Presenters: Anna Everett, College of Family, Home, and Social Sciences, Neuroscience
Authors: Erin Saito, Anna Everett, Darien Reed, Jeffrey Edwards
Faculty Advisor: Jeffrey Edwards, College of Life Sciences, Physiology and Developmental Biology
Institution: Brigham Young University
The ketogenic diet initially began as a significant treatment to prevent epilepsy. More recently it has seen a rise in popularity again, with many attributing positive physiological and cognitive benefits. The purpose of this study is to assess the validity of those claims in an animal model in order to examine this at the cellular level as well as identify possible molecular mechanisms for the changes observed. To quantify this, mice will be fed a diet high in fats and low in carbohydrates. A Morris water maze will be used to assess the diet’s effect on spatial memory. Next, field electrophysiology experiments will assess the cellular mechanism of memory known as long-term potentiation (LTP) in the hippocampus, which is the memory center of the brain. It was hypothesized that changes in concentration of an important development factor, brain-derived neurotrophic factor (BDNF), are a possible explanation for physiological changes caused by the keto diet. To determine this, ANA-12, a TrkB antagonist, will be intraperitoneally (IP) injected to block the effects caused by BDNF. Preliminary data gathered from bathed brain slices of both male and female animals have shown an enhancement of LTP. These data lead us to our hypothesis that the ketogenic diet will cause significant changes in behavioral memory and CA1 synaptic plasticity through altered BDNF levels. By understanding the mechanism of ketones on spatial learning, the ketogenic diet could be established as a viable intervention in disease and prevention in age-related cognitive decline.