investigated how deployment affects metabolomics profile changes within individuals independent of PTSD score changes. Untargeted metabolomics profiling of plasma has been completed using both liquid and gas chromatography with mass spectrometry. Our preliminary data indicates that deployment has complex metabolic effects that must be considered in evaluation of deployment-associated exposures in military personnel. Our in depth-data analysis may further elucidate pathways, novel compounds, and biomarkers associated with PTSD in its relation to military deployment. These findings may have clinical implications for understanding the pathogenesis of PTSD and provide insights to avert chronic PTSD

OBJECTIVE: Acute leukemia (AL) is associated with an immediate threat to life, an unpredictable clinical course, and substantial physical suffering. Traumatic stress symptoms that may meet criteria for acute stress disorder (ASD) may be common and disabling in this context, but have received little clinical attention. We investigated the incidence over time and risk factors for traumatic stress symptoms and ASD in the 3 months following diagnosis or relapse of AL. METHODS: Individuals with AL were recruited at a tertiary cancer centre in Canada within one month of diagnosis or relapse. Participants (N=230) completed self-report measures, including the Stanford Acute Stress Reaction Questionnaire, at baseline and monthly over 3 months. The incidence of traumatic stress symptoms over time was examined and a generalized logistic model was used to identify factors associated with ASD. RESULTS: Participants were 60% male, with a mean age of 48.9+/-15.2 years. Symptoms of ASD were identified in 24.3% of participants at baseline. Of these participants, ASD was identified in 37.3% at one follow-up and in 55.3% at >/=2 follow-ups. ASD was associated with having young children, being unmarried, acute lymphocytic leukemia (ALL), and greater physical symptom burden. Persistent or recurrent ASD was associated with female sex, ALL, greater attachment anxiety, less spiritual well-being, and less satisfactory patient-clinician communication. CONCLUSIONS: Symptoms of ASD are common and often persist or recur following diagnosis or relapse of AL. Research is urgently needed to determine the impact of interventions to prevent and treat psychological distress in this population.

Traumatic brain injury (TBI) and Alzheimer's disease (AD) are devastating neurological disorders, whose complex relationship is not completely understood. Cerebrovascular pathology, a key element in both conditions, could represent a mechanistic link between Aβ/tau deposition after TBI and the development of post concussive syndrome, dementia and chronic traumatic encephalopathy (CTE). In addition to debilitating acute effects, TBI-induced neurovascular injuries accelerate amyloid β (Aβ) production and perivascular accumulation, arterial stiffness, tau hyperphosphorylation and tau/Aβ-induced blood brain barrier damage, giving rise to a deleterious feed-forward loop. We postulate that TBI can initiate cerebrovascular pathology, which is causally involved in the development of multiple forms of neurodegeneration including AD-like dementias. In this review, we will explore how novel biomarkers, animal and human studies with a focus on cerebrovascular dysfunction are contributing to the understanding of the consequences of TBI on the development of AD-like pathology.