Short Description: Neuroendocrine-immune alterations (including underlying molecular mechanisms) observable at rest and after psychosocial stress challenge in participants with current major depression and/or a history of early life trauma, as well as interventions designed to normalize changes in behavior and mood that result from excessive inflammation.
Long Description: Dr. Pace's laboratory investigates alterations in resting and psychosocial stress-induced inflammatory immune function in participants with current major depression and/or a history of trauma in the formative years of life. Excessive inflammation is hypothesized to result from insufficient glucocorticoid inhibition of inflammatory signaling that occurs subsequent to abnormal corticosteroid receptor function and/or abnormal cortisol release. Routine measures include plasma levels of proinflammatory cytokines and glucocorticoids, activation of inflammatory signaling pathways in circulating immune cells, and in vitro assessments of glucocorticoid sensitivity (determined via proinflammatory endpoints). The lab also investigates the effectiveness of proinflammatory antagonists that target inflammatory signaling pathways (including the nuclear factor-kappa B pathway and mitogen activated protein kinase cascades) to reverse changes in behavior and mood associated with hyperinflammatory states.
No Associated Keywords on File