The FINANCIAL -- Mice with glaucoma, which were treated with a compound developed by researchers in Japan, showed signs that the treatment prevented or retarded damage to the nerves that cause blindness.
That was one of the findings in a study reported April 19 in the online journal Heliyon on the "Neuroprotective effects of VCP modulators in mouse models of glaucoma" by researchers at Kyoto University.
The novel, synthesized compounds—called Kyoto University Substances (KUSs)—inhibited the activities of valosin-containing proteins (VCP) and mitigated the death of retinal ganglion cells (RGCs), the researchers say. Over time, RGCs die in patients with glaucoma. There is no cure for glaucoma, but early diagnosis and treatment can preserve sight.
"In conclusion, KUSs (Kyoto University Substances) could provide convenient, novel therapeutics for neuroprotection in incurable eye diseases such as glaucoma," wrote researcher and study author Noriko Nakano. "Given that the major pathology of many incurable human disorders, e.g., neurodegenerative diseases, ischemic diseases, etc., is early cell death in the affected organs, which occurs long before somatic death, KUSs could also provide a novel strategy for cell protection in these disorders."
The research is promising, says Murray Fingeret, O.D., chief of optometry at the U.S. Department of Veterans Affairs, New York Harbor Healthcare System, in Brooklyn, New York. Dr. Fingeret is the first and only optometrist appointed to the board of directors of The Glaucoma Foundation, where he continues his life's work of research and collaboration into finding a cure.
He applauded the researchers for their out-of-the box thinking.
"Most agents that are being evaluated for glaucoma neuroprotection have come from medications used for neurologic conditions such as Alzheimer's disease, dementia and traumatic brain injury because there are similar final pathways in terms of how nerve cells die, though their origins are different," Dr. Fingeret says.
But more research needs to be done. Animal models don't easily translate to human beings, he says.
"Animal models typically use 'crush' models in which the optic nerve is crushed and histologic sections used," Dr. Fingeret says. "This is a very different method to determine outcomes than what is used clinically, such as monitoring the optic nerve or visual fields. Positive results in animal models rarely turn into commercially viable drugs. There are no approved neuroprotection agents, for example, though similar animal model results have been previously reported."