# From FASD to AUDs: Strategies for Preventing Alcohol Addictions

> **NIH NIH K00** · UNIVERSITY OF TEXAS AT AUSTIN · 2024 · $91,481

## Abstract

DESCRIPTION (provided by applicant): Prenatal alcohol exposure (PAE) is a leading cause of
intellectual and other brain disabilities, contributing to an estimated prevalence of Fetal Alcohol
Spectrum Disorder (FASD) at between 1 and 5% of school-aged children in the US. Despite prevention
guidelines, alcohol use during pregnancy continues to be a problem, and consequently, FASD is
difficult to prevent. Behind every child with an FASD is an adult with unmet mental health needs that
result in risky patterns of alcohol consumption or an Alcohol Use Disorder (AUDs). Therefore,
preventing FASD requires preventing risky alcohol consumption in adults. Preventing AUDs is
challenging due to the paucity of effective medications. In this application, I propose a transitioning plan
in which I complement my passion for the study of FASD (the F99 phase) with the study of AUDs (the
K00 phase), with the expectation that the route to preventing FASD lies through preventing AUDs.
However, in both phases, I plan to pursue my interests in the mediating biology of non-protein-coding
RNAs. In the first phase of my predoctoral studies, I focused on Oct4/Pouf51, a transcription factor that 
is a key determinant of stem cell identity, and target of ethanol. I also identified a novel pseudo- gene
duplication of the Oct4/Pou5f1 locus, encoding a long non-coding RNA that I termed, Oc4pg9 lncRNA.
Oct4pg9 lncRNA is upregulated in neural stem cells (NSCs), following ethanol exposure. I found that
Oct4pg9 lncRNA mediates many maturational effects of ethanol on NSCs. In the F99 phase, I plan to
assess, using single-cell RNA sequencing, whether the expression of Oct4pg9 lncRNA and
Oct4/Pou5f1 marks unique non-overlapping NSC subpopulations. Using an in vivo murine model for
PAE, I plan to determine the extent to which ethanol exposure disrupts, at the cellular level, the
association between Oct4Pou5f1 and Oct4pg9, leading to the emergence of new NSC subpopulations
with aberrant maturation signatures. In the K00 phase, I will transition to the field of adult alcoholism
and continue studying the regulation and function of lncRNAs in the context of AUDs. This research
direction will focus on developing and behaviorally phenotyping mouse models of AUD-sensitive
lncRNAs. Additionally, I will utilize transcriptomic signatures and high-throughput behavioral screening
to identify and test candidate compounds that show promise in decreasing excessive alcohol
consumption. This proposal provides a research and training plan for a transition from predoctoral
FASD training to post-doctoral training in the biology of adult alcoholism, with the aim of developing an
independent research program in the field of adult alcoholism.

## Key facts

- **NIH application ID:** 10908453
- **Project number:** 5K00AA029955-05
- **Recipient organization:** UNIVERSITY OF TEXAS AT AUSTIN
- **Principal Investigator:** Nihal A Salem
- **Activity code:** K00 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $91,481
- **Award type:** 5
- **Project period:** 2019-07-19 → 2025-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10908453

## Citation

> US National Institutes of Health, RePORTER application 10908453, From FASD to AUDs: Strategies for Preventing Alcohol Addictions (5K00AA029955-05). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10908453. Licensed CC0.

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