Neuroscientists continue to be amazed at the brain’s ability for adaptation and rewiring throughout life. Researchers discovered a way to restore sight to adult mice suffering from congenital blindness. This was despite the rodents being relatively mature.
The mice represented a rare human condition of the retina called “Retinal Disorder.” leber congenital amaurosis(LCA), which is often associated with severe visual impairment or blindness at birth.
This genetic condition appears to have been caused by mutations in any of the dozens of genes that are associated with the retina and light-sensing abilities.
For many decades, researchers have been trying to find ways to restore damaged or malfunctioning photoreceptors in the eye. Retinal implants, gene editing interventions and drug treatments are some of the options.
These therapies are all promising and have varying success rates. Synthetic compounds that target the retina seem particularly promising for people with rod photoreceptor mutations.
Rods are photoreceptors located at the back and sense dim light. These neurons are highly specialized. A series of biochemical reactionsTo convert sensory light into electrical signals that the rest of your brain can’read’.
Because light-sensitive pigments found in retinal rods absorb very low levels light, they Convert the molecule 11cis retinal to all-Trans-retinalThe impulse is then sent down the optic nerve to your brain.
Previous studiesChildren with LCA have seen that injecting synthetic retinoid solutions directly into the eyes can compensate for some vision loss. However, it is still not clear how these treatments will affect adults suffering from the condition.
Researchers stated that although some progress was made, it is still unclear if adult visual circuits can be restored fully functional at the level the visual cortex after correction of the retinal defect. Send an email.
Tradition has held that the brain’s vision system is built and strengthened during specific developmental windows. The brain’s visual network may not be properly wired for vision if the eye isn’t exercising during these crucial periods. This could result in lifelong vision problems.
A mammal’s vision potential may not be as strong as one might think.
This idea was explored by researchers who administered a synthetic vitamin for seven days in rodents that had retinal degeneration.
The treatment was successful in partially restoring light sensitivity and normal light-orienting behaviors of the animals for 27 days.
Nine days later, the optic nerve activated far more neurons in visual cortex.
This indicates that even in adult mice, retinoid treatment can significantly restore the central vision pathway that transmits information from the eyes to the visual cortex.
“Frankly, the treatment saved brain circuits that are involved in vision and we were stunned,” “Sunil Gandhi, neurobiologist at the University of California Irvine.
“Seeing is more than just functioning and intact retinae. It all starts with the eye, which transmits signals throughout the brain. Visual perception is actually created in the central circuits.
While the study was conducted only on mice, the neuroscientists have now concluded that the critical window of the human visual system might be wider than originally thought.
This means that a loss of vision in childhood doesn’t necessarily mean that sight cannot be restored in adulthood.
“The treatment activated twice as many neurons in the brain after it was completed,” “ Ghandi.
“What was more amazing was the fact that signals from the same side eye pathway activated five times more neurons in brain after treatment, and this remarkable effect was lasting.”
Additional research is required on animal models. Neuroscientists may one day be able to test whether LCA can have similar effects on older people.
Ghandi stated, “The fact this treatment works so well at the central visual pathway during adulthood supports a new idea. It is that there is latent vision potential that is just waiting for it to be activated.” This explains.
The study was published by Current Biology.
