You may be familiar with the research interest in heat shock proteins and their role in cellular health and repair. They are a part of the reaction to heat necessary to allow individuals to survive high temperatures. There is an analogous but different reaction to the other end of the temperature scale, also intended to assure survival under potentially damaging low temperatures. Here is an interesting result in which researchers investigate some of the mechanisms involved in the cellular reaction to cold, arising out of the study of hibernation in mammals:
It has long been known that during hibernation, where a mammal's core temperature cools to well below normal body temperature, synapses (the connections between brain cells) are depleted. This allows the animal to enter a state of 'torpor', similar to a very deep sleep but where no brain activity occurs, allowing the animal to survive without nutrition for weeks or months. As the animal comes out of hibernation and warms up, connections between brain cells are reformed and the number of synapses once again rises, restoring normal brain activity. In humans, a reduction in body temperature (hypothermia) is known to protect the brain. For example, people have survived hours after a cardiac arrest with no brain damage after falling into icy water. Artificially cooling the brains of babies that have suffered a loss of oxygen at birth is also used to protect against brain damage.
Cooling and hibernation lead to the production of a number of different proteins in the brain known as 'cold-shock' proteins. One of these, RBM3, has been associated with preventing brain cell death, but it has been unclear how it affects synapse degeneration and regeneration. Knowing how these proteins activate synapse regeneration might help scientists find a way of preventing synapse loss, without the need for actual cooling.
Researchers reduced the body temperature of healthy mice to 16-18ºC - similar to the temperature of a hibernating small mammal - for 45 minutes. They found that the synapses in the brains of these mice, which do not naturally hibernate, also dismantled on cooling and regenerated on re-warming. The team then repeated the cooling in mice bred to reproduce features of neurodegenerative diseases (Alzheimer's and prion disease) and found that the capacity for synapse regeneration disappeared as the disease progressed, accompanied by a disappearance of RBM3 levels. When the scientists artificially boosted levels of the RBM3 protein 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.