About 170 million people worldwide live with age-related macular degeneration, which strikes one in 10 people over the age of 55.
About 1.7 million people worldwide have the most common form of inherited blindness, retinitis pigmentosa, which typically leaves people blind by the age of 40.
Currently, options for such patients are limited to an electronic eye implant hooked to a video camera that sits on a pair of glasses.
This is an awkward, invasive, and expensive setup that produces an image on the retina that is equivalent, currently, to a few hundred pixels. But normal, sharp vision involves millions of pixels.
Correcting the genetic defect responsible for retinal degeneration is not straightforward, either, because there are more than 250 different genetic mutations responsible for retinitis pigmentosa alone.
About 90% of these kill the retina’s photoreceptor cells—the rods, sensitive to dim light, and the cones, for daylight color perception.
But retinal degeneration typically spares other layers of retinal cells, including the bipolar and the retinal ganglion cells, which can remain healthy, though insensitive to light, for decades after people become totally blind.
In a recent study from the University of California, Berkeley, researchers inserted a gene for a green-light receptor into the eyes of blind mice, and, a month later, the mice were navigating around as easily as mice with no vision problems.
They were able to see motion, brightness changes over a thousandfold range, and fine detail sufficient to distinguish letters.
The researchers say that within as little as three years, the gene therapy—delivered via an inactivated virus—could be tried in humans who’ve lost sight because of retinal degeneration,
Patients may have enough vision to move around and the therapy could potentially restore their ability to read or watch the video.
The study is published in Nature Communications. The lead author is Ehud Isacoff, a UC Berkeley professor of molecular and cell biology.
In the study, the UC Berkeley team succeeded in making 90% of ganglion cells light-sensitive.
Diagram of a setup in which mice were trained to respond to patterns on iPads instead of much brighter LEDs.
After the trained mice went blind from an inherited retinal disease, they were treated with a gene therapy that restored sufficient sight for them to respond to patterns on the iPads almost as well as before they went blind.
To reverse blindness in these mice, the researchers designed a virus targeted to retinal ganglion cells and loaded it with the gene for a light-sensitive receptor, the green (medium-wavelength) cone opsin.
Normally, this opsin is expressed only by cone photoreceptor cells and makes them sensitive to green-yellow light.
When injected into the eye, the virus carried the gene into ganglion cells, which normally are insensitive to light, and made them light-sensitive and able to send signals to the brain that were interpreted as sight.
In mice, the researchers were able to deliver the opsins to most of the ganglion cells in the retina.
To treat humans, they would need to inject many more virus particles because the human eye contains thousands of times more ganglion cells than the mouse eye.
But the team has developed the means to enhance viral delivery and hopes to insert the new light sensor into a similarly high percentage of ganglion cells, an amount equivalent to the very high pixel numbers in a camera.
The team is now at work testing variations on the theme that could restore color vision and further increase acuity and adaptation.
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