An English team from the University of Leicester has discovered that the RBM3 protein helps restore brain activity when animals come out of hibernation. This discovery may well be useful in research into treatments for neurodegenerative diseases like Alzheimers.
To better understand the challenge of this study, published in the scientific journal Nature, it is necessary to take an interest in the process of animal hibernation. When marmots, hedgehogs and bears hibernate, the number of brain connections, called synapses, decreases, allowing them to enter this state of “torpor”. This loss of synapses, of the order of 20 to 30%, causes the body’s temperature to drop, which then drops from 37 degrees to 16-18 degrees.
When the body wakes up and warms up, the synapses reform. This regeneration of synapses stimulates brain activity, without any loss of memory.
The English researchers found that this mechanism of synapse destruction-repair during hibernation, called synapse plasticity, was made possible by the activity of the RBM3 protein. In the experiment of the scientists, this formation of new nervous connections was noted only on young mice.
The results of this study will be further investigated to determine to what extent this protein could play a role in the protection of synapses, the reduction of which constitutes a marker of dementia such as Alzheimer’s disease.
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