Neurovascular Physiology Laboratory
Jody Greaney, PhD
Assistant Professor, Department of Kinesiology
Depression afflicts more than one in ten Americans and is a leading cause of disease and disability. Indeed, many studies demonstrate that people with depression have a much higher risk for developing cardiovascular disease. Our lab is interested in better understanding the link between mental illnesses like depression and cardiovascular disease risk. In particular, we study how and why the regulation of the nervous system and the blood vessels may be altered in people suffering from depression, with the hope that our research findings may help develop more effective strategies to reduce, or even prevent, cardiovascular disease in depressed adults.
Our laboratory is currently investigating the mechanisms underlying neurovascular dysfunction in human depression, with the ultimate goal of identifying novel therapeutic intervention strategies to prevent, slow, or reverse depression-associated cardiovascular disease. Our laboratory utilizes a multidisciplinary, integrative, and translational research strategy that combines a variety of experimental techniques that enable the interrogation of physiological and pathophysiological mechanisms of neurovascular function in humans.
Join the Lab - Graduates and Undergraduates Welcome
The Neurovascular Physiology Laboratory is seeking graduate student applications and is welcoming to undergraduates seeking research opportunities. Interested candidates should contact Dr. Jody Greaney (firstname.lastname@example.org) for additional information.
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Current Research Projects
Central Mechanisms of Neurovascular Dysfunction in Human Depression
Funding: NIH R00HL133414
The goal of this study is to understand the role of oxidative stress in contributing to altered sympathetic neural function in men and women with depression. We are further extending this line of inquiry by including an examination of the modulatory influence of chronic selective serotonin reuptake inhibitor (SSRI) treatment for depressive symptoms on sympathetic function. Our overall hypothesis is that oxidative stress mechanistically contributes to chronic sympathetic overactivity in depression, thus representing a link between depression and cardiovascular disease.
Cerebrovascular Function in Human Depression
The goal of this study is to examine brain blood vessel function in young adults with depression. Our working hypothesis is that vasodilatory responsiveness of the arteries in the brain is impaired in adults with depression. Further, we hypothesize that these deficits in brain blood vessel function will be related to alterations in cognitive function.
Stress Reactivity in Human Depression
We recently demonstrated that exposure to daily psychosocial stressors (e.g., arguments with a partner, job-related stress, etc.) is related to more severe impairments in microvascular endothelial function in adults with depression. To extend this line of inquiry, we are examining the relation between emotional and cognitive reactivity to psychosocial stress and neurovascular reactivity to acute physiological stressors. These studies have the potential to identify novel targets for intervention strategies to improve depression-associated neurovascular dysfunction.
- Greaney JL, Dillon GA, Saunders EFH, and Alexander LM. Peripheral microvascular serotoninergic signaling is dysregulated in young adults with Major Depressive Disorder. Under Review.
- Greaney JL, Koffer RE, Saunders EFH, Almeida DM, and Alexander LM. Self-reported everyday psychosocial stressors are associated with greater impairments in endothelial function in young adults with Major Depressive Disorder. J Am Heart Assoc 8(4), 2018.
- Greaney JL, Saunders EFH, Santhanam L, and Alexander LM. Oxidative stress contributes to microvascular endothelial dysfunction in men and women with Major Depressive Disorder. Circ Res 124(4): 564-574, 2019. *accompanied by editorial highlight
- Greaney JL and Kenney WL. Measuring and quantifying skin sympathetic nervous system activity in humans. J Neurophysiol. 118(4): 2181-2193, 2017. [Invited Review]