Lab-grown aging eye model reveals early AMD markers in weeks

The rods and cones in your eyes are responsible for helping you see, but what is responsible for helping them? Retinal pigment epithelium cells are their caretakers, but environmental, genetic and aging factors can strain them and make them less effective. This is known as age-related macular degeneration—a leading cause of blindness.

Age-related macular degeneration, often called AMD, is difficult to study because replicating the conditions of the aging eye in a laboratory is challenging. Researchers at Utah State University are working to change that.

USU Associate Professor Elizabeth Vargis and her doctoral student Dillon Weatherston, along with Associate Professor Justin Jones, developed a model to mimic the effects of aging and improve prevention and treatment while advancing research into other age-related diseases, such as Alzheimer’s.

After years of exploring how to control cell growth, Vargis and Weatherston’s latest research breakthrough came after they discovered that a membrane developed from hagfish proteins could be tuned to mimic natural aging. They then observed how retinal pigment epithelium cells from pig eyes responded to the changing hagfish membrane, with the goal of identifying early indicators of AMD.

The team’s findings were published in GeroScience, a leading journal covering aging and age-related diseases.

Using the new model, the researchers successfully replicated the onset of AMD in the same way it develops in a human eye. Similar to naturally occurring AMD, the model produced fatty deposits and protein markers that signal the early stages of the disease.

“AMD affects so many people, and the way to treat it is with vitamins or monthly injections into the eyeball,” said Vargis, the project’s principal investigator.

“It’s 2026, and I feel like we should have something better.”

Vitamin treatments can reduce the likelihood of developing AMD, but they are not as effective once progressive vision loss begins, and injections work only during the late stage of the disease.

“Now we’ve got this model, where over the course of a month of growing cells on it, the cells are behaving similarly to what happens to a person’s eye over the course of 60 years,” Weatherston said.

While the specific findings of the AMD study are important, Vargis said the real breakthrough comes in developing a model that is better able to mimic aging in cells.

Jones’s role in this project was to develop the tunable protein platform on which the RPE cells grow and which more accurately mimics human eyes. He said that by finding a way to imitate human physiology, future discoveries made with the model will be transferable to other fields of study.

“The power of this research is that it developed a model system that we can test drugs against to help treat and cure AMD,” he said.

The team’s latest research is central to MyxTek Bio, a USU technology spinout company guided by Jones and Vargis. The company has been recommended for funding from the National Science Foundation for its work in developing and commercializing the AMD model system. The team has filed a nonprovisional patent for the technology in hopes of making it more widely available.

“We are incredibly hopeful that through our efforts we can successfully transition this model system to help find a cure or more effective treatment for AMD,” Jones said.

Who’s behind this story?

Andrew Zinin

Master’s in physics with research experience. Long-time science news enthusiast. Plays key role in Science X’s editorial success.

Full profile →

Advertisements