# The neuroimmune model of excessive alcohol consumption: Transition to Alcohol Use Disorder.

> **NIH NIH R01** · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · 2020 · $573,750

## Abstract

Project Summary/Abstract
Activation of the innate immune system results in the release of pro-inflammatory cytokines, which may lead
to changes in neuroimmune signaling and behavioral abnormalities, such as high alcohol (ethanol)
consumption, which may ultimately lead to the development of alcohol use disorder (AUD). We lack
understanding of how changes in neuroimmune signaling are integrated into neuronal networks that
mediate the transition from normal (social) drinking to excessive alcohol consumption. Here, we propose the
neuroimmune model of excessive alcohol consumption, where repeated injections of the immune activator
Poly(I:C) produce progressive escalation of alcohol intake over several weeks of drinking. We hypothesize
that immune activation induces cell type-specific changes in gene expression, which are integrated to affect
neuronal functions and drive excessive drinking. We will use a combination of molecular, cellular, behavioral
and computational approaches to test this hypothesis. Gene expression will be measured in neurons,
astrocytes and microglia to investigate cell type-specific molecular mechanisms of immune activation. We
will then use molecular signatures from different cell types and computationally-driven drug-repurposing
approaches to identify and test pharmacological compounds with the potential to reduce high alcohol
drinking. We will investigate roles of specific neural networks in immune-induced escalation of drinking by
measuring neuronal functions and manipulating excitability of critical projection neurons. Temporal profiling
across three critical time points will identify dynamic changes in cell type-specific transcriptomes and
neuronal functions. Results of the proposed experiments will advance our understanding of the role of
neuroimmune signaling in the transition to AUD and will be widely applicable to brain disorders with pro-
inflammatory phenotypes.

## Key facts

- **NIH application ID:** 9778698
- **Project number:** 5R01AA027096-03
- **Recipient organization:** TEXAS TECH UNIVERSITY HEALTH SCIS CENTER
- **Principal Investigator:** Igor Ponomarev
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $573,750
- **Award type:** 5
- **Project period:** 2018-09-10 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9778698

## Citation

> US National Institutes of Health, RePORTER application 9778698, The neuroimmune model of excessive alcohol consumption: Transition to Alcohol Use Disorder. (5R01AA027096-03). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9778698. Licensed CC0.

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