Breakthrough in Amblyopia Treatment

Researchers believe they may have discovered a method to reverse “lazy eye,” even in adults who have lived with the condition since childhood.

The technique is currently untested in humans, having only been explored in animals thus far, which means there’s still a way to go before it can be applied to people.

A lazy eye, or amblyopia, emerges when the brain prefers one eye over the other during early childhood. This leads to a decline in vision in the less favored eye. The standard method of treatment involves patching the stronger eye, encouraging the brain to rely on the weaker one. Unfortunately, this approach is effective mainly during infancy and early childhood when the neural pathways for vision are still developing.

A recent study on mice, published on November 25 in Cell Reports, showcases a method for temporarily shutting down the weak eye. This temporary closure may facilitate recovery from amblyopia, even in cases of prolonged vision problems. Activating neurons that transmit visual signals from the retina to the visual cortex appears to “reboot” the lazy eye, enabling recovery.

Ben Thompson, a professor and director at the University of Waterloo’s School of Optometry and Vision Science, expressed optimism about the findings, noting that inactivation of the amblyopic eye has shown promise in the study. However, he cautioned that more research is necessary to evaluate whether this method will be safe and effective for human patients.

Dr. Dennis Levi, a professor of optometry and vision science at UC Berkeley, also felt hopeful but remained cautiously optimistic. Historical attempts to reverse lazy eye in mice did not yield significant results for humans, yet this new technique seems worthy of attention.

So, how does temporarily shutting down the weak eye aid in restoring its vision?

Previous studies led by MIT neuroscientist Mark Bear demonstrated that anesthetizing the non-lazy eye prompted visual recovery in older animals. This included cats and mice, and similar outcomes have also been observed in monkeys—potentially offering good news for humans.

The research team suggested that blocking input from one retina causes synchronized bursts of activity in the thalamus, which relays sensory information to the visual cortex. They theorized that mimicking these early activity patterns could help treat amblyopia.

In their study, the team used a local anesthetic called tetrodotoxin (TTX) in the retinas of mice, monitoring the activity of the neurons in the lateral geniculate nucleus (LGN), which is essential for visual processing. TTX, a neurotoxin found in pufferfish, has potential therapeutic applications, but ongoing research is necessary for its human use. In this instance, TTX effectively rebooted the mice’s retinas.

By shutting down either eye, they observed the same burst activity in the LGN. A separate experiment involved genetically modifying mice to block this burst of firing, which prevented improvement in amblyopia, indicating that the bursts themselves are vital for recovery.

The researchers then tested whether targeting only the weak eye could be effective. In one experiment, some mice received an injection to mute the weak eye’s signals for about two days, while others did not. A week after the injection, evaluations showed that the treated mice benefited from a more balanced input from both eyes compared to those that went untreated, suggesting that temporarily shutting down the weaker eye allowed it to “catch up” with the other eye.

Thompson noted that this is an encouraging finding, as the fellow eye is not exposed to treatment risks. Still, he emphasized that further research is needed to ensure the safety and efficacy of tetrodotoxin in humans.

Previous studies indicate that TTX’s effects may extend to cats and monkeys, raising hopes that this approach could one day assist humans as well.

The discovery that burst firing could enhance the brain’s capability for rewiring and forming new neural pathways is compelling. Thompson suggested that non-invasive methods to stimulate the brain might eventually be developed to trigger similar neural responses without requiring TTX injections.

This article is for informational purposes only and is not meant to offer medical advice.