Amnesia caused by head injury reversed in mouse study
Researchers at Georgetown University Medical Center, in collaboration with Trinity College Dublin, have found that amnesia and poor memory following head injury are due to inadequate reactivation of neurons involved in forming memories — and that such amnesia has the potential to be reversed. That’s according to a new study in mice, which has been published in The Journal of Neuroscience.
Georgetown investigators had previously found that the brain adapts to repeated head impacts by changing the way the synapses in the brain operate, which can cause trouble in forming new memories and remembering existing memories. But while most research in this area has been in human brains with chronic traumatic encephalopathy (CTE) — a degenerative brain disease found in people with a history of repetitive head impact — senior investigator Professor Mark Burns said he and his colleagues sought to understand “how the brain changes in response to the low-level head impacts that many young football players regularly experience”.
In the new study, the scientists gave two groups of mice a new memory by training them in a test they had never seen before. One group was exposed to a high frequency of mild head impacts for one week (designed to mimic a week of exposure for a college football player) and one group were controls that didn’t receive the impacts. The impacted mice were unable to recall the new memory a week later — despite the fact that neurons involved in learning new memories (the ‘memory engram’) were equally present in both the control mice and the experimental mice.
“We are good at associating memories with places, and that’s because being in a place, or seeing a photo of a place, causes a reactivation of our memory engrams,” explained first author Dr Daniel P Chapman. “This is why we examined the engram neurons to look for the specific signature of an activated neuron. When the mice see the room where they first learned the memory, the control mice are able to activate their memory engram, but the head impact mice were not. This is what was causing the amnesia.”
This confirmed that the memory loss attributed to head injury was not a permanent pathological event driven by a neurodegenerative disease; indeed, the researchers were able to reverse the amnesia to allow the mice to remember the lost memory by using lasers to activate the engram cells. But while this invasive technique was able to successfully reverse memory loss in the mice, Burns said it is not translatable to humans.
“Our research gives us hope that we can design treatments to return the head-impact brain to its normal condition and recover cognitive function in humans that have poor memory caused by repeated head impacts,” Burn said.
“We are currently studying a number of non-invasive techniques to try to communicate to the brain that it is no longer in danger, and to open a window of plasticity that can reset the brain to its former state.”
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