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dc.contributor.authorHayes, Hailey
dc.date2015-05-01
dc.date.accessioned2016-02-19T15:38:17Z
dc.date.available2016-02-19T15:38:17Z
dc.identifier.urihttps://repository.tcu.edu/handle/116099117/10342
dc.description.abstractAccording to the Alzheimer's Association, Alzheimer’s Disease (AD) is the sixth leading cause of death in the United States, and is the only leading cause of death that cannot be prevented or slowed. Nur77 is a member of the NR4A subfamily of orphan nuclear receptors. Nur77 is down regulated in transgenic APP + PS1 murine models of AD, and the pharmacological enhancement of the nuclear receptor leads to enhanced memory consolidation in wild type animals. Taken together, this information suggests that Nur77 inhibition may be a factor contributing to the characteristic memory loss seen in AD. Additionally, inflammatory cytokines induce Nur77 expression in target cells. Previous research in our lab indicates that the intraperitoneal administration of the inflammation-inducing agent lipopolysaccharide (LPS), over seven consecutive days, significantly increases Aβ peptide levels in the hippocampus of mice leading to reduced cognitive function (Kahn et al., 2012). Our lab has shown that Nur77 increases as cytokines increase during the first 5 days of the 7 –day LPS injection protocol. However, on the 7th day, when Aβ is elevated and mice exhibit endotoxin tolerance, Nur77 is reduced. Additionally, exercise has been shown to play a significant role in AD models. If mice are allowed to run for two weeks following the 7-day LPS injection protocol, the hippocampal Aβ-levels return to the amount expressed in the saline-injected control group. It is well-known that exercise enhances cognitive function. Recent studies have also shown that exercise enhances the expression of Nur77 in the skeletal muscle of mice.  In this study, we demonstrate that there is a trending decrease in Nur77 across treatment groups: both of the LPS groups expressed less Nur77 than both of the Sal groups. While there was not a significant difference between condition groups, the data suggests that there is a pattern of increased Nur77 expression in mice administered LPS that were allowed to exercise for 14 days, which may contribute to enhanced cognition.            
dc.subjectAlzheimer's Disease
dc.subjectNur77
dc.subjectInflammation
dc.subjectexercise
dc.titleThe Regulation of Nur77 in Response to Inflammation, Amyloid-Beta, and Exercise in an LPS-Induced Alzheimer's Disease Modelen_US
etd.degree.departmentBiology


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