By Adrian Galbreth
Many people's worst nightmare is to go blind, but this is a reality for those suffering from late-stage glaucoma, which is the second leading cause of blindness, affecting over 70 million worldwide.
However, new findings from Georgia Tech, published to mark Glaucoma Awareness Month in the Journal of Molecular Biology, explore one of the many molecular origins of glaucoma and could advance research dedicated to fighting the disease.
A study led by Raquel Lieberman, a Chemistry and Biochemistry assistant professor at the facility, focused on examining the structural properties of these myocilin deposits.
Normally, glaucoma is typically triggered when fluid is unable to circulate freely through the eye's trabecular meshwork (TM) tissue, resulting in intraocular pressure rising and damaging 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, which the experts sought to study in more detail.
"We were surprised to discover that both genetically defected as well as normal, or wild-type, myocilin are readily triggered to produce very stable fibrous residue containing a pathogenic material called amyloid," professor Lieberman explained.
She also highlighted that amyloid formation is recognised as a major contributor to numerous non-ocular disorders, including Alzheimer's, certain forms of diabetes and Mad Cow disease, with scientists currently studying ways to destroy amyloid fibrils as an option for treating these diseases.
However, further research, based on her findings, could potentially result in drugs that prevent or stop myocilin amyloid formation or destroy existing fibrils in glaucoma patients, she noted.
Until now, amyloids linked to glaucoma had been restricted to the retinal area, killing retina cells and leading to vision loss, but not affecting intraocular pressure.
"The amyloid-containing myocilin deposits we discovered kill cells that maintain the integrity of TM tissue. In addition to debris from dead cells, the fibrils themselves may also form an obstruction in the TM tissue. Together, these mechanisms may hasten the increase of intraocular pressure that impairs vision," professor Lieberman explained.
by Adrian Galbreth