Deposits of a mineral found in tooth enamel at the back of the eye could be hastening the progression of age-related macular degeneration, the leading cause of deteriorating eyesight in people over 50.

Now researchers have identified a protein called amelotin that experiments suggest is involved in producing the mineral deposits that are the hallmark of “dry” age-related macular degeneration, the most common of the two forms of the disease. Age-related macular degeneration, or AMD, affects about 3 million people in the United States. But the new finding, if confirmed, could change that.

While the “wet” form of AMD, which comprises up to 30 percent of AMD cases, can be treated with injections, there are currently no treatments for dry AMD.

“Finding amelotin in these deposits makes it a target to try to slow the progression of mineralization, which, if it’s borne out, could result in new therapies,” says Imre Lengyel, an ophthalmologist at Queen’s University Belfast in Northern Ireland who was not involved in the research.

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These deposits, first documented in 2015, are made of a type of mineralized calcium called hydroxyapatite and appear beneath the retinal pigment epithelium — a layer of cells just outside the retina that keeps its light-sensing rods and cones happy and healthy. The deposits may worsen vision by blocking the flow of oxygen and nutrients needed to nourish those light-sensitive cells of the retina. By contrast, in wet AMD abnormal blood vessels intrude into the retina and often leak. Both types of AMD distort a person’s central vision — the focused, detailed sight needed for reading and recognizing faces — which can make independent living difficult.

For the new study, published online February 26 in Translational Research, researchers grew retinal pigment epithelial cells in the lab, and then subjected them to a form of stress that may be common in aging eyes: a loss of nutrients.

“One of the problems with this disease and with aging is that blood vessels aren’t delivering the blood they used to, and that loss of nutrients and oxygen could be driving the course of the disease,” says Graeme Wistow, an ophthalmologist at the National Eye Institute at the National Institutes of Health in Bethesda, Md.

After Wistow and his colleagues deprived the cells of nutrients for nine days, a gene involved in producing amelotin called AMTN switched on and started making the protein, which in turn caused hydroxyapatite deposits to form. Blocking the gene’s activity prevented the deposits from forming in lab experiments, the scientists report. The team also found amelotin in cadaver eyes that suffered from dry AMD, concentrated in areas with large deposits of hydroxyapatite.

“It’s a ways off, but the best possible outcome would be finding a way to inhibit amelotin or its gene expression in a way that prevented or delayed the deposition of hydroxyapatite,” Wistow says. That “might allow people to keep their vision a bit longer.”

But Lengyel and other researchers want to see the results verified in mice or lab-grown cells that more closely resemble a living human eye. Wistow and his colleagues are currently working on breeding mice with eyes that more closely mimic those of humans suffering from dry AMD to test their findings.