Walker, AshleyWolf, JuliaReeve, Emily2021-07-272021-07-272021https://hdl.handle.net/1794/264851 page.With advancing age, large arteries experience increased stiffness in their walls, while small arteries maintain elasticity. Arterial stiffening can occur when advanced glycation end-products (AGEs) form, resulting in collagen in the extracellular matrix becoming cross-linked. Age-induced large artery stiffness is associated with cognitive impairment and heightened risk for developing neurodegenerative disease. The formation of AGEs and collagen cross-linking have been shown to be inhibited by pyridoxamine. It was hypothesized that pyridoxamine treatment would prevent age-related arterial stiffness and attenuate cognitive impairment. Pyridoxamine was administered via drinking water to old C57BL/6 mice for six months, with old and young control groups. Aortic stiffness was measured by pulse wave velocity (PWV), while carotid and middle cerebral artery stiffness were measured ex vivo. Nest building was performed to measure cognitive ability. Old pyridoxamine treated mice had lower aortic PWV and a trend for lower carotid stiffness compared with old control mice. There was no difference in cerebral artery stiffness across groups, indicating that pyridoxamine specifically targets age-related arterial stiffening. Nest building was impaired in old control mice compared with young, but old pyridoxamine treated mice were not different from either group. These results shed light onto potential pyridoxamine treatments for preventing large artery stiffness to preserve cognitive function.application/pdfen-USCC BY-NC-ND 4.0agingvascularphysiologypyridoxaminecognitivePresentationhttps://orcid.org/0000-0002-7424-3051