# Modeling poly-genomic risk in the relationship between brain structure and alcohol involvement from adolescence through adulthood

> **NIH NIH R21** · WASHINGTON UNIVERSITY · 2020 · $147,656

## Abstract

PROJECT SUMMARY/ABSTRACT
Alcohol use is associated with significant personal and socioeconomic costs (accounting for more than 5% of
global disease burden as well as worldwide deaths). Alcohol use initiation, progression to heavy episodic
drinking, and early onset alcohol use disorder commonly emerge during adolescence and young adulthood. This
developmental period of risk is theorized to result from typical patterns of regionally asynchronous brain
maturation (i.e., rapid and early development of limbic regions alongside relatively immature prefrontal and
multimodal association cortices) resulting in a diminished ability to suppress inappropriate emotions, desires,
and actions when salient environmental cues are present. During later young adulthood the stabilization,
reduction, or desistance of heavy use typically occurs alongside maturing cognitive control and emotional
regulation abilities coinciding with cortical development. Brain maturation may also be influenced by alcohol
use. However, whether alcohol use alters brain maturation and/or results from individual differences in neural
development attributable to predipsositional genomic background is unclear and can only be addressed by
genomically-informed longitudinal research with extensive alcohol phenotyping. In this 2-year R21, we propose
to add genome-wide association study (GWAS) content to 2 longitudinal neuroimaging studies of adolescents
and young adults (n=696; spanning ages 12-33 with annual neuroimaging and biannual alcohol characterization)
to examine whether brain changes during adolescence and young adulthood associated with alcohol use may
represent polygenic risk factors and/or represent consequences of heavy alcohol exposure. Disentangling the
contributions of predisposing factors from consequences of alcohol on structural brain trajectories will inform our
etiologic understanding of alcohol use during adolescence and young adulthood that could contribute to alcohol-
related policy, education, nosology, prevention, and treatment. Primary deliverables from this project will be
manuscripts examining whether polygenic propensity to alcohol use, as well as risk for impulsivity and negative
affect and deficits in cognition, modify trajectories of brain maturation and further alter the course of youth alcohol
engagement. Further, due to the extensive scope of longitudinal data available in these studies (e.g., other neural
phenotypes, psychiatric, sleep, trauma, biosensor assessments), the addition of GWAS data will provide benefits
to the broader research community through data sharing (e.g., dbGaP) and contribute to consortia-based gene
discovery efforts (e.g., ENIGMA, PGC).

## Key facts

- **NIH application ID:** 10013119
- **Project number:** 5R21AA027827-02
- **Recipient organization:** WASHINGTON UNIVERSITY
- **Principal Investigator:** RYAN H BOGDAN
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $147,656
- **Award type:** 5
- **Project period:** 2019-09-09 → 2023-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10013119

## Citation

> US National Institutes of Health, RePORTER application 10013119, Modeling poly-genomic risk in the relationship between brain structure and alcohol involvement from adolescence through adulthood (5R21AA027827-02). Retrieved via AI Analytics 2026-05-25 from https://api.ai-analytics.org/grant/nih/10013119. Licensed CC0.

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