Scientists find a hidden retinal defense against vision loss

Researchers at Scripps Research, working with scientists at UC San Diego and the Lowy Medical Research Institute, have now identified a naturally occurring molecule called erucamide that appears to help coordinate communication between cells in the retina. In a study published in Nature Neuroscience on June 19, 2026, the team found that erucamide levels decline as photoreceptors, the light-sensing cells responsible for detecting visual information, begin to die.

When the researchers restored erucamide, however, it activated cellular responses that helped stabilize retinal tissue. The results suggest that the molecule may be part of the retina's own protective system and could eventually point toward new ways to slow diseases that cause progressive vision loss.

"The retina doesn't simply deteriorate; in fact, it actively responds to injury," says senior author Martin Friedlander, a professor at Scripps Research. "Our work identifies erucamide as a signaling molecule that helps coordinate that response."

How the Retina Tries to Protect Itself

Keeping the retina healthy requires constant coordination among neurons, glia, blood vessels and immune cells. Together, these components form what scientists call the neurovascular unit, a closely connected system that helps maintain the tissue needed for vision.

That coordination begins to break down in diseases such as diabetic retinopathy, retinitis pigmentosa and age-related macular degeneration. As the disease advances, photoreceptors die, and vision progressively declines.

Friedlander's team began pursuing the new study after earlier research produced an intriguing result. Transplanted stem cell-derived retinal cells appeared to slow degeneration even after the transplanted cells themselves had disappeared.

That finding suggested the cells might have been releasing protective chemical signals whose effects lasted longer than the cells. The researchers therefore began searching for the molecules that might be responsible.

Searching for Hidden Molecular Signals

Scientists have long known that lipids, a broad group of fat-like compounds, can do much more than store energy or form cell membranes. Some also act as signaling molecules, carrying instructions between cells.

Yet many lipid-related molecules have received relatively little attention in retinal disease.

To look for possible protective signals, the team used mass spectrometry-based metabolomics: a technique that measures many small molecules in tissue at once. They applied the method to several well-established preclinical models of retinal degeneration and tracked how different molecules changed as the disease progressed.

Erucamide quickly attracted their attention.

Its levels dropped sharply as photoreceptors began to deteriorate, raising the possibility that the change might play an active role in the disease process rather than simply reflect ongoing damage.

"That was a pivotal moment for us," recalls co-author Dale Boger, the Richard and Alice Cramer Professor of Chemistry at Scripps Research. "It raised the possibility that erucamide could be influencing how tissue responds and wasn't just changing as a consequence of disease."

Restoring Erucamide to the Retina

The next question was whether replacing erucamide could alter the course of retinal degeneration.

To test that idea, the scientists delivered erucamide into the eye using porous silicon nanoparticles, tiny engineered carriers capable of releasing molecules in a controlled manner.

That delivery system was particularly important because erucamide is hydrophobic (meaning it doesn't dissolve well in water) and can form clumps when injected. The nanoparticles helped keep the molecule stable and distributed more evenly inside the eye.

What happened next surprised the researchers.

Erucamide did not appear to act directly on the photoreceptors themselves. Instead, it activated immune cells in the retina known as CD11b⁺ myeloid cells. These cells respond to injury and contribute to tissue maintenance throughout the body.

The researchers also identified a protein called TMEM19 that erucamide binds to. When TMEM19 levels were reduced, the myeloid cells were no longer activated in the same way, and erucamide's protective effects disappeared.

Helping Retinal Tissue Stay Stable

Once activated, the myeloid cells released signals linked to neurovascular stabilization. These signals supported both nerve cells and the blood vessels that supply them with nutrients and oxygen.

Erucamide did not reverse retinal degeneration outright. Instead, it slowed certain aspects of the process by helping preserve the structure and function of tissue that remained.

"Instead of targeting the photoreceptors themselves, erucamide appears to work by engaging the surrounding environment," explains first author Guoqin Wei, a staff scientist at Scripps Research who began working on this project as a postdoctoral research associate in Friedlander's lab seven years earlier. "That shift in perspective could be important for treating degenerative retinal diseases going forward."

A Possible New Strategy for Retinal Disease

The researchers have now identified several important pieces of the pathway, but many questions remain about exactly how erucamide produces its effects.

Future studies will examine how erucamide signaling behaves across different retinal diseases and whether manipulating the pathway can deliver meaningful benefits over longer periods.

Turning erucamide itself into a treatment could also be challenging. Because erucamide is hydrophobic and most eye medications are water-based, researchers will need better ways to formulate and deliver it.

The team plans to test modified forms of erucamide to determine whether they can produce stronger or longer-lasting effects. Researchers will also examine related lipid molecules to see whether any are even more effective at activating the retina's protective responses.

Strengthening a Defense the Eye Already Uses

More broadly, the findings support the idea that naturally occurring molecules already present in the body might be used to help tissues withstand disease.

Rather than introducing an entirely new biological process, a future treatment based on this approach might strengthen a protective signal the retina already relies on when it is under stress.

The early findings suggest that enhancing this natural response could become one strategy for slowing retinal degeneration and preserving functioning tissue for longer.

"The goal is to reinforce a signal that's already present," notes Friedlander. "If we can learn how to modulate that response carefully, it could offer a new path for slowing the progression of retinal diseases where treatment options remain limited."

In addition to Friedlander, Boger and Wei, authors of the study, "A fatty acid amide activates myeloid cells and improves neurovascular outcomes in retinal degeneration," include Shreyosree Chatterjee, Daisuke Ogasawara, Katie Biscocho, Peter Westenskow, Junhua Wang, Helena Pham, Edith Aguilar, Jacob Robinson, Ayumi Usui-Ouchi, Gary Siuzdak and Benjamin Cravatt of Scripps Research; Qinglin Yang, Sanahan Vijayakumar, Ruhan Fan and Michael J. Sailor of UC San Diego; and Sarah Giles, Roberto Bonelli and Kevin Eade of the Lowy Medical Research Institute.

This work was supported by funding from the Lowy Medical Research Institute; the National Eye Institute (grants R01EY11254 and 5R24EY017540); the California Institute for Regenerative Medicine (grant TR1-01219); the National Science Foundation through the UC San Diego Materials Research Science and Engineering Center (grant DMR-2011924); the National Institutes of Health (grants 2R01AI132413, R35 GM130385, U01 CA235493 and U01 CA305256); the National Institute on Drug Abuse (grant DA015648), the San Diego Nanotechnology Infrastructure of UC San Diego, a member of the National Nanotechnology Coordinated Infrastructure, which is supported by the National Science Foundation (grant ECCS-2025752); and the Natural Sciences and Engineering Research Council of Canada Postgraduate Scholarship-Doctoral program (grant NSERC PGS-D).