Age-related macular degeneration is one of the leading causes of blindness in the elderly, affecting more than 2 million people in the United States and leading to progressive loss of central vision.
Genome-wide studies have identified almost three dozen genes that play a role in the disease, but exactly where in the eye they inflict damage was not well known.
In a new study, researchers found glial cells (or support cells), and vasculature cells tasked with providing blood to the retina as well as cone cells contribute to the degeneration of the macula, in the central part of the retina.
The research was conducted by a team from Yale University, MIT, and Harvard University.
There are a limited number of effective long-term treatments available for the two forms of macular degeneration.
The wet form is caused by the growth of abnormal blood vessels underneath the macula, which can be mitigated by regular injections in the eye.
Other than eye vitamin supplements, there is no treatment for the dry form of the disease, which is marked by accumulations of yellow deposits called drusen in the macula.
While current treatments provide some benefits, over time there can be a continued, progressive loss of vision in both forms of the disease.
In the study, the Yale/Harvard/MIT team used new single-cell sequencing to generate the first comprehensive human retinal atlas and employed data analysis technology to localize their effects to specific cell types associated with the disease.
While they found risk genes associated with cones, the cell type key to central vision, the researchers also found an association with glial and vascular cells—providing possible targets for novel therapies to improve and restore vision.
This study helps pinpoint cell types that can be examined closely to develop new types of treatments.
One author of the study is Brian Hafler, an assistant professor of ophthalmology and visual science and of pathology at Yale.
The study is published in the journal Nature Communication.
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