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New treatment could reverse vision loss caused by retinopathy

Researchers have developed an experimental compound that could treat vision loss in premature infants and adults. 

Retinopathy

According to researchers, a new discovery could pave the way for therapies to reverse vision loss common in premature infants and adults. The scientists have identified a compound that could give rise to therapies for a host of eye diseases that include retinopathy of prematurity and diabetic retinopathy.

The study was conducted at the Oklahoma Medical Research Foundation (OMRF), US. 

The researchers say that several eye disorders occur when blood vessels grow out of control in the retina, the tissue that lines the back of the eye. In these forms of retinopathy, a web of vessels blocks light from reaching the retina. The overgrowth causes vision issues that can advance to total blindness.

Retinopathy in premature babies – linked to high oxygen levels in NICU incubators that interrupts normal vessel development in the eye – often resolves naturally over time, but not always. In those cases and in adult diseases like diabetic retinopathy, vision damage can be irreversible.

The researchers thought there might be clues to thinning this tangle of vessels if they analysed a different set of vessels that naturally regress and disappear in mice soon after birth. When they studied newborn mice, the team found that levels of a specific class of cellular proteins crashed as the mice experienced normal blood vessel loss in the eye.

“Dr Chris Schafer hypothesised that these cellular proteins might be an important ‘off switch’ to eliminate these vessels in a neonatal model,” said Dr Courtney Griffin, the senior author of the study. “This is a new way of approaching these diseases. The current methods – invasive surgeries or life-long injections into the eye – only prevent the disease from advancing and often have serious complications.”

Schafer identified an experimental compound that disables the proteins. It allowed him to flip the switch and test the idea.

“We wanted to trick blood vessels in diseased mice into thinking they were supposed to be regressing and naturally dying off,” said Schafer. “This appears to be what happened.”

Even more encouraging, Griffin said, the compound only impacted abnormal blood vessels with slow blood flow. The normal vessels needed in a healthy eye were not affected. 

The researchers say these findings open the door to tailored therapies to reverse vision loss. It may also have implications in shrinking tumours that contain abnormal blood vessels in other parts of the body.

“We’ve shown that once these abnormal vessels have formed in the young eye, they’re susceptible to being treated,” said Griffin.

The research team will now study the compound in models of adult eye diseases.

The study was published in Proceedings of the National Academy of Sciences