Restoring Vision: A Breakthrough in Treating Glaucoma-Induced Blindness

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In a remarkable leap forward, researchers have partially restored the vision of mice with damaged optic nerves by generating new nerve cells in the eye. This innovative approach holds promise for treating conditions like glaucoma, which can lead to blindness by damaging the optic nerve.

Restoring Vision: A Breakthrough in Treating Glaucoma-Induced Blindness

"We can regenerate those cells," says Biraj Mahato at the Children’s Hospital Los Angeles, highlighting the potential of this technique. However, before human trials can begin, further studies in larger animals are necessary to ensure its safety and efficacy.

Glaucoma stands as one of the leading causes of blindness worldwide, affecting approximately 80 million people. It progressively damages the optic nerve, which transmits visual information from the eyes to the brain. While the condition can be managed once diagnosed, it is often detected only after significant vision loss has occurred, and there is currently no way to restore lost vision.

Efforts to replace the nerve cells in the optic nerve, specifically the retinal ganglion cells that perish in glaucoma, are underway globally. These cells have long projections, or axons, that stretch from the retina to the brain. One approach to restore lost vision involves generating new retinal ganglion cells from stem cells in a lab and then transplanting them into the eye.

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Scientists have made a remarkable breakthrough in restoring vision lost to glaucoma. By coaxing existing cells in the eye to regenerate, they've partially restored sight in mice with damaged optic nerves. Could this innovation be the key to treating blindness caused by optic nerve damage in humans?


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However, Mahato and his team have taken a different route, coaxing existing cells within the eye, known as Müller glia, to transform into nerve cells. By developing a cocktail of eight chemicals, they were able to induce these support cells to adopt the characteristics of retinal ganglion cells.

When this cocktail was tested in mice with chemically damaged optic nerves, the researchers observed signs of vision recovery starting as early as two weeks post-treatment and lasting for at least four months. In one experiment, mice were placed on a transparent surface with a visual drop on one side, resembling a visual cliff. While almost all non-glaucoma mice instinctively avoided the edge, mice with damaged optic nerves showed no such preference. However, 45 days after treatment, 72 percent of the treated mice chose the safer-looking side.

Further studies confirmed that the newly developed retinal ganglion-like cells had indeed originated from Müller glia and were extending axons towards the brain. Additionally, the cocktail successfully converted human Müller glia cells into retinal ganglion-like cells in laboratory settings.

Mahato believes that this approach offers advantages over cell transplantation, as it is quicker and avoids issues related to immune rejection. Ted Garway-Heath from the UCL Institute of Ophthalmology in the UK agrees, calling it "an approach worth pursuing." However, he cautions that much work remains before human trials can commence, as the success in mice does not guarantee effectiveness in humans, especially considering the longer axon growth required in human nerves to reach the brain.

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