Understanding how the brain preserves vision in retinitis pigmentosa
Official title: The role of plasticity in loss of vision caused by retinitis pigmentosa
Funded at University of Arizona · NIH-11000382 · Data updated 2026-11-12
This grant studies why people with retinitis pigmentosa keep some visual sharpness even as their eye cells fail, by looking at brain and eye circuits in mice and figuring out if changing plasticity could slow vision loss.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | University of Arizona NIH-funded |
| Lab location | 1 site (Tucson, United States) |
| Project start | January 1, 2025 |
| Project end | December 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $357,759 |
| NIH project number | 5R01EY035885-03 |
| Project ID | NIH-11000382 on NIH RePORTER |
Who could benefit from this research
✓Could help
Not applicable to patients directly in this grant; the study uses a mouse model to understand mechanisms that could benefit people with RP in the future.
✕Less likely to help
Direct patient benefit is not immediate; outcomes depend on future translation to human therapies.
What this research studies
Retinitis pigmentosa gradually damages vision, but acuity declines more slowly than retinal function. Researchers will study visual cortex and retina in a mouse model that mimics human RP to understand how the brain adapts to reduced input. They will test whether increasing or decreasing experience-driven brain plasticity changes the course of vision loss, using mice with genetic tweaks that alter plasticity. Findings could reveal targets to slow vision decline and sustain acuity for patients with RP.
Why it matters
Potential benefit: If successful, this work could identify ways to preserve visual sharpness in RP patients by guiding plastic changes in the brain and retina.
How similar studies have gone: Animal studies of plasticity and vision have informed understanding of RP progression, with ongoing exploration translating to human trials.
Where this research is happening
-
University of Arizona
Tucson, United States Active
Researchers
- Principal investigator: Mcgee, Aaron W — University of Arizona
- Study coordinator: Mcgee, Aaron W
Related research
Other NIH-funded projects on the same topics.
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Inflammation in MERTK-related retinitis pigmentosa
This project aims to understand whether losing the MERTK gene causes retinal inflammation that leads to vision loss in people with MERTK-related retinitis pigmentosa.
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Enhancing cone survival in RP through targeted cell-specific CRISPR therapy
A patient-friendly look at a new approach to protect cone cells in retinitis pigmentosa using precise gene editing to support vision.
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Oral, once-daily MC16 medicine for retinitis pigmentosa
A gene-mutation-agnostic pill (MC16) is being studied to help people with retinitis pigmentosa by addressing a common cellular problem in the eye.
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Role of IPM Proteoglycans in Retinal Health and Inherited Blindness
This grant studies how specific retinal extracellular matrix proteins (IMPG1 and IMPG2) affect eye health and contribute to retinitis pigmentosa, with potential implications for people who have or are at risk for inherited blindness.
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NAC Attack: a late-stage trial for preserving vision in RP patients
A large, multi-site study is testing whether taking a daily NAC pill can help people with retinitis pigmentosa keep more of their vision.
-
Non-invasive biomarker for mitochondria health in retinitis pigmentosa
Aims to test a new, non-invasive OCT-based biomarker to explain and predict how mitochondria function affects cone cells in people with retinitis pigmentosa.
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.