Targeting p38 MAPK to slow ALS-related axonal damage
Official title: Inhibiting specific kinases in the p38 MAPK pathway module to treat different genetic forms of ALS
Funded at University of Illinois at Chicago · NIH-11607932 · Data updated 2026-11-12
Aims to block a specific brain-wide signaling pathway (p38 MAPK) to reduce nerve damage in people with various genetic forms of ALS.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Illinois at Chicago NIH-funded |
| Lab location | 1 site (Chicago, UNITED STATES) |
| Project start | September 1, 2026 |
| Project end | August 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $528,643 |
| NIH project number | 1R56NS146375-01A1 |
| Project ID | NIH-11607932 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals with ALS or genetic forms showing axonal transport defects who could benefit from therapies targeting p38 MAPK.
✕Less likely to help
Patients whose disease is not driven by FAT defects or who cannot tolerate kinase inhibitors may not benefit from this approach.
What this research studies
Amyotrophic lateral sclerosis (ALS) damages nerves early on by impairing the fast transport of cellular components within axons. This project tests whether inhibiting a key kinase in the p38 MAPK pathway can prevent or lessen axon degeneration caused by ALS-linked gene changes. The study uses a special ex vivo model to understand how mutant ALS proteins trigger harmful signaling and whether blocking p38a helps protect axons in living systems. If successful, this approach could point to a new therapeutic strategy for multiple ALS forms that share this axonal problem.
Why it matters
Potential benefit: If successful, patients with ALS may gain a new treatment approach that protects nerve fibers and potentially slows disease progression.
How similar studies have gone: Preclinical studies have shown that blocking p38 MAPK can reduce axonal transport defects in ALS models, supporting this approach.
Where this research is happening
-
University of Illinois at Chicago
Chicago, United States Active
Researchers
- Principal investigator: Morfini, Gerardo Andres — University of Illinois at Chicago
- Study coordinator: Morfini, Gerardo Andres
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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.