Modulating the DNA Repair System to Protect Nerve Cells After Eye Injury
Official title: Modulating the DNA Damage Repair System in Traumatic Optic Neuropathy
Funded at Stanford University · NIH-11387494 · Data updated 2026-11-12
A physician-scientist at Stanford is testing whether tweaking the DNA damage repair process can keep retinal nerve cells alive after optic nerve injury to prevent vision loss.
Quick facts
| Grant type | Career grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Stanford University NIH-funded |
| Lab location | 1 site (Stanford, United States) |
| Project start | September 1, 2025 |
| Project end | August 31, 2030 |
| Funding year | 2026 |
| Award (this year) | $257,785 |
| NIH project number | 5K08EY037381-02 |
| Project ID | NIH-11387494 on NIH RePORTER |
Who could benefit from this research
✓Could help
Ideal candidates are individuals with or at risk for optic nerve injuries where neuroprotection strategies could preserve vision.
✕Less likely to help
Patients without optic nerve injury or those unlikely to benefit from neuroprotection strategies may not benefit.
What this research studies
Traumatic optic neuropathy can cause irreversible vision loss, and this grant explores a potential therapy that protects retinal cells by adjusting DNA damage response pathways. The project focuses on Chk1, a protein involved in cell survival after injury, to see if inhibiting it helps retinal ganglion cells survive and regenerate. The team will study this effect in lab models and map the molecular partners of Chk1 in retinal cells to understand how it supports cell survival. If successful, the approach could open new avenues for treating TON and related optic neuropathies.
Why it matters
Potential benefit: If successful, patients with TON could retain vision or avoid progression after injury.
How similar studies have gone: Early preclinical work suggests targeting DNA damage response can influence neuron survival, but human data in TON are limited.
Where this research is happening
-
Stanford University
Stanford, United States Active
Researchers
- Principal investigator: Kinde, Benyam Z — Stanford University
- Study coordinator: Kinde, Benyam Z
Related research
Other NIH-funded projects on the same topics.
-
Non-invasive, microscopic biomarkers to detect CIPN in chemotherapy patients
This grant aims to develop a non-invasive imaging method to measure nerve changes in patients undergoing chemotherapy to better understand and monitor chemotherapy-induced peripheral neuropathy (CIPN).
-
Neonatal Fc receptor blockade by efgartigimod to help inflammatory nerve disease
Aims to test how blocking a specific antibody trafficking receptor with efgartigimod could improve nerve inflammation in a model of AIDP/GBS-type neuropathy.
-
Schwann cell aging and secretions linked to diabetic nerve damage
A research project looking at how aging nerve cells and their secretions may drive nerve damage in people with type 2 diabetes.
-
Diabetic bladder problems in diabetes mice show sex-specific nerve and inflammation roles
Aims to understand why bladder problems happen in diabetes, exploring how inflammation and nerves differ between male and female mice.
-
Prenyltransferase inhibitor as a new therapy for inflammatory neuropathy
A new drug candidate called FGTI-2734 is being studied to calm nerve inflammation in conditions like AIDP/Guillain-Barré syndrome, with the goal of protecting nerves and reducing symptoms.
-
KCTD11-related CMT neuropathy: uncovering how it damages nerves
We are studying a genetic form of Charcot–Marie–Tooth disease to understand what goes wrong in nerves and support future treatments.
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.