Published on: Oct 20, 2025
Age-related macular degeneration (AMD), the leading cause of blindness in adults over the age of 55, progressively degrades the macula, the part of the eye responsible for straight-ahead vision enabling reading, facial recognition and driving. The disease is more prevalent in women than in men, although the reason is not well-understood.
UB ophthalmology researchers have received a $2.2 million grant from the National Institute on Aging of the National Institutes of Health to study sex-specific mechanisms for AMD. The goal is to identify novel sex-specific biological mechanisms to lay the groundwork for development of therapies that would be targeted to men or women.
AMD is a chronic neurological condition and there’s no cure and no way to prevent it, says Margaret DeAngelis, principal investigator and Ira G. Ross and Elizabeth Olmsted Ross Endowed Chair and professor of ophthalmology in the Jacobs School of Medicine and Biomedical Sciences. Because most people don’t exhibit symptoms early in the disease, she says it’s difficult to detect the disease in its early and intermediate stages. For that reason, most AMD studies have focused on the late stages.
We want to stop progression at an early stage, says DeAngelis, who also has an appointment in the Department of Biochemistry. It has been published that women get the worst form of the disease, known as wet AMD, and that it progresses faster in women than men. Wet AMD can cause vision loss suddenly, sometimes as quickly as overnight.
Studying human eye postmortem
The UB team’s hypothesis is based on preliminary data it gathered studying intermediate and advanced forms of AMD in well-characterized human donor eyes. The donor eyes are from the unique human donor eye repository in the DeAngelis lab, which she and her colleagues have been curating since 2012 and which provides a key advantage.
Like other chronic progressive neurological diseases, one of the challenges facing AMD researchers is the fact that there are no animal models of the disease because animals don’t get AMD, DeAngelis says.
This is because the tissues affected by AMD are unique to the human eye. Our repository, the first of its kind, gives us direct access to the tissue affected by the disease and we use some of the same imaging techniques used in the clinic on living patients.
She stresses that the repository would not be possible without the generosity of patients willing to be organ donors and the scientists and clinicians who work to rapidly process and rigorously phenotype the donor eyes according to a standardized published protocol. In this manner, she says, the eyes have the greatest translational impact when they are used for research.
Epigenetic dysfunction
There is increasing evidence that dysfunction in the epigenetics — changes to the expression of DNA without changing the actual DNA sequence — that is associated with chronic neurodegenerative diseases of aging may be more prevalent in women.
And the UB team’s published and preliminary data suggest the sex differences in AMD may originate in some dysfunction that occurs in the epigenetic interplay or crosstalk observed between the nuclear and mitochondrial genomes in the macula from the donor eyes from the biorepository.
Their plan is to leverage their already annotated and well-characterized sex- and age-matched donors with and without different types of AMD and to use a systems biology approach, harnessing a variety of techniques to characterize the interplay between these genomes in the macula.
Researchers will also be look at the question of susceptibility and who is more likely to develop AMD. The team has data showing, for example, that there are DNA differences — or variants— in the mitochondrial genomes of people with AMD. This suggests that some mitochondrial DNA variants may make people more susceptible to AMD.
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