Central OC Times

A study co-led by the University of California, Irvine, has identified accumulated DNA damage in the retina as a significant factor contributing to age-related macular degeneration (AMD). The research suggests that targeting specific retinal cell types could lead to treatments that slow or stop the progression of this condition.

AMD affects around 200,000 Americans each year and is a leading cause of blindness in individuals over 50. It presents in two forms: wet AMD, which can be treated with established therapies, and dry AMD, for which effective treatments are currently lacking.

The findings were published online in the journal Aging Cell. They demonstrate how DNA damage, commonly associated with aging, impairs retinal function and accelerates vision loss. "Our findings highlight the critical role DNA damage repair plays in maintaining retina health for good vision," said Dorota Skowronska-Krawczyk, UC Irvine associate professor of physiology and biophysics. "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."

The retina relies on the retinal pigment epithelium cell layer to function properly. Due to its exposure to light and high metabolic activity, it is particularly susceptible to oxidative stress and DNA damage accumulation over time. Understanding this relationship is crucial for developing new approaches to combat AMD.

Researchers compared a mouse model with reduced levels of ERCC1-XPF—a DNA repair enzyme—with young healthy mice and naturally aging mice. By three months old, these models exhibited signs of visual impairment similar to those seen in human eye aging.

"The more we know about how DNA damage contributes to eye diseases like AMD," Skowronska-Krawczyk noted, "the better we can develop interventions that address the root causes of vision loss." She added that future research would focus on identifying cell types driving age-related changes by selectively impairing DNA mechanisms.

The team included William Cho from UC Irvine; Dr. Laura J. Niedernhofer from the University of Minnesota; and faculty from other institutions such as Columbia University and the University of Florida.

This research was supported by funding from various sources including NIH grants and contributions from Cecilee Faster.