How the receptor FSHR-1 helps nerves and muscles communicate during normal and stress conditions
Official title: Investigation of the role of the G protein-coupled receptor FSHR-1 in multi-tissue control of neuromuscular signaling in normal and oxidative stress conditions
Funded at Butler University · NIH-11221240 · Data updated 2026-11-12
This project looks at whether a receptor called FSHR-1 helps protect nerve-to-muscle signaling from oxidative stress that can contribute to conditions like Alzheimer’s disease.
Quick facts
| Grant type | R15 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Butler University NIH-funded |
| Lab location | 1 site (Indianapolis, United States) |
| Project start | August 20, 2022 |
| Project end | July 31, 2028 |
| Funding year | 2025 |
| Award (this year) | $516,307 |
| NIH project number | 2R15NS112918-02 |
| Project ID | NIH-11221240 on NIH RePORTER |
Who could benefit from this research
✓Could help
This project does not enroll people because it is laboratory research in worms, though future clinical work informed by these findings would likely focus on patients with Alzheimer’s or other neurodegenerative diseases involving oxidative stress.
✕Less likely to help
Patients seeking immediate treatment or participation will not benefit directly from this grant because it conducts basic experiments in a non-human model.
What this research studies
Researchers will use the roundworm C. elegans to change or remove the FSHR-1 receptor in specific tissues such as the intestine and glial cells and then watch how nerve-to-muscle communication and movement change. They will expose worms to oxidative stress and compare signaling and behavior under normal and stressed conditions to map which tissues and molecules are involved. The team will test candidate signaling partners and downstream effectors to trace how signals travel between tissues to affect cholinergic motor neurons and muscle activity. Results aim to define molecular steps that could later guide treatments for human neurodegenerative conditions linked to oxidative damage.
Why it matters
Potential benefit: If successful, the work could reveal molecular targets to protect synapses and slow nerve damage in conditions like Alzheimer’s disease.
How similar studies have gone: Related studies in model organisms have shown that GPCR signaling and oxidative stress affect synaptic function, but the specific role of FSHR-1 in multi-tissue control is a newer, less-tested area.
Where this research is happening
-
Butler University
Indianapolis, United States Active
Researchers
- Principal investigator: Kowalski, Jennifer — Butler University
- Study coordinator: Kowalski, Jennifer
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About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page.