Hibernation regenerates the brain
Each year, bears and other mammals experience a drastic drop in body temperature during hibernation. To conserve resources, within their brains are many connections between neurons-the synapses disappear. Last winter, these animals create new connections and lose memory. It is an exercise of regeneration that haunts many scientists seeking a remedy against the effects of Alzheimer’s and other diseases characterized by loss of these neural connections. Now, British researchers have forced hibernation in mice and discovered a molecule that appears to be critical to the repairing effect. Its effects even help prevent neuronal death when animals suffer similar to those of Alzheimer’s damage.
Until now, it was known that hypothermia may have a protective effect on the brain, and is exploring its potential after stroke. It has also been shown that cold prevents choking baby during childbirth. Now, the new study explores whether a sudden drop in temperature also protects the brain from degeneration and memory loss characteristic of neurodegenerative diseases.
The study, published in Nature, has used mice suffering from a form of Alzheimer’s or being infected with prions that cause neurodegenerative diseases. A stroke of hypothermia from 45 minutes to about 16 degree was enough for mice to lose much of their synapses in the hippocampus, a brain epicenters of memory. Upon return to normal temperature, the younger mice regained their connections between neurons but older did not.
Researchers have shown that part of the explanation was a protein called Rbm3. Its levels were multiplied by the cold in young mice but not in older. The work also shows how to artificially increase the levels of this protein without hypothermia, also protects the brains of diseased mice whose neurons cease to die and improve symptoms. All this is far from being applicable in humans, although, according to the authors, provides a new way to look inspired by the beneficial effects of hibernation treatments.
The study gives a target to develop a drug, just as paracetamol for fever – used more than a cold water bath. And yet still no treatment able to slow the disease. No protein or lipid or drug recall a neuron or synapse when this is gone. The most this protein or drug can do is to slow the loss if administered before it happens. Before that we should know whether Rbm3 causes or simple effect of the progressive degeneration of neurons and synapses. Another question to be explored – what makes only a few elderly have pathology when all have apparently lost Rbm3.
The greatest contribution of the study may not have to do with Alzheimer’s. The results draw attention to a point that seems to be a key in neurodegenerative diseases and that has not been given the necessary importance: maybe not so much to avoid the loss of synapses, otherwise to maintain or improve the ability to repair.