Cathepsin L's role in changing nuclear proteins linked to aging and Alzheimer’s
Official title: Cathepsin-L mediated remodeling of the nuclear proteome
Funded at Saint Louis University · NIH-11231249 · Data updated 2026-11-12
Seeing if changing levels of the enzyme cathepsin L can reduce harmful nuclear proteins in people with Alzheimer’s disease and premature-aging syndromes.
Quick facts
| Grant type | R21 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Saint Louis University NIH-funded |
| Lab location | 1 site (Saint Louis, United States) |
| Project start | November 15, 2024 |
| Project end | October 31, 2026 |
| Funding year | 2026 |
| Award (this year) | $189,375 |
| NIH project number | 5R21AG089917-02 |
| Project ID | NIH-11231249 on NIH RePORTER |
Who could benefit from this research
✓Could help
Patients with Alzheimer’s disease or with Hutchinson–Gilford Progeria Syndrome (or their caregivers) would be most directly interested and could consider contributing biological samples in future related work.
✕Less likely to help
People with conditions unrelated to nuclear lamins or those seeking immediate clinical therapies are unlikely to benefit directly from this early laboratory research.
What this research studies
This project looks at an enzyme called cathepsin L that can alter proteins inside the cell nucleus that are linked to aging and Alzheimer’s. Researchers will work with patient-derived cells (including cells from people with progeria) and lab experiments to see how cathepsin L trims or remodels nuclear proteins such as lamin B1 and progerin. They will test whether drugs like chloroquine that raise nuclear cathepsin L levels reduce toxic protein fragments and signs of cellular aging. The goal is to identify molecular steps that could become targets for future treatments to protect brain cells or reduce damage in rare premature-aging conditions.
Why it matters
Potential benefit: If successful, this work could point to new ways to reduce toxic nuclear proteins and potentially slow progression of Alzheimer’s or lessen symptoms of progeria.
How similar studies have gone: Prior laboratory studies showed that raising nuclear cathepsin L improved cellular features in progeria cells and similar nuclear changes are seen in Alzheimer’s, but this approach has not yet produced proven treatments for people.
Where this research is happening
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Saint Louis University
Saint Louis, United States Active
Researchers
- Principal investigator: Gonzalo Hervas, Susana — Saint Louis University
- Study coordinator: Gonzalo Hervas, Susana
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.