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Breakthrough Study Reverses Amblyopia Vision Loss

Study Identifies Method to Restore Vision in Amblyopia

Male ophthalmologist examining a senior female patient's eyes using a slit lamp biomicroscope in a bright clinical office.
MIT researchers have identified a potential method to treat amblyopia, or ‘lazy eye,’ in adults by temporarily anesthetizing the retina to reset visual connections.

WASHINGTON Scientists have reported a potential method to restore vision in individuals with a common developmental eye disorder by temporarily “rebooting” the retina, allowing it to regenerate and restore function.

Researchers at the Massachusetts Institute of Technology in the United States found that briefly anesthetising the retina can reverse the visual system to an earlier developmental state, addressing amblyopia, commonly known as “lazy eye”.

Amblyopia occurs when vision in one or both eyes does not develop correctly during childhood, as the brain suppresses input from one eye.

Existing treatments are largely effective only during infancy, when neural connections are still forming.

The MIT team discovered that anesthetising the retina of the amblyopic eye in mice for several days restored the brain’s visual response to that eye even in adulthood, according to a study published in the journal Cell Reports.

The researchers intend to investigate whether this treatment is effective in other animal species and eventually in humans.

Study author Mark Bears noted that if the approach translates to humans, it would allow the amblyopic eye to be reactivated without disrupting vision in the unaffected eye. “The amblyopic eye, which is not doing much, could be inactivated and ‘brought back to life’ instead,” he said.

The research focused on the lateral geniculate nucleus, a network of brain neurons that conveys visual information from the eyes to the visual cortex for processing.

Previous research in 2008 demonstrated that blocking retinal signals to this network triggered synchronous bursts of electrical activity in neurons of the visual cortex.

The current study explored whether these bursts play a role in potential amblyopia treatments. Researchers injected anaesthesia into the eyes of amblyopic mice and compared them with a control group, temporarily taking the retina offline for two days.

Subsequent measurements of neuron activity in the visual cortex revealed that the ratio of signals from each eye was higher in treated mice than in untreated mice, indicating that the injection could “reboot” the eye. This suggested that input from the amblyopic eye increased to match that of the normal eye after anesthetisation.

The researchers concluded that the findings offer cautious optimism for developing a new treatment approach for human amblyopia, particularly given the effectiveness of silencing the amblyopic eye.