Bionic Eye Soon Available

A bionic eye being developed by a team of biomedical researchers at the University of Sydney and UNSW has shown to be safe and stable for long-term implantation in a three-month study, paving the way towards human trials.

The Phoenix99 Bionic Eye is an implantable system, designed to restore a form of vision to patients living with severe vision impairment and blindness caused by degenerative diseases, such as retinitis pigmentosa. The device has two main components which need to be implanted: a stimulator attached to the eye and a communication module positioned under the skin behind the ear.

Publishing in Biomaterials, the researchers used a sheep model to observe how the body responds and heals when implanted with the device, with the results allowing for further refinement of the surgical procedure. The biomedical research team is now confident the device could be trialed in human patients.

The Phoenix99 Bionic Eye works by stimulating the retina—a thin stack of neurones lining the back of the eye. In healthy eyes, the cells in one of the layers turn incoming light into electrical messages which are sent to the brain. In some retinal diseases, the cells responsible for this crucial conversion degenerate, causing vision impairment. The system bypasses these malfunctioning cells by stimulating the remaining cells directly, effectively tricking the brain into believing that light was sensed.

Importantly, we found the device has a very low impact on the neurons required to ‘trick’ the brain. There were no unexpected reactions from the tissue around the device and we expect it could safely remain in place for many years,” said Mr Samuel Eggenberger, a biomedical engineer who is completing his doctorate with Head of School of Biomedical Engineering Professor Gregg Suaning.

Our team is thrilled by this extraordinary result, which gives us confidence to push on towards human trials of the device. We hope that through this technology, people living with profound vision loss from degenerative retinal disorders may be able to regain a useful sense of vision,” added Mr Eggenberger.

Source: https://neurosciencenews.com/

 

How To Reverse Congenital Blindness

Researchers funded by the  American National Eye Institute (NEI) have reversed congenital blindness in mice by changing supportive cells in the retina called Müller glia into rod photoreceptors. The findings advance efforts toward regenerative therapies for blinding diseases such as age-related macular degeneration and retinitis pigmentosa. A report of the findings appears online today in Nature. NEI is part of the National Institutes of Health.

This is the first report of scientists reprogramming Müller glia to become functional in the mammalian ,” said Thomas N. Greenwell, Ph.D., NEI program director for retinal neuroscience. “Rods allow us to see in low light, but they may also help preserve cone photoreceptors, which are important for color vision and high visual acuity. Cones tend to die in later-stage eye diseases. If rods can be regenerated from inside the eye, this might be a strategy for treating diseases of the eye that affect photoreceptors.”

Photoreceptors are light-sensitive cells in the retina in the back of the eye that signal the brain when activated. In mammals, including and humans, photoreceptors fail to regenerate on their own. Like most neurons, once mature they don’t divide.

Scientists have long studied the regenerative potential of Müller glia because in other species, such as zebrafish, they divide in response to injury and can turn into photoreceptors and other retinal neurons. The zebrafish can thus regain vision after severe retinal injury. In the lab, however, scientists can coax mammalian Müller glia to behave more like they do in the fish. But it requires injuring the tissue.

From a practical standpoint, if you’re trying to regenerate the retina to restore a person’s vision, it is counterproductive to injure it first to activate the Müller glia,” said Bo Chen, Ph.D., associate professor of ophthalmology and director of the Ocular Stem Cell Program at the Icahn School of Medicine at Mount Sinai, New York.

We wanted to see if we could program Müller glia to become rod photoreceptors in a living mouse without having to injure its retina,” added Chen, the study’s lead investigator.

Source: https://www.nih.gov/
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