Retinal Device Restores Sight to Blind Mice
Researchers hope to start human trials next
MONDAY, Aug. 13, 2012 (HealthDay News) -- Researchers report they have developed in mice what they believe might one day become a breakthrough for humans: a retinal prosthesis that could restore near-normal sight to those who have lost their vision.
That would be a welcome development for the roughly 25 million people worldwide who are blind because of retinal disease, most notably macular degeneration.
The notion of using prosthetics to combat blindness is not new, with prior efforts involving retinal electrode implantation and/or gene therapy restoring a limited ability to pick out spots and rough edges of light.
The current effort takes matters to a new level. The scientists fashioned a prosthetic system packed with computer chips that replicate the "neural impulse codes" the eye uses to transmit light signals to the brain.
"This is a unique approach that hasn't really been explored before, and we're really very excited about it," said study author Sheila Nirenberg, a professor and computational neuroscientist in the department of physiology and biophysics at Weill Medical College of Cornell University in New York City. "I've actually been working on this for 10 years. And suddenly, after a lot of work, I knew immediately that I could make a prosthetic that would work, by making one that could take in images and process them into a code that the brain can understand."
Nirenberg and her co-author Chethan Pandarinath (a former Cornell graduate student now conducting postdoctoral research at Stanford University School of Medicine) report their work in the Aug. 14 issue of Proceedings of the National Academy of Sciences. Their efforts were funded by the U.S. National Institutes of Health and Cornell University's Institute for Computational Biomedicine.
The study authors explained that retinal diseases destroy the light-catching photoreceptor cells on the retina's surface. Without those, the eye cannot convert light into neural signals that can be sent to the brain.
However, most of these patients retain the use of their retina's "output cells" -- called ganglion cells -- whose job it is to actually send these impulses to the brain. The goal, therefore, would be to jumpstart these ganglion cells by using a light-catching device that could produce critical neural signaling.
But past efforts to implant electrodes directly into the eye have only achieved a small degree of ganglion stimulation, and alternate strategies using gene therapy to insert light-sensitive proteins directly into the retina have also fallen short, the researchers said.
Nirenberg theorized that stimulation alone wasn't enough if the neural signals weren't exact replicas of those the brain receives from a healthy retina.
"So, what we did is figure out this code, the right set of mathematical equations," Nirenberg explained. And by incorporating the code right into their prosthetic device's chip, she and Pandarinath generated the kind of electrical and light impulses that the brain understood.
The team also used gene therapy to hypersensitize the ganglion output cells and get them to deliver the visual message up the chain of command.
Behavioral tests were then conducted among blind mice given a code-outfitted retinal prosthetic and among those given a prosthetic that lacked the code in question.
The result: The code group fared dramatically better on visual tracking than the non-code group, with the former able to distinguish images nearly as well as mice with healthy retinas.
"Now we hope to move on to human trials as soon as possible," said Nirenberg. "Of course, we have to conduct standard safety studies before we get there. And I would say that we're looking at five to seven years before this is something that might be ready to go, in the best possible case. But we do hope to start clinical trials in the next one to two years."
Results achieved in animal studies don't necessarily translate to humans.
Dr. Alfred Sommer, a professor of ophthalmology at Johns Hopkins University in Baltimore and dean emeritus of Hopkins' Bloomberg School of Public Health, urged caution about the findings.
"This could be revolutionary," he said. "But I doubt it. It's a very, very complicated business. And people have been working on it intensively and incrementally for the last 30 years."
"The fact that they have done something that sounds a little bit better than the last set of results is great," Sommer added. "It's terrific. But this approach is really in its infancy. And I guarantee that it will be a long time before they get to the point where they can really restore vision to people using prosthetics."
Other advances may offer benefits in the meantime, he said. "We now have new therapies that we didn't have even five years ago," Sommer said. "So we may be reaching a state where the amount of people losing their sight will decline even as these new techniques for providing artificial vision improve. It may not be as sci-fi. But I think it's infinitely more important at this stage."
For more on retinal degeneration, visit the U.S. National Institutes of Health.
SOURCES: Sheila Nirenberg, Ph.D., professor and computational neuroscientist, department of physiology and biophysics, Weill Medical College of Cornell University, New York City; Alfred Sommer, M.D., professor, ophthalmology, and dean emeritus, Bloomberg School of Public Health, Johns Hopkins University, Baltimore; Aug. 14, 2012, Proceedings of the National Academy of Sciences
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