A research team co-led by the University of California, Irvine, discovered that accumulated DNA damage in the retina is a key contributor to AMD and that targeting specific retinal cell types may lead to treatments that slow or stop progression.

The study, recently published online in the journal Aging Cell, reveals how DNA damage, a hallmark of aging, compromises the retina’s function and accelerates vision loss.

The team compared a mouse model with reduced levels of ERCC1-XPF, a DNA repair enzyme, with both young, healthy mice and naturally aging mice. By just 3 months of age, the model showed signs of visual impairment, structural alterations in the retina, abnormal blood vessel formation, and shifts in gene expression and metabolism, as well as mitochondrial dysfunction in the retinal pigment epithelium. All these changes mirror those seen in natural human eye aging.

“Our findings highlight the critical role DNA damage repair plays in maintaining retina health for good vision,” said co-corresponding author Dorota Skowronska-Krawczyk, UC Irvine associate professor of physiology and biophysics, in a UC Irvine press release. “Because age is the strongest risk factor for AMD, gaining deeper insights into the underlying biology of aging in the eye is essential for developing effective therapies.”