Current Scholars

Sex differences in the effects of early childhood adversity in laboratory-induced stress and craving among individuals with Opioid Use Disorder

Delisa Brown, Ph.D. (Sudie Back, Ph.D., Primary Mentor)

Stress has been shown to play an important role in substance use initiation, maintenance, and relapse.  Psychosocial stressors such as early life stress have been linked to the initiation of substance use and the development of substance use disorders, although little research in this area has focused on Opioid Use Disorder (OUD). Early childhood adversity (ECA), as measured by the Adverse Childhood Experiences (ACEs) scale, may negatively impact neurobiological sensitivity to stress, impair the ability to manage negative emotions, and increase vulnerability to the development of substance use disorders. Several studies show an association between ECA and OUD, but the impact of ECA may be different for men and women. To date, no studies have investigated the relationship between ECA and response to stress and drug cues among individuals with OUD, and sex differences in this area remain poorly understood. This project directly addressed this knowledge gap by investigating sex differences in subjective, physiological and neuroendocrine responses to personalized imagery scripts (stress, opioid, neutral cues) among individuals with OUD.

Sex-associated difference in mitochondrial stress response following Traumatic Brain Injury

Onder Albayram, Ph.D. (Besim Ogretmen, Ph.D., Primary Mentor)

The overarching goal of this project  is to elucidate the different cellular and molecular mechanisms of the endogenous neuroprotective effects of mitochondrial stress response and mitophagy in the male and female brain following brain injury. This hypothesis will be tested by pursuing two specific aims. In Aim 1, the sex-specific effects of p17-mediated mitochondrial stress response in the development and progression of pathological processes  and long-term neurobehavioral sequelae after TBI will be elucidated. In Aim 2, how sexual dimorphism in p17-mediatedmitochondrial stress response may contribute to disease pathogenesis and mitochondrial adaptation following TBI will be elucidated. These aims will allow us to explore the biological significance of sex-associated differences in mitochondrial stress response and mitophagy on pathophysiology of brain injury.