Authors:

Lazar Isakharov

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About Paper:

Dietary zinc affects cerebrovascular but not cognitive function in young Alzheimer's model mice. Co-Author(s): Skylyn Ferguson, Abby Cullen, Ashley Walker Prevalence of Alzheimer's disease (AD) is rising with the aging population, exacerbated by oxidative stress and cerebrovascular dysfunction. Zinc, a vital antioxidant, is a global nutritional deficiency impacted by both diet and age. We aimed to elucidate zinc's role in the cerebrovascular pathology of AD. We hypothesized that low-zinc diet decreases cognitive function through endothelial impairment and dysfunctional antioxidant response compared to normal- and high-zinc diets in AD model mice. Male and female mice were fed normal (30 ppm), low (2-5 ppm) and high-zinc (300 ppm) diets for 8 wk starting at 4 m. We evaluated cognition via Morris Water Maze and Novel Object Recognition tests. Cerebrovascular function was assessed via pressure myography and brain immunofluorescent staining. Our data revealed no significant effect of zinc on cognition. Endothelium-dependent dilation to acetylcholine (ACh) and insulin had sex and zinc-dependent effects. Max ACh dilation was significantly lower in low-zinc males vs. other males and low-zinc females. High-zinc females trended toward increased max ACh dilation than normal. High-zinc males dilated more to insulin than normal- and low-zinc, while the responses in females were not different. However, high-zinc females dilated significantly less to insulin than high-zinc males. Antioxidant analysis is ongoing, but we expect to find dysregulation in low-zinc diet animals. This study advances understanding of zinc's impact on AD pathology.

Source:

University of Oregon / 2025

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Co-authors:

Lazar Isakharov