University of Kentucky
High fat diet induces behavioral deficits and an altered inflammatory profile that is partially restored by dietary reversal.
Grade Level at Time of Presentation
Junior
Major
Psychology and Public Health
Institution 24-25
University of Kentucky
KY House District #
1
KY Senate District #
1
Faculty Advisor/ Mentor
Linda J. Van Eldik, PhD; David J. Braun, PhD
Department
Dept. of Neuroscience
Abstract
Introduction: Obesity is a risk factor that can increase the likelihood of Alzheimer’s disease (AD). Kentucky has a higher prevalence of obesity compared to other states in the US, posing a significant risk of diet-related neurodegeneration and instances of AD and related dementias. Recent studies have shown robust impacts of dietary intervention in preventing later cognitive decline. Specifically in rodents, high-fat diet reversal can decrease memory deficits and neuroinflammation. These models need to be further explored to better identify the mechanisms underlying preservation of memory with an eye toward therapeutic targets for treatment of obesity-related cognitive decline in humans.
Purpose: The purpose of this study was to determine the role of dietary reversal on body weight, biomarker levels, and memory impairment in mice receiving a high-fat diet.
Methods: Twenty male mice were placed on a high-fat diet (HFD) at 6w of age. At 14w, the diet for half of the mice was switched to standard mouse chow (STD) for the remainder of the study. Mouse weights were collected weekly as a measure of metabolic health. Observable health was assessed using frailty index tests. Memory impairment was assessed in the Y-maze apparatus. Following observational and behavioral assessments, blood samples were collected at baseline, one month, and two months post-diet change. Brain tissue was collected at the conclusion of the study.
Results: At 1mo post-diet change, mice in the HFD group were frailer compared than baseline and frailer compared to mice in the Rev group at 1mo. HFD produced spatial memory deficits in the Y-maze. Several plasma and brain biomarkers were also significantly altered.
Conclusion: These findings indicate that HFD reversal can preserve cognitive and metabolic health and is associated with alterations in peripheral and central neuroinflammatory biomarkers that altogether provide future therapeutic targets which may ultimately benefit people in the Commonwealth.
High fat diet induces behavioral deficits and an altered inflammatory profile that is partially restored by dietary reversal.
Introduction: Obesity is a risk factor that can increase the likelihood of Alzheimer’s disease (AD). Kentucky has a higher prevalence of obesity compared to other states in the US, posing a significant risk of diet-related neurodegeneration and instances of AD and related dementias. Recent studies have shown robust impacts of dietary intervention in preventing later cognitive decline. Specifically in rodents, high-fat diet reversal can decrease memory deficits and neuroinflammation. These models need to be further explored to better identify the mechanisms underlying preservation of memory with an eye toward therapeutic targets for treatment of obesity-related cognitive decline in humans.
Purpose: The purpose of this study was to determine the role of dietary reversal on body weight, biomarker levels, and memory impairment in mice receiving a high-fat diet.
Methods: Twenty male mice were placed on a high-fat diet (HFD) at 6w of age. At 14w, the diet for half of the mice was switched to standard mouse chow (STD) for the remainder of the study. Mouse weights were collected weekly as a measure of metabolic health. Observable health was assessed using frailty index tests. Memory impairment was assessed in the Y-maze apparatus. Following observational and behavioral assessments, blood samples were collected at baseline, one month, and two months post-diet change. Brain tissue was collected at the conclusion of the study.
Results: At 1mo post-diet change, mice in the HFD group were frailer compared than baseline and frailer compared to mice in the Rev group at 1mo. HFD produced spatial memory deficits in the Y-maze. Several plasma and brain biomarkers were also significantly altered.
Conclusion: These findings indicate that HFD reversal can preserve cognitive and metabolic health and is associated with alterations in peripheral and central neuroinflammatory biomarkers that altogether provide future therapeutic targets which may ultimately benefit people in the Commonwealth.