The Aging & Vascular Physiology Laboratory is interested in age-related vascular dysfunction including impaired endothelial cell function, increased large artery stiffness, and increased atherosclerotic risk. Specific projects include:
Large artery stiffness: As we age, our large elastic arteries, namely the aorta and carotid arteries, become stiffer. These stiffer large arteries can lead to an increase in the blood pressure pulse in the brain. This bigger blood pressure pulse potentially damages the small blood vessels in the brain. Epidemiology studies in human patients find correlations between large artery stiffness, a greater pulse in cerebral arteries, and dementia; however, these previous studies do not provide definitive evidence or explain the mechanisms for these connections. Thus, our goal is to understand the role of age-related increases in large artery stiffness on cerebrovascular function. This work is funded by the National Institute on Aging (K01 AG046326) and the Oregon Medical Research Foundation.
Alzheimer’s disease: Alzheimer’s disease is the 6th leading cause of death in the United States, yet there is no cure for this disease and current treatments to slow the progression are ineffective. It is now recognized that dysfunction of the vasculature in the brain is a likely contributor to Alzheimer’s disease. Alzheimer’s disease is associated with greater vascular permeability, changes to blood flow, and increased large artery stiffness. Still, we do not know the direct effects of age-related vascular changes on Alzheimer’s disease outcomes. We seek to understand the causes of Alzheimer’s disease in hope of identifying new treatment targets. This work is funded by the National Institute on Aging (R56 AG064016) and the Oregon Tax Check-off Alzheimer’s Research Fund through the Oregon Partnership for Alzheimer’s Research.
Sex differences: There are inherent differences between men and women in the mechanisms leading to vascular dysfunction in older age. These differences may increase the risk for disease more in one sex. For example, women are two times more likely to develop Alzheimer’s disease than men. However, surprising little is known about the cellular mechanisms underlying the sex difference in the risk for vascular dysfunction and Alzheimer’s disease. Our previous studies demonstrated that with aging there is more dysfunction of telomeres (the ends of each chromosome) in the arteries of women compared to men. We are now particularly interested in determining the role of estrogen deficiency after menopause on the cellular and molecular changes in the vasculature with age.
Hemorrhagic shock: Obese patients who suffer hemorrhagic trauma have a higher incidence of organ failure and mortality compared with non-obese patients. We seek to understand the vascular mechanisms related to the poor outcomes in this patient population after trauma. This project is a collaboration with Dr. Belinda McCully at OHSU and is funded by a UO-OHSU Seed Grant.