Physical activity is clearly beneficial to our cardiovascular and brain health; it can even improve motor and cognitive function in certain forms of neurodegenerative diseases. Still, the underlying mechanisms by which exercise prevents or protects against neurodegeneration remain poorly understood. But researchers at the Department of cellular and molecular medicine (University of Ottawa, Canada) were able to find out more, at least in mice. Does running promote brain repair?

Among these many benefits, we know that physical exercise promotes neurogenesis (the production of new neurons). In addition, although their role in delaying neurodegeneration is not yet clear, nerve growth factors (VGF), neuropeptide precursors, are upregulated during physical exertion. It is these precursors that Matias Alvarez-Saavedra and his team examined in their study.

To study the mechanisms linking physical exercise to neural protection or even repair, they used genetically modified mice whose cerebellums had been reduced (by one third in comparison to their control counterparts), causing motor difficulties and reducing their life expectancy (between 25 and 45 days). Once these conditions were established, the scientists gave the impaired mice unlimited access to a wheel. The results were surprising!

Active mice were able to extend their lives to over a year. In addition to their survival rates, running improved their motor function and balance. A significant increase in myelination was seen in the brains of exercising rats; myelin is the lipid-based substance that coats most nerve endings and allows nerves to effectively and quickly transmit various messages. Consequently, the circuits damaged in the mice (who were missing part of their cerebellum) functioned better with physical exercise. However, as soon as the rats stopped running (in some of the experiments, the scientists removed the wheel), the "repair" process was interrupted. The VGFs produced during physical exercise are clearly facilitating the repair of the damaged brain areas.

Overall, the results of this study suggest that, thanks to VGFs, “the damaged cerebellar neurons can be substantially saved by an increase in myelination, by using an endogenous brain repair mechanism.” While further studies are needed, this work already sheds light on new paths for potentially treating certain neuronal pathologies. In the meantime, let’s get some exercise!