Honors Scholars Collaborative Projects

Publication Date

Spring 2020

Abstract

The geriatric population of America has grown exponentially in the past century. Health degradations and expensive medical care are characteristic of this population with many of these costs due to age-related cognitive decline. It is essential to completely understand the mechanisms of normal and abnormal aging in the search for treatments for cognitive decline. A reduction of neurogenesis is a common factor in aging, but this reduction is even more drastic in individuals experiencing cognitive decline. It is unclear what effect reduced neurogenesis has on the extracellular environment, including glial cells. In particular, changes in microglial activation could be related to cognitive decline, and it is possible that reduced neurogenesis could influence microglial activation. To determine the functional effect of prolonged ablation of neurogenesis on microglial activation, a pharmacogenetic rat model (GFAP-TK) was used. Wild type (WT) rats had normal neurogenesis throughout the experiment, while transgenic (TK) rats given valganciclovir (VGCV) had neurogenesis inhibited starting at eight weeks old. Microglial activation and hippocampal volume were measured for three different age groups (VGCV treatment for 4, 13, and 22 weeks) in both WT and TK rats to determine effects of prolonged neurogenesis-ablation on markers related to aging. It was found that the TK rats experienced no differences of microglia activation or hippocampal volume when compared to the WT rats. Differences between age groups regardless of genotype were evident. The oldest age groups had the smallest hippocampal volume, and the most microglial activation. Ablating neurogenesis had no effect on the surrounding microglia, but aging increasing their activity.

Faculty Advisor

Dr. Timothy Schoenfeld

Document Type

Honors Thesis

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