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Retinal Device Restores Sight to Blind Mice
Date:8/13/2012

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 n
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