A research team co-led by the University of California, Irvine has discovered that accumulated DNA damage in the retina is a key contributor to age-related macular degeneration and that targeting specific retinal cell types may lead to treatments that slow or stop progression.
The study reveals how DNA damage, a hallmark of aging, compromises the retina’s function and accelerates vision loss. The retina's regular exposure to light and intense metabolic activity makes it highly vulnerable to oxidative stress and the accumulation of DNA damage over time, a process closely linked to aging.
The team compared mice bred to have reduced levels a DNA repair enzyme with young, healthy mice and with 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.
The team hopes to develop interventions that will reduce these signs of aging and help prevent age-related eye disease.