Proteasome Boost to Protect Vision in Retinitis Pigmentosa
Official title: Role of Proteasome Overload in Pathogenesis of Retinitis Pigmentosa
Funded at Duke University · NIH-11312607 · Data updated 2026-11-12
A study to see if boosting the cell’s protein-cleanup machines can slow vision loss in people with retinitis pigmentosa.
Quick facts
| Grant type | Career grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Duke University NIH-funded |
| Lab location | 1 site (Durham, United States) |
| Project start | May 1, 2022 |
| Project end | April 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $170,704 |
| NIH project number | 5K08EY033857-05 |
| Project ID | NIH-11312607 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates would be individuals with retinitis pigmentosa or related retinal degeneration, particularly those interested in future trials targeting proteasome pathways.
✕Less likely to help
Patients whose RP is not related to proteostasis imbalance or who cannot participate in preclinical-to-clinical translation steps may not benefit.
What this research studies
Retinitis pigmentosa is a leading cause of inherited blindness with many different genetic causes. This project focuses on restoring balance in how cells degrade misfolded proteins in the eye, using mouse models to test whether targeting the 20S proteasome core can reduce retinal degeneration. The research will explore drug-like approaches that enhance proteasomal activity to protect photoreceptors, aiming to identify potential targets and strategies suitable for translation to patients. If successful, this work could lay the groundwork for therapies that help many RP patients regardless of their specific mutation.
Why it matters
Potential benefit: If successful, the work could lead to treatments that slow or prevent vision loss for many people with RP.
How similar studies have gone: Preclinical studies in models of retinal degeneration have shown that improving proteostasis can delay photoreceptor loss.
Where this research is happening
-
Duke University
Durham, United States Active
Researchers
- Principal investigator: Alekseev, Oleg — Duke University
- Study coordinator: Alekseev, Oleg
Related research
Other NIH-funded projects on the same topics.
-
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.
-
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.
-
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.
-
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.