Heredized blindness, closer than ever

According to RCO News Agency, A new and successful treatment allows the damaged retina cells to rebuild themselves.

Current research has been done on mice, but the way it is done is the same in humans, hoping for a new way to treat certain types of blindness, according to the New Atlas.

Pigantosa retinitis (retina), while regarding a relatively rare disease, affects approximately 1.5 million people worldwide and is considered as the number one factor in hereditary blindness associated with retinal degeneration.

It breaks down light -sensitive cells called optical receptors in the retina, which results in a gradual reduction of vision and ultimately the complete loss of central vision.

There is currently no well -known treatment for “Pigantosa Retinite”, but researchers at the Korean Institute of Advanced Science and Technology (Kaist) have recently made progress in its treatment that can certainly lead to complete treatment.

Scientists were inspired by fish (especially zebra) in their research. This is because when the retina is damaged, they have a strange ability to regenerate damaged cells. The reason for this seems to be due to the cells of the Glia Glia. A coating of these cells creates a connection between the inner and outer layers of the retina, in addition to helping to remove nerve waste from the eye and help transmit light.

When the retina is damaged, the Golia Muller cells distinguish the retina precursor cells that produce new neurons and help the fish maintain their vision properly.

This does not apply to mammals, and Kaist researchers studied human donated eyes and the eyes of mice designed for retinal damage.

This is due to a protein called Prox1 that is present in the damaged eye of humans and mice. The Prox1 protein prevents the distinction between Golia Muller cells in mammals. By blocking this ability, Golia cells cannot work to regenerate retinal cells.

So the researchers developed an antibody that connected to the prox1 protein. When the antibody was injected into the retina of mice with “retinitis pigtanosa”, the prox1 protein function was blocked, the retina was rebuilt and the vision returned for more than six months.

The team is currently developing the prox1 antibodies through a Cellia startupmaster and hopes to begin human experiments for patients with Pigantosa retinitis and other retina that are currently not cured.

Eun Jung Lee, a senior writer of the study, says: “We are completing the prox1 -neutralized antibody optimization, and we move to pre -clutch studies before prescribing it in patients with retina.”

“Our goal is to provide a solution for patients that are currently lacking in proper treatment options,” he said.

This research is published in the journal Nature Communications.

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