All ETDs from UAB

Advisory Committee Chair

Karen L Gamble

Advisory Committee Members

Jeremy J Day

Kirk M Habegger

Lori L McMahon

David M Pollock

Document Type


Date of Award


Degree Name by School

Doctor of Philosophy (PhD) Heersink School of Medicine


Circadian rhythms are biological processes that cycle every ~24 hours and have allowed life to adapt for optimal function across the day. These rhythms are present in all tissues in the body and are coordinated to the light/dark cycle by the suprachiasmatic nucleus (SCN) in the hypothalamus. Along with active-rest cycles, cognitive performance fluctuates across the course of the day, peaking during the active phase. In addition to the light cycle, food and meal timing can provide signaling cues to extra-SCN tissues. Food access only during the inactive phase results in weight gain and memory impairment. High fat diet protocols are well-established models of obesity and impair cognition along with other metabolic functions. High fat diets also rapidly disrupt rhythms in meal timing and activity. Although high sucrose diets similarly impair cognition, the effect on circadian behavior is unknown. It also remains unknown whether either high fat or high sucrose diets disrupt rhythmic hippocampal function. The goal of this dissertation is to test the hypothesis that calorically dense diets impair cognition through altered circadian behaviors, namely meal timing, resulting in disruption to the hippocampal molecular clock, using multiple feeding strategies, memory tasks, slice electrophysiology, and western blot analysis. In the main chapters, we show that: 1) both high fat and high sucrose diets result in loss of day night differences in working memory, synaptic plasticity, and alter many components of the hippocampal molecular clock, and 2) restricting access to high fat diet to the active phase rescues cognitive impairment and synaptic plasticity independent of rescuing the hippocampal molecular clock. The results presented here are the first to demonstrate that high caloric diet disrupts rhythms in cognition and that this impaired rhythmicity in cognition can be rescued with restricted meal timing. We also discovered that this rescue is independent of restoring rhythmicity of the hippocampal molecular clock. As obesity is linked to increased risk of dementia and cognitive impairment later in life, practical strategies involving meal timing may provide beneficial areas of study for human health.



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