When a bear beds down for the winter, his brain is going into a kind of sleep, too. As the body cools, some brain synapses (the connection between brain cells) are cut off, putting the animal into a state of torpor, or deep sleep. But in the spring, when the bear’s body warms and he prepares to wake up, those synapses are restored without loss of memory.
Human brains have a similar protective mechanism triggered by rapid cooling. Think of those stories about people whose hearts have stopped as a result of hypothermia but are revived without experiencing significant brain damage.
At play in the brains of both hypothermic humans and hibernating animals is the production of “cold shock” proteins triggered during cooling, says a team of researchers at the University of Leicester. One of these proteins, RBM3, is the focus of the team's study, recently published in Nature. They set out to better understand how RBM3 influences the degeneration and regeneration of synapses, and, in doing so, were able to determine the role the protein may play in preventing brain cell death in those suffering from neurodegenerative disorders.
For the study, mice specially bred to reproduce features of Alzheimer’s and prion diseases had their body temperatures dropped to levels similar to those of hibernating animals. In the older mice whose diseases were further progressed, RBM3 proteins disappeared and brain synapses failed to regenerate after warming.
When the scientists artificially boosted levels of RBM3 they found that this alone was sufficient to protect the Alzheimer and prion mice, preventing synapse and brain cell depletion, reducing memory loss and extending lifespan.
The researchers were therefore able to conclude that RBM3 – and perhaps other cold-shock proteins – affects the ability of neurons to regenerate synapses in neurodegenerative diseases, which is essential to prevent synapse loss during disease progression.
In essence, the study showed that the process protecting brain synapses in those with neurodegenerative disorders may be defective, thereby contributing to brain cell death. Restoring this process could help restore synapses, and contribute to the prevention of brain cell loss in these patients.
Scientists now hope to develop medicine that could reproduce the protective effects of hibernation on the human brain—but without having to drop a patient’s body temperature. Such a development could change the way doctors prevent and treat diseases like Alzheimer’s, and, according to some, may one day even help restore lost memories.