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A Treatment for Alzheimer's Might Lie in the Brains of Hibernating Bears

When mammals emerge from hibernation, a protein called RBM3 helps to regenerate connections between dormant brain cells — a process which scientists have now been able to simulate in laboratory mice.
Image via Flickr

Chances are that if you've been somewhere cold during the winter months you've had to fight off the urge to curl up under the covers, imitating the tranquil state of a hibernating bear.

Well, it turns out, according to scientists, hibernation might provide some lessons for treating the five million Americans that suffer from Alzheimer's and other neurodegenerative brain disorders.

A group of Leicester, England-based researchers simulated the process of hibernation in mice, which do not do so naturally, and identified a process for preventing the loss of brain cells and the connections between them.


When a bear hibernates for the winter, its core body temperature declines, which depletes the synapses between brain cells, allowing the mammal to fall into a deep torpor for extended periods of time without the need for nutrition. When body temperature is increased in the bear at the end of the season, the connections between its brain cells are restored, causing brain function to return to normal.

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At the heart of that process are "cold shock" proteins, one of which scientists identify as RBM3 and, they say, helps to regenerate the connections between brain cells.

The researchers took two sets of mice, one of which was bred to develop neurological disorders and another that was healthy. They reduced the body temperatures of the mice by 16 -18 degrees Celsius for 45 minutes. In the healthy mice, they found that brain cell synapses degenerated during cooling but regenerated during re-warming. In the mice bred to develop neurological disorders, however, they found that brain cell regeneration deteriorated as the disease advanced, as did levels of RBM3.

The researchers then took a group of neurologically compromised mice and boosted their levels of RBM3. In this set of mice, they found that by boosting the protein, brain cells and the connections between them were protected from deterioration.

RBM3 alone, they concluded, could help protect brain function without the need for cooling core body temperature. Their findings were published in the journal Nature.


"We've known for some time that cooling can slow down or even prevent damage to brain cells," Giovanna Mallucci of the UK Medical Research Council (MRC) said. "But reducing body temperature is rarely feasible in practice: it's unpleasant and involves risks such as pneumonia and blood clots."

"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," Mallucci said.

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There is no known cure for Alzheimer's and, treatment costs are estimated to be $215 billion annually. Currently 225 clinical studies are underway seeking to identify ways to combat Alzheimer's, according to the Alzheimer's Foundation of America. And, says the US Centers for Disease Control, it is the sixth leading cause of death in the United States.

The most common form of dementia, Alzheimer's causes memory loss, problems with language, disorientation, and mood swings. Risk of suffering from Alzheimer's increases significantly after the age of 65. Those 85 years or older have a 50 percent chance of contracting Alzheimer's.

"The neuroprotective pathway identified in this study could be an important step forward," Hugh Perry, chairman of MRC's Neurosciences and Mental Health Board, said. "We now need to find something to reproduce the effect of brain cooling. Just as anti-inflammatory drugs are preferable to cold baths in bringing down a high temperature, we need to find drugs which can induce the effects of hibernation and hypothermia."

Consider that when curling up this winter.

Follow G. Vaughn on Twitter: @gingervaughn100

Image via Flickr