# Omega-3 supplementation as a therapeutic agent in PAE-induced neuroinflammation

> **NIH NIH F32** · UNIV OF NORTH CAROLINA CHAPEL HILL · 2022 · $72,082

## Abstract

Abstract
An estimated 10% of pregnant women in the US report consuming alcohol within the past 30 days, and 3%
report binge drinking. Prenatal alcohol exposure (PAE) causes significant cognitive impairment in humans and
in animal models, and persistent PAE-induced neuroinflammation may contribute to these impairments,
although underlying mechanisms are not well understood. Understanding these mechanisms will inform
strategies that may improve outcomes for these individuals.
Neuroinflammation is induced through a complex and dynamic network of lipid mediators, cytokines, and
chemokines produced from various neuroimmune cells, including microglia which are the resident
macrophage-like innate immune cells of the brain. They are the first line of innate immunity and mediate
immune regulation and resolution of inflammation. Polyunsaturated fatty acids (PUFAs) provide critical
structural and functional components in the brain and in resident immune cells. Long-chain PUFAs can elicit
immunomodulatory effects via their metabolites; these lipid mediators can alter the intensity and/or duration of
inflammation. Omega-3 PUFAs are well known for their anti-inflammatory and pro-resolving properties;
relevant lipid metabolites include E-series resolvins derived from eicosapentaenoic acid (EPA) that elicit their
anti-inflammatory effects by binding to the chemerin receptor (ChemR23). Microglia have high levels of EPA
and ChemR23. Activation of ChemR23 suppresses neuroinflammation, while its removal increases
inflammation. Alcohol consumption during pregnancy is associated with decreased PUFA accumulation in the
developing brain which may disrupt the ability of microglia to resolve neuroinflammation. The long-term goal of
the proposed research is to evaluate the role of resolvins in PAE-induced neuroinflammation. Specifically, this
study will utilize a ChemR23 knockout (KO) mouse strain. Pregnant mice will be exposed to alcohol and
provided an EPA-enriched diet. Offspring will be assessed for lipid and resolvin concentrations in the brain
(Aim 1) and neuroinflammation (Aim 2) at weaning. Experiments will be done in KO and background
(C57BL/B6J) mice to functionally test the role of EPA-derived resolvins in PAE-induced neuroinflammation.
The Nutrition Research Institute of UNC Chapel Hill (NRI) is located on the North Carolina Research Campus
(NCRC). The campus maintains a collaborative atmosphere among multiple universities, companies and
community partners and provides state-of-the-art lab and animal facilities housing all necessary equipment for
the proposed research. My mentor Dr. Sandra Mooney sustains a strong scholarship in PAE,
neurodevelopment, behavioral studies, grantsmanship, and academic collaboration. Taken together, Dr.
Mooney’s mentorship and the NRI will help me to achieve my goals of; strengthening my background in PAE,
nutrition, neurodevelopment and neuroimmunology research, build a strong neurodevelopment and
neuroimmunology assessment skill ...

## Key facts

- **NIH application ID:** 10387762
- **Project number:** 1F32AA029287-01A1
- **Recipient organization:** UNIV OF NORTH CAROLINA CHAPEL HILL
- **Principal Investigator:** Kathleen Rose Walter
- **Activity code:** F32 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $72,082
- **Award type:** 1
- **Project period:** 2022-02-01 → 2023-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10387762

## Citation

> US National Institutes of Health, RePORTER application 10387762, Omega-3 supplementation as a therapeutic agent in PAE-induced neuroinflammation (1F32AA029287-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10387762. Licensed CC0.

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