Inflammation, and Amyloid-Beta in Conjunction with Isolation Stress in C57BL6/J Mice Hagen, C.2, Peterman, J. L.1, Eimerbrink, M. J.1, White, J. D.1, Cooksey, M.2, Boehm, G. W.1, Chumley, M. J.2 1Department of Psychology, Texas Christian University; 2Department of Biology, Texas Christian University
As current research explores the connection between inflammation and neurodegenerative diseases, one area of serious concern is how psychological stress impacts this interaction. Moreover, this interaction is especially relevant in Alzheimer's disease (AD). Here, we investigate how stress influences both inflammatory pathways and as well as the production of amyloid beta (Aβ), a protein responsible for plaque formation in AD. In these experiments, social isolation was used in C57BL6/J mice at varying durations to model psychological stress. To measure changes to inflammation in response to stress, lipopolysaccharide (LPS; 250 g/kg, i.p.) was administered post isolation and inflammatory markers were quantified 4 hours later. To determine how isolation stress affects amyloid beta production, the stress paradigm was repeated with 7 daily administrations of either LPS or saline, as our lab has previously demonstrated this results in significant hippocampal Aβ production. Hippocampal tissue was then collected to measure levels of amyloid beta. Cognition was also assessed through contextual fear conditioning (CFC). Further, experiments were conducted with both males and females to explore potential sex differences. Together, these experiments further expand on the negative impact stress has on brain health. This research is particularly important in today's society where stress has become an unavoidable reality.
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