Brain forms complex new neural circuits when its primary "learning centre" is damaged to compensate for lost function, a new study has found.
Scientists from University of California, Los Angeles and Australia also pinpointed the regions of the brain involved in creating those alternate pathways - often far from the damaged site.
Researchers found that parts of the prefrontal cortex take over when the hippocampus, the brain's key centre of learning and memory formation, is disabled.
Their breakthrough discovery, the first demonstration of such neural-circuit plasticity, could potentially help scientists develop new treatments for Alzheimer's disease, stroke and other conditions involving damage to the brain.
For the study, Michael Fanselow and Moriel Zelikowsky conducted laboratory experiments with rats showing that the rodents were able to learn new tasks even after damage to the hippocampus.
While the rats needed more training than they would have normally, they nonetheless learned from their experiences - a surprising finding.
After discovering the rats could, in fact, learn to solve problems, Zelikowsky, travelled to Australia to work with Bryce Vissel, a group leader of the neuroscience research program at Sydney's Garvan Institute of Medical Research.
They analysed the anatomy of the changes that had taken place in the rats' brains. Their analysis identified significant functional changes in two specific regions of the prefrontal cortex.
"Interestingly, previous studies had shown that these prefrontal cortex regions also light up in the brains of Alzheimer's patients, suggesting that similar compensatory circuits develop in people," Vissel said.
"While it's probable that the brains of Alzheimer's sufferers are already compensating for damage, this discovery has significant potential for extending that compensation and improving the lives of many," Vissel added.
The hippocampus, a seahorse-shaped structure where memories are formed in the brain, plays critical roles in processing, storing and recalling information. The hippocampus is highly susceptible to damage through stroke or lack of oxygen and is critically involved in Alzheimer's disease, Fanselow said.
"Until now, we've been trying to figure out how to stimulate repair within the hippocampus. Now we can see other structures stepping in and whole new brain circuits coming into being," he said.
Zelikowsky said that sub-regions in the prefrontal cortex compensated in different ways, with one sub-region - the infralimbic cortex - silencing its activity and another sub-region - the prelimbic cortex - increasing its activity.
The study was published in Proceedings of the National Academy of Sciences journal.
