- OT
- Science and vision
- Research
- An energy boost for the eye
An energy boost for the eye
New Japanese therapeutic allows the eye to power through glaucoma
19 April 2016
A little extra pep might be all the eye’s neural cells need to survive glaucoma, according to a Japanese trial of a novel therapy that boosts the cells’ own fuel.
Kyoto University researchers were able to slow the progression of glaucoma in mice, using such a method, in a paper published today (19 April) in the journal Heliyon.
University ophthalmology assistant professor, Dr Hanako Ikeda, said that she started looking at boosting energy because many glaucoma patients continued to lose their sight even after surgery, or while taking drugs to lower intraocular pressure.
Dr Ikeda told OT that previous research had found that an enzyme, known as valosin-containing protein (VCP), was involved in neural cell death in glaucoma.
The enzyme breaks apart ATP molecules, which cells use to transfer energy between them. Dr Ikeda’s team believes stopping this breakdown could yield positive results.
She explained: “Inhibiting … VCP frees up ATP for other essential cellular processes and consequently prevents, or retards, cell death.”
The team has designed compounds, which the researchers have named Kyoto University substances (KUSs), to stop the action of VCP. When given to mice with the disease, the animals showed thicker retinal nerve fibre layers and better visual function, Dr Ikeda said.
She emphasised: “We did not see any evidence of side effects in the mice during the 10-month administration of KUSs.”
The substances work when given orally or by injection, she highlighted, adding: “Both showed significant efficacies … Another, probably more ideal, route is via eye drops. Next we will modify the dosage forms of KUSs for eye drops, and we will then examine their efficacies.”
The team is planning a phase I/II clinical trial. Though a trial of the therapeutic in people is likely to be between three and five years away, Dr Ikeda concluded.
Advertisement
Comments (0)
You must be logged in to join the discussion. Log in