Thekabarnews.com – Researchers at the Massachusetts Institute of Technology (MIT) may have found a new way to cure amblyopia, also known as “lazy eye.” Patients previously believed to be beyond the reach of effective therapy now have new hope. Studies have found a promising new way to tackle the issues caused by “lazy eyes” in such patients.

When the brain favors one eye over the other, it makes the less dominant eye’s vision worse. Eye patching, medicated eye drops, or corrective surgery are all traditional ways to try to bring the eyes back into equilibrium. But these methods do not always work well. This is particularly true if the treatment commences in the teenage years or later, or if patients struggle to adhere to the prescribed regimen.

The MIT researchers did not just look at the eyes; they also studied how the brain processes visual information. They were especially interested in how disturbed neural impulses make it harder for the weaker eye to send signals to the visual cortex. This condition leads to “lazy eyes,” according to studies.

Reconnecting the eye and brain

Researchers used tetrodotoxin, a strong neurotoxin that stops neuronal activity, to temporarily numb the retina of the weaker eye in mice with amblyopia. After only two days after retinal inactivation, the animals made an amazing recovery. The neuronal responses in the visual cortex returned to normal, which “rebooted” the broken connection between the eye and brain. The weaker eye’s vision got a lot better, whereas the stronger eye’s function stayed the same.

The results expand on years of work by neuroscientist Mark Bear and his team, which has looked at how blocking retinal input can make the brain more flexible again, like it was during early development. Previous research revealed that putting both eyes to sleep or momentarily turning off the stronger eye could bring back vision. But those methods have big hazards, like temporary blindness or problems with normal eyesight.

The important role of calcium channels

The current study improves the method by simply focusing on the amblyopic eye. The researchers discovered that recovery is contingent upon particular T-type calcium channels in the brain. These channels provide bursts of neuronal activity that change the way visual circuits work. They wake up pathways that were asleep and help the brain learn how to process visual data from the weaker eye again. Studies have found a promising new insight into the roles calcium channels play in this process.

What comes next after mice?

The researchers are cautiously hopeful, even though the method is still experimental and invasive and has only been tried on mice so far. The next stage is to test the technology on animals with more complicated visual systems. The study is an important step before going on to human clinical trials.

Applying the results to humans could significantly transform the treatment of amblyopia. Patients may eventually benefit from a quick, biologically driven “reset” of the visual system. This would improve eyesight in the long run, even later in life, instead of relying on long-term behavioral therapy.

The study implies that the time frame for treating amblyopia may be far longer than previously thought for the millions of people around the world who have it. Studies have found a promising new way that suggests more extended treatment periods for “lazy eyes” are possible.