There’s a tremendous amount of hope when it comes to Alzheimer’s treatment research, thanks to a cooling protein. Conducting a study on mice, scientist lead Giovanna Mallucci and his team of researchers found a mechanism which releases a ‘cold shock’ protein, RBM3, to the brain, preventing synapse, and the loss of brain cells.
“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 (because) it’s unpleasant and involves risks such as pneumonia and blood clots,” said Giovanna Mallucci who led the research. “By identifying how cooling activates a process that prevents the loss of brain cells, we can now work toward finding a means to develop drugs that might mimic the protective effects of cold on the brain.”
In terms of hibernating animals, cooling triggers production of specific brain proteins, referred to as ‘cold-shock’ proteins, and RBM3 is a fine example of this. This protein has been known to prohibit the loss of brain cells and synapses, but researchers are still unaware of the reasoning behind it; therefore a connection would undoubtedly pave the way to help re-produce this as treatment for brain-related diseases.
All the mice used in the study had neurodegenerative diseases like Alzheimer’s. During tests that were similar to the hibernation process for mice, researchers decreased the body temperatures of their specimens to 16-18 degrees Celsius for 45 minutes. What they found was that the synapses of the mice broke down when cold, and revamped when warmed up. The research team repeated this cooling process, and found that the increased levels of the RBM3 protein helped to prevent synapse and brain cell damage.
Hugh Perry, chairman of Britain’s Medical Research Council’s neurosciences and mental health board, funded the research and had this to say, “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.”