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Researchers at Yale Have Pinpointed Cells That Are Linked to Macular Degeneration

Researchers have found the cells linked to the leading cause of blindness in elderly.

In the Oct. 25 issue of the journal Nature Communications, Yale researchers reported that glial cells, also called support cells and vasculature cells, which supply blood to the retina as well as cone cells, contribute to macular degeneration.

Genome-wide studies have identified almost three dozen genes that play a role in the disease, but the exact location where they inflict damage had remained unknown until now.

The Yale/Harvard/MIT team used new single-cell sequencing to generate the first comprehensive human retinal atlas. They used data analysis technology to localize their effects to specific cell types associated with the disease.

This new information can help find treatments for macular degeneration in the future. “This study helps pinpoint cell types that can be investigated closely to develop new types of therapeutics,” said co-senior author Brian Hafler, assistant professor of ophthalmology and visual science and of pathology at Yale.

While age is the most significant risk factor for developing age-related macular degeneration (AMD), other risk factors such as heredity, blue eyes, high blood pressure, cardiovascular disease, and smoking have also been identified. AMD accounts for 90% of new cases of legal blindness in Canada.

While current treatments of both the dry and wet form of macular degeneration of injections, photodynamic therapy and vitamin supplements can provide some benefits, there can be continued progressive vision loss even with treatment. There is still a gap for effective treatments for the largely affected population. The identification of these risk cells provides possible points of interest for new therapies to improve and restore vision in AMD patients.

References:

http://.news.yale.edu/2019/10/24/yale-researchers-find-cells-linked-leading-cause-blindness-elderly

https://www.nature.com/articles/s41467-019-12780-8

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