During hibernation, animals like bears and mice lose as much as 30% of their synapses as the creatures cool; but those brain connections are recreated when they wake back up however many weeks or months later. Synapses are similarly lost (but, of course, not reformed) in the brains of Alzheimer's patients, and that loss correlates with memory loss. Now a team out of the UK is reporting in the journal Nature on the role a "cold-shock" protein called RBM3 may play. The team found then when both young and old mice (in this case, a non-hibernating version) with Alzheimer's disease were chilled and then warmed up, only the young ones were able to reform their connections. And in those young mice, RBM3 levels jumped as they cooled; the same wasn't true for their elderly counterparts, reports the BBC. But by boosting RBM3 levels, the team found they could prevent "synapse and brain cell depletion."
"This gives us a target to develop a drug in the same way paracetamol is used for a fever rather than a cold bath," one of the lead researchers says. And though it's too early to say whether such an effect will be similar in humans, the lab behind this discovery—the Medical Research Council's Toxicology Unit in Leicester—is the one that first prevented the death of brain tissue in a neurodegenerative disease. "While we don't think body cooling is a feasible treatment for long-term, progressive conditions like Alzheimer's disease, this research opens up the possibility of finding drugs that can have the same effect," an outside researcher says. (Hibernating bears have been called a "metabolic marvel.")