The brain’s ability to adapt and rewire itself throughout life continues to amaze neuroscientists. Researchers have discovered treatment that restores sight to adult mice with a form of congenital blindness, despite the rodents’ relative maturity.
The mice had a rare human retinal disorder called Leber congenital amaurosis (LCA), which often causes blindness or severe visual impairment at birth.
This inherited condition appears to be caused by a mutation in any of dozens of genes associated with the retina and its ability to perceive light.
Vision-restoring treatment is getting closer to reality
Researchers have worked for several decades on treatment that restores vision by restoring damaged or dysfunctional photoreceptors in this part of the eye. Some strategies include retinal implants, gene-editing interventions, and drug treatments.
All of these emerging therapies improve vision with varying degrees of success, but synthetic compounds that target the retina appear particularly promising for those with mutations involving rod photoreceptors.
Rods are the photoreceptors at the back of the eye that sense dim light. These specialized neurons use a series of biochemical reactions to convert sensory light into electrical signals that the rest of the brain can “read”.
As the light-sensitive pigments in the retinal rods absorb low levels of light, they convert the 11-cis retinal molecule to all-trans-retinine, which in turn generates an impulse that travels through the optic nerve to the brain.
The study that changes what was previously known about vision
Previous studies on children with ACL have shown that synthetic retinoid treatments can help compensate for vision loss when injected directly into the eye. But how these treatments work in adults with the condition is not as well understood.
“Although some progress has been made, it remains unclear to what extent adult visual circuits can be restored to a fully functional state in the visual cortex after retinal defect correction,” the researchers write.
Traditionally, the brain’s visual system was thought to be formed and consolidated during certain developmental windows early in life. If the eye is not used during these critical periods, then the visual networks in the brain will never connect properly for vision, leading to lifelong vision deficits, he writes Science Alert.
But a mammal’s potential to see might not be so rigidly wired; it could be much more plastic than previously thought.
The sight-restoring treatment has shown promising results
To explore this idea, the researchers administered a synthetic retinoid for seven days to adult rodents born with retinal degeneration.
The vision-restoring treatment was ultimately successful in partially restoring the animals’ light sensitivity and their typical light-orienting behaviors for 27 days.
Nine days after treatment, many more neurons in the visual cortex were being activated by the optic nerve.
This suggests that the central visual pathway that carries information from the eye to the visual cortex can be significantly restored by retinoid treatment, even in adult mice.
“Honestly, we were amazed at how much the treatment saved the brain circuits involved in vision,” says neurobiologist Sunil Gandhi, of the University of California, Irvine, in the US.
“Vision involves more than an intact and functioning retina. It starts in the eye, which sends signals throughout the brain. It is only in the central circuits of the brain that visual perception actually occurs,” explains Gandhi.
People with vision problems at birth may recover their sight later in life
The study was conducted only in mice, but the finding leads neuroscientists to believe that the critical window for the human visual system may also be larger than once thought.
In other words, the lack of vision in childhood does not necessarily mean that vision cannot be recovered in adulthood.
“Immediately after treatment, signals from the opposite eye, which is the dominant pathway in the mouse, activated twice as many neurons in the brain,” says Ghandi.
“What was even more extraordinary was that signals coming from the eye pathway on the same side activated five times as many neurons in the brain after treatment, and this impressive effect was long-lasting,” added the researcher.
Further research in animal models is needed. But maybe one day, neuroscientists will be able to test whether similar benefits could be triggered in older people with some versions of LCA.
The study was published in Current Biology.