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New findings at Georgia Tech, published in January during Glaucoma Awareness Month, explore one of the many molecular origins of glaucoma and advance research dedicated to fighting the disease.
Glaucoma is typically triggered when fluid is unable to circulate freely through the eye’s trabecular meshwork tissue. Intraocular pressure rises and damages the retina and optic nerve, which causes vision loss. In certain cases of glaucoma, this blockage results from a build-up of the protein myocilin. Georgia Tech Chemistry and Biochemistry Assistant Professor Raquel Lieberman focused on examining the structural properties of these myocilin deposits.
“We were surprised to discover that both genetically defected as well as normal, or wild-type (WT), myocilin are readily triggered to produce very stable fibrous residue containing a pathogenic material called amyloid,” said Lieberman, whose work was published in the most recent Journal of Molecular Biology.
Amyloid formation, in which a protein is converted from its normal form into fibers, is recognized as a major contributor to numerous non-ocular disorders, including Alzheimer’s and certain forms of diabetes. Scientists are currently studying ways to destroy amyloid fibrils as an option for treating these diseases. Further research, based on Lieberman’s findings, could potentially result in drugs that prevent or stop myocilin amyloid formation or destroy existing fibrils in glaucoma patients.
Dr. Lieberman received a $40,000 Shaffer Grant from the Glaucoma Research Foundation in 2008. Her current research at Georgia Tech is funded by the National Eye Institute, National Institutes of Health.
Last reviewed on January 18, 2012