Scientists have developed a retinal implant that can restore lost vision in rats, and are planning to trial the procedure in humans later this year.

The implant, which converts light into an electrical signal that stimulates retinal neurons, could give hope to millions who experience retinal degeneration – including retinitis pigmentosa – in which photoreceptor cells in the eye begin to break down, leading to blindness.

The retina is located at the back of the eye, and is made up of millions of these light-sensitive photoreceptors. But mutations in any one of the 240 identified genes can lead to retinal degeneration, where these photoreceptor cells die off, even while the retinal neurons around them are unaffected.

Because the retinal nerves remain intact and functional, previous research has looked at treating retinitis pigmentosa with bionic eye devices that stimulate the neurons with lights, while other scientists have investigated using CRISPR gene editing to repair the mutations that cause blindness.

Now, a team led by the Italian Institute of Technology has developed a new approach, with a prosthesis implanted into the eye that serves as a working replacement for a damaged retina.

The implant is made from a thin layer of conductive polymer, placed on a silk-based substrate and covered with a semiconducting polymer.

The semiconducting polymer acts as a photovoltaic material, absorbing photons when light enters the lens of the eye. When this happens, electricity stimulates retinal neurons, filling in the gap left by the eye's natural but damaged photoreceptors.

To test the device, the researchers implanted the artificial retina into the eyes of rats bred to develop a rodent model of retinal degeneration – called Royal College of Surgeons (RCS) rats.

After the rats had healed from the operation 30 days later, the researchers tested how sensitive they were to light – called the pupillary reflex – compared to healthy rats and untreated RCS rats.

At the low intensity of 1 lux – a bit brighter than the light from a full moon – the treated rats weren't much more responsive than untreated RCS rats.

But as the light increased to around 4–5 lux – about the same as a dark twilight sky – the pupillary response of treated rats was largely indistinguishable from healthy animals.

When they retested the rats at six and 10 months after surgery, the implant was still effective in the rats – although all the rats in the tests (including the treated rats, the healthy animals, and the RCS controls) had suffered minor vision impairment due to being older.

Using positron emission tomography (PET) to monitor the rats' brain activity during the light sensitivity tests, the researchers saw an increase in the activity of the primary visual cortex, which processes visual information.

Based on the results, the team concludes that the implant directly activates "residual neuronal circuitries in the degenerate retina", but further research will be required to explain exactly how the stimulation works on a biological level.

"[T]he detailed principle of operation of the prosthesis remains uncertain," they explain in their paper.

While there are no guarantees that the results seen in rats will translate to people, the team is hopeful that it will – and from the sounds of things, it won't be too long until we find out.

"We hope to replicate in humans the excellent results obtained in animal models," says one of the researchers, ophthalmologist Grazia Pertile from the Sacred Heart Don Calabria in Negrar, Italy.

"We plan to carry out the first human trials in the second half of this year and gather preliminary results during 2018. This [implant] could be a turning point in the treatment of extremely debilitating retinal diseases."

The findings are reported in Nature Materials.