NEI-funded research identifies molecule that strengthens the eye’s response to damage in retinal disease

This artistic rendering depicts the retina as a landscape at night, where blood vessels appear as luminous rivers across hills of neural tissue. A constellation of erucamide molecules descends in light and engages TMEM19 on microglial cells, rousing them from their resting state. As the activated cells begin to glow, the surrounding tissue brightens, illustrating how erucamide-mediated activation of retinal microglial cells improved vascular and neuroretinal outcomes in models of retinal degeneration. Credit: Katie Biscocho, Scripps Research

Research funded by the National Eye Institute shows that a naturally occurring molecule called erucamide plays a role in how cells communicate in the retina, the light-sensing tissue at the back of the eye. While erucamide levels drop as light-sensing cells known as photoreceptors begin to die, restoring the molecule activates cellular responses that support retinal stability. These findings suggest that erucamide may be part of a natural protective response in the retina, and could offer a new way to slow the progression of diseases that lead to vision loss. The findings published in Nature Neuroscience.

Many conditions that cause vision loss share a common feature: the gradual breakdown of the retina. Although scientists know some of the structural changes that ensue as this damage progresses, less is understood about the molecular signals that shape how the retina copes with disease.

"The retina doesn't simply deteriorate; in fact, it actively responds to injury," says senior author Martin Friedlander, M.D., Ph.D., a professor at Scripps Research. "Our work identifies erucamide as a signaling molecule that helps coordinate that response." Scripps Research conducted the study in collaboration with University of California San Diego and the Lowy Medical Research Institute.

The retina depends on constant communication between neurons, glia, blood vessels and immune cells. This system, the neurovascular unit, keeps visual tissue functioning. But in diseases associated with loss of vision such as diabetic retinopathy, retinitis pigmentosa and age-related macular degeneration, that tight coordination wanes. Photoreceptors start dying, and eyesight fades.

The work from Friedlander's team builds on earlier observations that transplanted stem cell-derived retinal cells could slow degeneration long after the cells had disappeared, suggesting they were releasing protective signals that outlasted their own survival. This insight prompted the team to search for the specific molecules responsible.

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Reference:

Wei, G., Chatterjee, S., Yang, Q. et al. A fatty acid amide activates myeloid cells and improves neurovascular outcomes in retinal degeneration. Nat Neurosci (2026). doi.org/10.1038/s41593-026-02341-w