By studying the process of hibernation, scientists have identified ‘cold shock’ proteins that regenerate the connections between brain cells, which they say could be key to a new treatment for Alzheimer’s disease.
In order to survive the winter months in some of the world’s coldest climates, animals such as bears, hedgehogs and bats hibernate. First their core temperatures decrease dramatically, which causes up to 30 percent of the synapses that form connections between the brain cells to deplete. This allows the animals to fall into a deep torpor, so they can while away the harshest weeks of the year without worrying about finding food that isn’t there.
Once the cold subsides and these animals’ body temperatures rise, a whole bunch of synapses are suddenly restored, allowing them to wake and continue on with their perfect brain function restored, and no loss of memory.
This process of synapse restoration relies on ‘cold shock’ proteins known as RBM3 to restore the connections between a hibernating creature’s brain cells, and scientists are looking into how they can apply them to new treatments for dementia.
The team, led by Giovanna Mallucci from the UK Medical Research Council, investigated the effects of RBM3 in non-hibernating mice, split into two groups - one that was bred to develop neurological disorders, and one that wasn’t. Both groups had their body temperatures cooled to 16 to 18 degrees Celsius for 45 minutes to simulate a mini hibernation episode.
When they observed the healthy mice, the team found that their synapses decreased dramatically as their bodies were cooled right down, but when it came time for warming up, their levels of RBM3 sky-rocketed and everything was regenerated back to regular levels. The mice with neurological disorders, on the other hand, struggled to regenerate the connections between their brain cells, and their levels of RBM3 started to deteriorate. And this only got worse as their disease advanced.
So the researchers worked with a new group of mice bred to develop neurological disorders and then increased their levels of RBM3. Publishing in the journal Nature, they report that all the extra RBM3 prevented the synapses from deteriorating. "RBM3 alone, they concluded, could help protect brain function without the need for cooling core body temperature,” G. Vaughn writes for Vice News.
"We've known for some time that cooling can slow down or even prevent damage to brain cells. But reducing body temperature is rarely feasible in practice: it's unpleasant and involves risks such as pneumonia and blood clots,” Mallucci told Vaughn. "By identifying how cooling activates a process that prevents the loss of brain cells, we can now work towards finding a means to develop drugs that might mimic the protective effects of cold on the brain."
Interestingly, the team thinks that if they can figure out how to get this treatment to work in humans, they will be able to restore the memories that have been lost to people affected by Alzheimer’s disease. As James Gallagher writes at BBC News, this is because only the receiving end of the synapse shuts down during cooling or hibernation.
"I asked Prof Mallucci if memories could be restored in people if their synapses could be restored: 'Absolutely, because a lot of memory decline is correlated with synapse loss, which is the early stage of dementia, so you might get back some of the synapse you've lost.’"
According to the US Alzheimer’s Association, the likelihood of developing Alzheimer’s disease doubles just about every five years after age 65. And after 85, the risk reaches nearly 50 percent. Any step closer to figuring out how to prevent and treat this devastating disease is a welcome development, especially if it involves big, sleepy bears.