A potential ‘game changer’ for eye disease
By Jan Jarvis
A novel pharmacological intervention to control retinal ganglion cell death caused by glaucoma is in preclinical development, said Katalin Prokai-Tatrai, PhD, Associate Professor in the Center for Neuroscience Discovery and the Department of Pharmaceutical Sciences in the UNT System College of Pharmacy.
“We believe that this novel therapeutic intervention will be effective for other blinding eye diseases associated with neurodegeneration, such as age-related macular degeneration,” said Dr. Prokai-Tatrai. “We are very hopeful we will generate data that shows we can prevent and stop the damage that leads to blindness.
“If it works, it will be a game-changer in terms of how neurodegenerative eye diseases are treated.”
Initially the study will target the effectiveness of the drug for glaucoma, the second-leading cause of blindness. The study will then be expanded to treat other neurodegenerative diseases impacting the brain.
“The beauty of our drug is that it remains inactive until it reaches the retina when applied in eye drops,” Dr. Prokai –Tatrai said.
Scientists know that glaucoma is caused by elevated pressure, but the mechanism behind it is not fully clear. Several possibilities are under investigation. Dr. Prokai-Tatrai said her translational research focuses on neuroprotection, not the mechanism that causes the elevated pressure.
“Our goal is to prevent neuron death using the eye drops, because once those neurons die they are gone forever,” she said. “Our preliminary data is unprecedented and very promising in terms of preserving visual acuity.
“This gives us hope, that if the approach is successful, we can develop a complementary therapy used together with conventional medications for those with glaucoma.”
The multidisciplinary research involves medicinal chemistry-driven drug discovery and delivery, retina proteomics and ophthalmology and is in collaboration with other researchers at UNTHSC and at the University of Missouri-Kansas City School of Medicine.
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