Many conditions that cause vision loss have common characteristics. It is the gradual destruction of the retina, the light-sensing tissue at the back of the eye. Although scientists know some of the structural changes that occur as this damage progresses, little is understood about the molecular signals that shape how the retina copes with the disease.
Now, a team at the Scripps Research Institute, in collaboration with the University of California, San Diego and the Lowy Medical Institute, has discovered that a naturally occurring molecule called erucamide plays a role in communication between cells in the retina.. Their research is natural neuroscience June 19, 2026 Researchers found that when light-sensing cells known as photoreceptors begin to die, erucamide levels drop, but when the molecule is restored it activates cellular responses that support retinal stability. These findings suggest that erucamide may be part of a natural protective response in the retina and may provide a new way to slow the progression of diseases that lead to vision loss.
The retina doesn’t just deteriorate. In fact, they respond positively to injury. Our research identified erucamide as a signaling molecule that helps orchestrate that response. ”
Martin Friedlander, senior author, professor at The Scripps Research Institute
The retina relies on constant communication between neurons, glia, blood vessels, and immune cells. This system, the neurovascular unit, maintains the function of visual tissues. However, in diseases that involve vision loss, such as diabetic retinopathy, retinitis pigmentosa, and age-related macular degeneration, this close coordination is weakened. Photoreceptors begin to die and vision deteriorates.
Friedlander’s team’s research builds on previous observations that transplanting stem cell-derived retinal cells can slow degeneration even after the cells have disappeared, suggesting that retinal cells emit protective signals that persist beyond their own lifetime. This insight led the team to search for the specific molecules responsible.
Although it has long been recognized that fat-like compounds called lipids function as signaling molecules in the body, many of these compounds have not been carefully studied in the context of retinal diseases. To look for overlooked players, the scientists used mass spectrometry-based metabolomics. This is a technique that measures many small molecules in tissues at once. The research team applied this approach to several established preclinical models of retinal degeneration to explore molecules that change as the disease progresses.
Among the many molecules detected, erucamide stood out. As photoreceptors begin to deteriorate, their levels drop rapidly, suggesting that this drop may not be a coincidence.
“That was a pivotal moment for us,” recalls co-author Dale Borger, the Richard and Alice Kramer Professor of Chemistry at the Scripps Research Institute. “That raised the possibility that erucamide may be influencing tissue responses and not just changing as a result of the disease.”
The team then set out to determine whether restoring erucamide could impact the retinal degeneration process. The scientists reintroduced erucamide into the eye using porous silicon nanoparticles, tiny delivery vehicles designed to release the molecule in a controlled manner. Since erucamide is hydrophobic (poorly soluble in water) and can form clumps upon injection, the nanoparticles helped to stabilize and evenly disperse the molecule.
Rather than acting directly on photoreceptors, Erucamide activates a group of immune cells in the retina known as CD11b+ myeloid cells, which support tissue health throughout the body in response to injury. The research team also identified a protein called TMEM19 that erucamide binds to. Reducing TMEM19 levels prevented the activation of these myeloid cells and blocked the protective effects of erucamide.
When stimulated, bone marrow cells release signals associated with neurovascular stabilization, supporting both nerve cells and the blood vessels that feed them. Although this effect did not completely reverse the retinal damage, it slowed down aspects of degeneration by preserving the structure and function of the remaining tissue.
“Erucuamide appears to work by engaging the surrounding environment rather than targeting the photoreceptors themselves,” explains lead author Guoqing Wei, a staff scientist at Scripps Research who began working on the project as a postdoctoral fellow in Friedlaender’s lab seven years ago. “That change in perspective could be important for future treatments of retinal degenerative diseases.”
The research team’s findings provide a glimpse into how erucamide’s effects occur at the molecular level, but additional research is needed to elucidate the full pathway. Future research will focus on erucamide signaling in various retinal diseases and whether targeting this pathway can provide meaningful long-term benefits.
And since most eye medicines are water-based, erucamide’s hydrophobic nature poses challenges to formulation, so scientists are aiming to improve ways to deliver the molecule as a therapy. They also plan to test modified forms of erucamide to see if they produce stronger or more stable effects, as well as to investigate whether related lipid molecules are even more effective than erucamide at activating defense responses.
Still, the discovery highlights the broader concept that some molecules already present in the body can be harnessed to support tissues under stress. Initial results point to a potential strategy to slow retinal degeneration by enhancing the tissue’s own response to injury.
“The goal is to strengthen the signals that are already there,” Friedlander points out. “If we can learn how to carefully tune that response, we may offer new avenues for slowing the progression of retinal diseases for which treatment options are limited.”
sauce:
Scripps Research Institute
Reference magazines:
Wei, G. others. (2026). Fatty acid amides activate bone marrow cells and improve neurovascular outcomes in retinal degeneration. natural neuroscience. DOI: 10.1038/s41593-026-02341-w. https://www.nature.com/articles/s41593-026-02341-w
