What does animal hibernation have to do with Alzheimer's? More than you might think. According to new research, the way that critters wake up from a long winter's rest could help scientists devise new treatments for dementia.
Research from Leicester University have isolated a cold-activated protein, RBM3, which helps restore brain activity of animals that are coming out of long hibernation periods. Though the protein also exists in humans, it's been found to be missing among Alzheimer's patients, whose brains also commonly have a reduced number of synapses.
Here's how it works: When animals go into hibernation, their number of brain synapses decreases so as to allow them to enter a prolonged state of inactivity. Then, the cold-activated protein RBM3 rebuilds the synapses when the animal wakes up, thereby restoring normal brain activity. The research believe that a drug that mimics the effect of this protein may have the potential to restore lost brain function among individuals suffering from neurodegenerative disorders.
“The neuroprotective pathway identified in this study could be an important step forward Dr. Hugh Perry, chairman of the Medical Research Counsil’s Neurosciences and Mental Health Board, which funded the study," told the Telegraph. "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.”
Hypothermia is known to protect the brain -- and the Leicester researchers sought to determine whether cooling the brains of Alzheimer's patients could help prevent synaptic loss.
To test this theory, the researchers lowered the body temperatures of a group of mice with Alzheimer's and a healthy control group to 60-64 degrees Fahrenheit (comparable to that of a small mammal in hibernation) for 45 minutes. When the 45 minutes were up, the RBM3 protein was activated in the healthy mice, restoring brain function as they woke up. In the mice with Alzheimer's, the protein did not kick in.
Researchers suggest that enhancing cold-shock pathways in the brain -- without cooling the body -- could act as a protective therapy for treating neurodegenerative disorders.
"While we don't think body cooling is a feasible treatment for long-term, progressive conditions like Alzheimer's disease, this research opens up the possibility of finding drugs that can have the same effect," Dr. Doug Brown of the Alzheimer's Society said in a statement. "We are very much looking forward to seeing this research taken forward to the next stage.'
The findings were published in the journal Nature.