# Examination of gut-microbiome-brain interactions in a novel gene x environment model of neurodevelopmental disorders

> **NIH NIH F99** · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · 2022 · $41,352

## Abstract

PROJECT SUMMARY / ABSTRACT
The development of the nervous system is a complex, dynamic process that is dysregulated in
neurodevelopmental disorders (NDDs). Although progress has been made to identify genetic and environmental
NDD-risk factors, we lag behind with rigorous investigation of how environmental factors may act on certain
genetic vulnerabilities to alter neurodevelopment. My dissertation project builds on my co-sponsor, Dr. Blaser’s,
recent human epidemiological study that identified infant cephalosporin antibiotic exposure as an environmental
factor associated with increased NDD risk. It is well established that antibiotics decrease the diversity and
abundance of beneficial microbial taxa in the gut, which can consequently alter brain structure and function.
However, the mechanism(s) by which an antibiotic-induced perturbed microbiome affects early
neurodevelopmental processes implicated in NDD pathogenesis remains largely unexplored. My current work
addresses this research gap by investigating gut-microbiome-brain interactions in a novel gene by environment
(GxE) mouse model of NDDs under the supervision of Drs. Emanuel DiCicco-Bloom (sponsor, neuroscience)
and Martin Blaser (co-sponsor, microbiology). The primary goal of Aim 1 is to receive rigorous training in
microbiology and developmental neurobiology during the F99 phase to examine how early life cephalosporin
exposure alters the gut microbiome and consequentially dysregulates neurodevelopment. The proposed
experiments will utilize both wildtype and 16p11.2 microdeletion copy number variation (+/16pDel CNV) mice,
which are a robust genetic risk model for investigating NDD pathogenesis due to their highly conserved 28 gene
deletion region also observed in human +/16pDel heterozygotes. My preliminary findings indicate sex- and
genotype-dependent effects of cephalosporin exposure on altered neurodevelopment. For the remaining F99
phase, I will finish characterizing how early life cephalosporin exposure alters neurodevelopment and the gut-
microbiome and then incorporate a mechanistic approach to determine if microbiome restoration can rescue
altered neurodevelopment. This training will provide me with a strong technical and intellectual skillset to continue
investigating gut-microbiome-brain research as a postdoctoral scholar. However, a gap in my skillset that Aim 2
will expand on is the ability to analyze and interpret the metabolome and epigenome, two intermediate systems
that mediate gut-microbiome-brain GxE interactions. To ensure I address this gap, I will identify a postdoctoral
laboratory that can train me in routine and cutting-edge techniques to study and manipulate the metabolome and
epigenome during the K00 phase. These studies will collectively establish and build on a mechanistic framework
to investigate gut-microbiome-brain GxE interactions while simultaneously facilitating my path towards
independence as a neuroscience investigator.

## Key facts

- **NIH application ID:** 10610587
- **Project number:** 1F99NS130926-01
- **Recipient organization:** RUTGERS BIOMEDICAL AND HEALTH SCIENCES
- **Principal Investigator:** Courtney R. McDermott
- **Activity code:** F99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $41,352
- **Award type:** 1
- **Project period:** 2022-09-15 → 2024-09-14

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10610587

## Citation

> US National Institutes of Health, RePORTER application 10610587, Examination of gut-microbiome-brain interactions in a novel gene x environment model of neurodevelopmental disorders (1F99NS130926-01). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10610587. Licensed CC0.

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