How mitochondrial, lysosome, and immune problems affect dry age-related macular degeneration
Official title: The mechanistic role of the interconnected mitochondrial-lysosomal-immune dysfunction axis in early, dry AMD
Funded at Johns Hopkins University · NIH-11609399 · Data updated 2026-11-12
This grant looks at how stress in eye cells’ powerhouses, waste disposal systems, and immune signals may contribute to early dry AMD in people who carry specific genetic risk.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Johns Hopkins University NIH-funded |
| Lab location | 1 site (Baltimore, United States) |
| Project start | September 4, 2026 |
| Project end | August 31, 2027 |
| Funding year | 2026 |
| Award (this year) | $773,165 |
| NIH project number | 1R56EY037703-01A1 |
| Project ID | NIH-11609399 on NIH RePORTER |
Who could benefit from this research
✓Could help
Individuals with AMD risk factors, including the CFHY402H variant, and access to patient-derived iPSC-RPE cells.
✕Less likely to help
People without AMD risk variants or those not willing to provide cells or samples may not benefit.
What this research studies
Researchers will study eye cells derived from patients to see how mitochondrial and lysosome problems trigger immune signals that could damage the retina. They will focus on the CFHY402H genetic variant and how it worsens harmful processes inside retinal pigment epithelium cells. The project uses patient-derived cells to model the disease mechanism and test the chain of events leading to vision loss. If the mechanism is clarified, it could point to new ways to slow or prevent progression in people at risk.
Why it matters
Potential benefit: Understanding these pathways could lead to new targets for preventing or delaying vision loss in people with AMD, especially those with the CFHY402H risk variant.
How similar studies have gone: precedent in iPSC-derived retinal models supports studying disease pathways, but direct links to CFH variant–driven cGAS/STING activation are still being explored.
Where this research is happening
-
Johns Hopkins University
Baltimore, United States Active
Researchers
- Principal investigator: Sinha, Debasish — Johns Hopkins University
- Study coordinator: Sinha, Debasish
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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.