- Robert Preidt
- Posted August 10, 2018
New Research Suggests Glaucoma May Be an Autoimmune Disease
FRIDAY, Aug. 10, 2018 (HealthDay News) -- The eye disease glaucoma may be an autoimmune disorder, a new study suggests.
Glaucoma affects nearly 70 million people worldwide. It damages the retina and optic nerve and can lead to blindness.
In research with mice, scientists found that immune system T-cells cause the retinal damage that occurs in glaucoma, and that previous interactions with bacteria normally found in the body trigger the T-cell attacks on the retina.
"This opens a new approach to prevent and treat glaucoma," senior co-author Jianzhu Chen said in a Massachusetts Institute of Technology news release. He is a professor of biology at MIT.
Most glaucoma treatments today aim to lower pressure in the eye, but the disease gets worse in many people even after pressure is normalized. Researchers found the same thing in mice, although research in animals doesn't always produce the same results in humans.
"That led us to the thought that this pressure change must be triggering something progressive, and the first thing that came to mind is that it has to be an immune response," senior co-author Dr. Dong Feng Chen said in the release.
She is an associate professor of ophthalmology at Harvard Medical School and the Schepens Eye Research Institute of Massachusetts Eye and Ear in Boston.
The discovery suggests blocking the autoimmune activity could offer a new approach to treating glaucoma.
Further research will try to determine whether other parts of the immune system play a role in glaucoma, and whether autoimmunity is a factor in degenerative brain diseases, the researchers said.
"What we learn from the eye can be applied to the brain diseases, and may eventually help develop new methods of treatment and diagnosis," Chen said.
The findings were published Aug. 10 in the journal Nature Communications.
The U.S. National Eye Institute has more on glaucoma.
SOURCE: Massachusetts Institute of Technology, news release, Aug. 10, 2018
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