# Investigating the effects of the microbiota on vagal afferent sensory neuronal activity in an animal model of Parkinson’s disease

> **NIH NIH F31** · UNIVERSITY OF CALIFORNIA LOS ANGELES · 2021 · $37,808

## Abstract

PROJECT SUMMARY
Neurological disorders are recognized by the World Health Organization as “one of the greatest threats to
public health.” Parkinson's disease (PD) in particular is estimated to afflict nearly 10 million people worldwide,
1 million of whom reside in the US. Recent evidence suggests a causal role for the microbiota in promoting
motor behaviorial abnormalities and alpha-synuclein pathology in animal models of PD, but the precise
mechanisms that mediate these effects remain elusive. In addition, the vagus nerve has been extensively
hypothesized to play a role in the spread of amyloid pathology from the enteric nervous system to the central
nervous system during development of PD, but there has been no interrogation to date into the consequences
of microbiome-induced alterations in vagal activity on the development of PD symptoms. These fundamental
gaps in knowledge surrounding precisely how the microbiome modulates PD symptoms motivates my research
on uncovering interactions between microbes and vagal activity in a PD mouse model. I hypothesize that vagal
chemosensation of microbially-modulated metabolites contributes to the development of PD-related symptoms.
The proposed research has the potential to inform novel therapeutic targets for early intervention or diagnosis
of PD, and aligns directly with the NINDS mission to “seek fundamental knowledge about the brain and
nervous system to reduce the burden of neurological disease.”
My preliminary data support the central hypothesis that the microbiome modulates vagal fiber activity in vivo,
and that alterations in vagal activity result from active sensation of bacterial stimuli occurring on short time
scales. Further, results from my experiments indicate that vagal fiber activity is elevated in a PD mouse model,
supporting a role for vagal hyperactivity as a contributing factor to the development of PD-related behaviors. In
light of these data, I hypothesize that functional alterations in vagal afferent signaling to the CNS arise from
dysregulated microbial signals in the intestinal lumen and that microbiome-induced vagal hyperactivity
contributes to the development of PD symptoms. I propose to test these hypotheses through the following
aims. Aim 1: Identify select microbially-mediated metabolites that regulate vagal neuronal activity; Aim 2:
Determine the role of mcirobiota-driven alterations in vagal activity in the development of PD-related
symptoms. Findings from these aims will reveal novel insights into the molecular and cellular signaling
mechanisms underlying microbiota-gut-brain communication at homeostasis and during the progression of PD
symptoms.

## Key facts

- **NIH application ID:** 10221619
- **Project number:** 5F31NS118966-02
- **Recipient organization:** UNIVERSITY OF CALIFORNIA LOS ANGELES
- **Principal Investigator:** Kelly Jameson
- **Activity code:** F31 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $37,808
- **Award type:** 5
- **Project period:** 2020-08-01 → 2022-07-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10221619

## Citation

> US National Institutes of Health, RePORTER application 10221619, Investigating the effects of the microbiota on vagal afferent sensory neuronal activity in an animal model of Parkinson’s disease (5F31NS118966-02). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10221619. Licensed CC0.

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