CURRENT RESEARCH AREAS:
Research in the Neigh Lab broadly focuses on how genetics and experience interact to modify the brain's function and interactions with other organ systems. We are a question-driven lab and believe that the techniques and approaches we use must meet the demands of those questions.
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Currently, there are three main focuses of research underway in the lab: the implications of chronic adolescent stress, the endocrine/immune balance disruptions of HIV, and the metabolic drivers of stress-induced neural compromise. These divisions are fluid and responsive to the new information provided by the data that we generate, the innovative ideas of the research team, and the availability of funds to complete the work in the most rigorous manner possible.
ADULT IMPLICATIONS OF CHRONIC ADOLESCENT STRESS MEDIATORS AND MODIFIERS
Stress is a part of life; however, stressors during development can lead to increased adult incidence of depression and PTSD, metabolic syndrome, inflammatory disorders, and cardiovascular disease. Further, evidence over the past decade has demonstrated that adolescence is an additional developmental period of increased risk to prolonged consequences of stress exposure. Both males and females exhibit the adult consequences of chronic adolescent stress exposure in the clinic, and in studies using model animals; however, despite the clear clinical sex differences in adult disorders following early life stress, the question of what mediates these sex differences remains unresolved.
We propose that chronic adolescent stress (CAS) alters regulation and function of transcription factors deferentially in males and females. Given that transcription factors control the flow of genetic information from DNA to mRNA and thereby protein, increased or decreased activity of transcription factors can exert wide-ranging effects on both physiology and behavior and may account for the range of observed sex differences in the effects of CAS. The novel contribution of the proposed research will be identification of the extent to which CAS alters adult regulation and function of the transcription factors related to glucocorticoid receptor activation.