Term | Value | Language |
---|---|---|
dc.contributor.advisor | Walker, Ashley | |
dc.contributor.author | Arora, Nayantara | |
dc.date.accessioned | 2024-08-30T19:08:14Z | |
dc.date.available | 2024-08-30T19:08:14Z | |
dc.date.issued | 2024 | |
dc.identifier.uri | https://scholarsbank.uoregon.edu/xmlui/handle/1794/29878 | |
dc.description | 39 pages | |
dc.description.abstract | Alzheimer’s disease (AD) is a type of dementia characterized by loss of cognitive function and build-up of amyloid-ß (Aß) plaques. Aging and cardiovascular decline, indicated by increased arterial stiffness, are primary AD risk factors. I aimed to identify if modeling large artery stiffness (LAS) in the context of AD at young age mimics the impairments in cognitive and cerebrovascular function seen in old age. I hypothesized that LAS in conjunction with AD exacerbates cerebral microvascular and cognitive impairment compared to AD alone. By crossing elastin haploinsufficient (Eln HET) and amyloid precursor protein knock-in (NLGF) animals, we generated a mouse model of LAS and AD. We used young (6 m) male and female mice. Cognition was assessed by novel object recognition, nest building, and rotarod tests. Cerebrovascular function was measured in posterior cerebral arteries using pressure myography. To assess LAS, aortas were cryosectioned and stained to measure elastin, collagen, and wall thickness. Our model of LAS and AD shows no effect on cognition or cerebrovascular function. There were no main or interaction effects of Aß and LAS on nest building, rotarod, or novel object recognition tests, nor for wall thickness, collagen composition, or vasoreactivity to acetylcholine. NLGF x Eln HET animals displayed lower vasoreactivity to sodium nitroprusside, an endothelium-independent vasodilator (p < 0.05), suggesting endothelium-independent dilation may be related to arterial stiffness. Data suggest that at a young age, LAS and Aß do not significantly impact cognition or cerebrovascular function, and that age is a primary contributor to these issues in AD. The insights from this study will aid in understanding how the cardiovascular system contributes to the development of AD. | en_US |
dc.language.iso | en_US | |
dc.publisher | University of Oregon | |
dc.rights | CC BY-NC-ND 4.0 | |
dc.subject | Alzheimer's | en_US |
dc.subject | Vascular | en_US |
dc.subject | Brain | en_US |
dc.subject | Neuroscience | en_US |
dc.subject | Human Physiology | en_US |
dc.title | Exploring Alzheimer's Disease: The Interaction Between Increased Aß And Large Artery Stiffness On Cognitive And Cerebrovascular Function And Structure | |
dc.type | Thesis/Dissertation | |
dc.identifier.orcid | 0009-0001-0675-6437 |