What is it about?
When the optic nerve is injured — for example, from trauma — the light-sensing cells that connect the eye to the brain (called retinal ganglion cells, or RGCs) start to die, and vision is permanently lost. This happens for two main reasons: the cells lose access to protective proteins called neurotrophic factors, and toxic levels of zinc build up inside the eye. In this study, we designed tiny nanoparticles that slowly release two protective proteins (CNTF and BDNF) together with a zinc-binding compound (DPA) that removes the excess zinc. In rats with optic nerve injury, a single injection of these particles kept releasing the proteins for up to two months and the zinc-binder for about a month. Compared to untreated animals, treated animals retained far more of their retinal ganglion cells, and their nerve fibers stayed intact over a much greater distance — extending from the eye all the way into the vision centers of the brain.
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Why is it important?
Currently, there's no established way to protect the optic nerve after injury, partly because protective proteins break down quickly in the body and typically require repeated injections directly into the eye. Our nanoparticle system addresses this by packaging both treatments into a single, long-lasting injection, and by directly tackling zinc toxicity — a contributor to nerve damage that most existing approaches don't target. The results show that combining protein delivery with zinc removal protects nerve cells and their connections to the brain more effectively than either approach alone, offering a promising new strategy for treating traumatic optic nerve injuries.
Perspectives
Most of my work has focused on brain-related biomaterials, so this project was a rewarding change of scope — applying similar delivery principles to protect vision instead. Working with the Ophthalmology team taught me just how few real treatment options exist for optic nerve injury, and how much protein delivery and zinc regulation depend on each other for real therapeutic benefit — neither works well alone. I hope this encourages more people to think about neuroprotection as a combination problem rather than a single-target one.
HUYNH QUANG DIEU NGUYEN
University of Colorado Anschutz Medical Campus
Read the Original
This page is a summary of: Co-delivery of neurotrophic factors and a zinc chelator substantially increases retinal ganglion cell survival and axon protection in the optic nerve crush model, Acta Biomaterialia, July 2025, Elsevier,
DOI: 10.1016/j.actbio.2025.06.007.
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