# Neuroprotection of retinal ganglion cells.

> **NIH NIH R16** · YORK COLLEGE · 2024 · $159,998

## Abstract

Project Summary
Mitochondrial dysfunction contributes to the death of retinal ganglion cells and their
axons in a variety of neurodegenerative conditions, including glaucoma, diabetic
retinopathy, and traumatic optic neuropathy. Retinal ganglion cells are particularly
vulnerable to dysfunction because the cells have high metabolic demands and axons
that are prone to damage as they exit the eye. Under normal conditions, ganglion cells
require an abundance of ATP to maintain cellular membrane potential, regulate calcium
levels, and to remove glutamate from synapses; these demands increase when exposed
to oxidative stress. A proposed treatment to manage oxidative stress following trauma to
the optic nerve is administration of compounds to support mitochondrial function. Our
laboratory has identified a high-density aromatic peptide (HDAP2) that targets cardiolipin
on the inner mitochondrial membrane and optimizes the mitochondrial membrane
potential under conditions of oxidative stress.
We propose to study the effect of HDAP2 in adult mice following optic nerve crush on
the survival of retinal ganglion cells, their dendritic arbors and the morphology of
mitochondria within affected neurons. Optic nerve crush closely approximates the partial
loss of optic nerve function and secondary loss of retinal ganglion cells observed in
many neurodegenerative diseases (Goldblum and Mittag, 2002; Levkovitch-Verbin et al.,
2000) and allows study of both primary and secondary effects of the trauma. Our
preliminary results have shown that administration of HDAP2 following optic nerve crush
significantly increases the survival of retinal ganglion cells following the procedure,
demonstrating its potential for preserving neuronal function.

## Key facts

- **NIH application ID:** 10841320
- **Project number:** 1R16GM149428-01A1
- **Recipient organization:** YORK COLLEGE
- **Principal Investigator:** MARGARET MACNEIL
- **Activity code:** R16 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $159,998
- **Award type:** 1
- **Project period:** 2024-04-01 → 2028-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10841320

## Citation

> US National Institutes of Health, RePORTER application 10841320, Neuroprotection of retinal ganglion cells. (1R16GM149428-01A1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10841320. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*