The brain adapts to find new visual information when a person gets eye disease causing blindness, according to a study from the Massachusetts Institute of Technology.

Researchers found that when people lose their sight because of macular degeneration, the affected neurons simply start seeking visual input from other, non-affected parts of the eye.

Their findings were published Wednesday in the Journal of Neuroscience.

"This study shows us one way that the brain changes when its inputs change. Neurons seem to 'want' to receive input: when their usual input disappears, they start responding to the next best thing," wrote lead researcher Nancy Kanwisher of the McGovern Institute for Brain Research at MIT.

It appears the long-term change in visual behaviour is not driving the brain's remapping; rather, it's the brain's relatively passive response to visual deprivation.

Macular degeneration is the most common form of adult blindness. It affects 800,000 people in Canada. Those suffering from it progressively lose vision in the central visual field of their retina, or their fovea. That means the corresponding part of the visual cortex in the brain also loses input.

"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said in a news release. "If scientists could one day develop technologies to replace the lost light-sensitive cells in the fovea, patients might be able to recover central vision since the neurons there are still alive and well."

Previously, researchers found deprived neurons would begin responding to visual input from another spot on the retina, essentially building a new visual map on the cortex. That information provided evidence of plasticity in the adult cortex. However, there were still questions as to how that happened.

MIT's study sheds light on the underlying neural mechanism.

"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information processing strategy," said Kanwisher.

Typically, people suffering from MD will compensate by using an adjacent patch of undamaged retina. They'll roll their eyes upward to look at someone's face instead of focusing straight on, for instance. That undamaged patch becomes their new "preferred retinal locus," or PRL.

The researchers wanted to find out if the cortical change was caused by chronic prior use of the PRL, said another study author, Daniel D. Dilks, a postdoctoral fellow in the Kanwisher lab.

"Or, do the deprived neurons respond to stimulation at any peripheral location, regardless of prior visual behaviour," he wrote.

The previous studies could not answer this question because they had only tested patients' PRL. This new study tests both the PRL and another peripheral location, using functional magnetic resonance imaging to scan two macular degeneration patients who had no central vision, and consequently had a deprived central visual cortex.

Because patients habitually use the PRL like a new fovea, it could be that the deprived cortex might respond preferentially to this location.

But that is not what the researchers found. Instead, the deprived region responded equally to stimuli at both the preferred and nonpreferred locations.