# Exploring HFD-induced alterations in long-term potentiation in aged hippocampus and amygdala

> **NIH NIH R03** · OHIO STATE UNIVERSITY · 2021 · $78,000

## Abstract

PROJECT SUMMARY/ABSTRACT
Consumption of saturated fats and refined sugars has dramatically increased in the last century and, not
surprisingly, obesity rates have risen concomitantly. Approximately 30% of older adults (65 and older) are obese,
and this is alarming because obesity among this age group has been associated with cognitive impairments and
dementia, such as Alzheimer’s Disease. There is growing evidence that obesity-related neuroinflammation may
play a prominent role in Alzheimer’s disease initiation and/or progression. However, there is a fundamental gap
in understanding the underlying mechanisms involved in this relationship. Preclinical data indicate that even
short-term consumption of high-fat diets (HFD) triggers a potent neuroinflammatory response in the
hippocampus and amygdala, causing profound spatial, contextual, and emotional memory deficits. The long-
term goal is to develop effective interventions to prevent and reverse debilitating memory declines in the aged
population caused by unhealthy diets or obesity. The objective of this application is to understand the
mechanisms that underlie aging-associated HFD-induced hippocampal- and amygdalar-dependent memory
impairments. Short-term HFD consumption will be used in this proposal to avoid having the many co-morbidities
associated with obesity confound results and interpretations. The central hypothesis is that the interaction of
aging and HFD causes profound memory impairments through neuroinflammation-evoked deterioration of
synaptic plasticity, as measured by long-term potentiation, in both the hippocampus and the amygdala. Guided
by strong preliminary data, this hypothesis will be tested by pursuing two specific aims: 1) Determine the extent
to which HFD consumption disrupts LTP in the hippocampus and amygdala, and 2) Determine the extent to
which central IL-1b mediates HFD-induced LTP disruptions in aged rats. The approach is innovative, in the
applicant’s opinion, because it will determine, for the first time, whether neuroinflammation, caused by HFD
consumption, in the amygdala and hippocampus leads to impairments in LTP. The proposed research is
significant because it is expected to advance and expand understanding of early mechanisms of hippocampal
and amygdalar dysfunction in the aged population following HFD consumption. Ultimately, such knowledge will
lead to novel approaches to slow or prevent further cognitive declines that could otherwise develop into
Alzheimer’s disease.

## Key facts

- **NIH application ID:** 10137869
- **Project number:** 5R03AG067061-02
- **Recipient organization:** OHIO STATE UNIVERSITY
- **Principal Investigator:** RUTH M BARRIENTOS
- **Activity code:** R03 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $78,000
- **Award type:** 5
- **Project period:** 2020-04-15 → 2024-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10137869

## Citation

> US National Institutes of Health, RePORTER application 10137869, Exploring HFD-induced alterations in long-term potentiation in aged hippocampus and amygdala (5R03AG067061-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10137869. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*