CURRENT AND RECENTLY COMPLETED PROJECTS

Daily stress and redox-immunological function in adults with depression

 UD IRB: 2056784

 Psychosocial stress can trigger circulating immune cells to produce proinflammatory cytokines and mitochondrial-derived superoxide, both of which have damaging effects on the peripheral vasculature. The aim of this study is to determine whether exposure and emotional responsiveness to daily stressors (e.g., argument with a partner, malfunctioning computer) are linked to excessive inflammation and disrupted mitochondrial redox balance in adults with depression. By better understanding how common and naturally occurring stressful events in everyday life influence redox-immunological function in adults with depression, this project will set the stage for future studies examining novel strategies to sever this link, thereby improving cardiovascular health in adults with depression.

Daily stress processes and sympathetic-cardiovascular reactivity in depression

Funded by the NIH (MH123928)

This project interrogated the link between multiple dynamic aspects of daily stress processes and sympathetic-cardiovascular reactivity to acute physical, cognitive, and emotional stress stimuli in adults with depression. A supplemental project examined whether daily memory lapses, a unique type of daily stressor, predict exaggerated acute stress reactivity in adults with depression. Together, the results of these projects have the potential to highlight a novel biosignature of cardiovascular and neurocognitive disease risk in stress-susceptible adults.

Peripheral and central mechanisms of neurovascular dysfunction in human depression

 Funded by the NIH (R00 HL133414)

 This project provided the first direct mechanistic evidence that oxidative stress (specifically superoxide) contributes to reductions in nitric oxide bioavailability and function, thereby driving peripheral microvascular endothelial dysfunction in unmedicated adults with major depressive disorder. Interestingly, endothelial function was preserved in adults with major depressive disorder who were treated with a selective serotonin reuptake inhibitor (SSRI) and in remission. Collectively, these findings provide clinically relevant insight into the pathophysiological mechanisms through which depression increases future cardiovascular and neurocognitive disease risk. We are currently developing follow-up projects to determine if the direct effects of SSRIs on neurovascular function are independent from improvements in depressive symptomatology and predictive of antidepressant treatment efficacy.