A protein in brains that helps to control cooling could be utilized to help treat cases of dementia, including Alzheimer's disease. This finding could lead to treat methods taking advantage of body systems used by some animals during hibernation.

Brain connections in bears, mice, and hedgehogs are regularly destroyed as the animals enter their long winter slumbers. Between 20 and 30 percent of synapses - connections in the brain - can be lost each year as hibernation begins, preserving bodily resources for the long sleep. As these animals return to consciousness in the Spring, the structures are naturally repaired, without loss of memory.

Mice with and without Alzheimer's and prion disease were cooled by researchers, and their brain structures were analyzed. Brain synapses were lost by the rodents as their temperature cooled, but regrew in younger animals, although older mice did not recover lost connections.

Alzheimer's patients lose vast quantities of brain synapses in early stages of the disease, and the disorder soon goes on to damage entire brain cells.

On variety of "cold-shock" proteins called RBM3 was prevalent in the bodies of young mice as they chilled, but did not build up in older rodents. The team conducted additional research that revealed deaths of brain cells could be reduced through the application of RBM3. Investigators believe this chemical could be responsible for rebuilding synapses lost as bodies cool.

"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," Giovanna Mallucci of the Medical Research Council Toxicology Unit at the University of Leicester, said.

Cooling bodies can often provide protection against brain damage, including in people who suffer cardiac arrest following a fall into frigid water. Babies suffering from oxygen deprivation at birth can often be saved from brain damage by doctors quickly chilling the infant. Researchers now hope to be able to mimic the effects of hibernation in humans without having to physically cool a patient, which can lead to blood clots and other health problems.

"We now need to find something to reproduce the effect of brain cooling. We need to find drugs which can induce the effects of hibernation and hypothermia," Hugh Perry, chairman of the neurosciences and mental health board at the Medical Research Council in Britain, told reporters.

RBM3 mediates structural plasticity and protective effects of cooling in neurodegeneration, a letter detailing the study into hibernation and brain synapses, was published in the journal Nature

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