Authors:

Ainsley Hogan

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Arterial Stiffness Co-Author(s): Emily Reeve, Abigail Cullen, Ashley Walker The pathophysiology of Alzheimer's Disease (AD) is still poorly understood despite its prevalence. Epidemiological studies have shown a link between increased large artery stiffness (LAS) and the development of neurodegenerative diseases such as AD. Increased LAS is a common age-related change in the vasculature and is primarily caused by the increased fragmentation and degradation of elastin. To assess the contribution of LAS on cerebrovascular, neuroinflammation, and cognitive function, a mouse model haploinsufficient in elastin (Eln+/-) was employed in young (6 months) and old (24 months) mice. Cerebrovascular function was investigated by assessing endothelial-dependent and independent dilation using ex vivo pressure myography experiments. Neuroinflammation was assessed through gene expression from cortex samples. A decline in endothelial-dependent dilation, measured by maximal dilation to acetylcholine (ACh), was observed with age in both Eln+/- mice (p<0. 05) and wild-type mice (p<0. 0005), however endothelial-independent dilation remained unaffected. Expression of the cytokine interleukin-1b (IL-1b) was higher with age in both Eln+/- mice (p<0. 0001) and wild-type mice (p<0. 0001). Additionally, wild-type, but not Eln+/- mice had higher expression of another cytokine, tumor necrosis factor a (TNFa) with age (p<0. 05). These results suggest that age is a primary risk factor for cerebrovascular dysfunction and neuroinflammation. 178 UNIVERSITY OF OREGON • 2025 UNDERGRADUATE RESEARCH SYMPOSIUM TABLE OF CONTENTS

Source:

University of Oregon / 2025

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Co-authors:

Ainsley Hogan