Exercise Found to Raise Brain Energy Levels in Mice

Patricia Silva, PhD avatar

by Patricia Silva, PhD |

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A new study published in the journal Cell Metabolism revealed that exercise can energize brain cell function in animal models by increasing the levels of a specific mitochondrial enzyme. The finding may have important therapeutic implications for the treatment of age-related cognitive decline and neurodegenerative diseases.

The study is titled “Mitochondrial SIRT3 Mediates Adaptive Responses of Neurons to Exercise and Metabolic and Excitatory Challenges” and was led by researchers at the National Institute on Aging Intramural Research Program and the Johns Hopkins University School of Medicine, both in Baltimore.

Brain cells, either as part of the natural aging process or in the context of neurodegenerative diseases, are known to stop producing the levels of energy required for them to remain fully functional. In the study, researchers used animal models relevant for neurodegenerative diseases, such as Huntington’s disease and epilepsy, and found that an enzyme called SIRT3 (sirtuin [silent mating type information regulation 2 homolog] 3) could protect mice brains from stressors thought to be involved in brain cell energy loss. SIRT3 is present in mitochondria, the small cellular organelles where energy for the body is produced.

Interestingly, the team found that normal mice that exercised (running on a wheel) had increased levels of the SIRT3 enzyme in neurons, being protected from degeneration. In contrast, neurons in mice lacking SIRT3 showed increased vulnerability to stressors, such as neurotoxins known to cause brain degeneration and epileptic seizures. Exercise in animals lacking SIRT3 also failed to offer protection from neurodegeneration and neuronal death.

Researchers reported that SIRT3 deficiency had an impact in the neuron responses to metabolic, oxidative and excitatory stress, as well as in several mitochondrial proteins and functions, including superoxide dismutase 2, a protein that clears mitochondrial reactive oxygen species (ROS) contributing to neuronal protection against damage and cell death.

Based on the finding, the research team concluded that SIRT3 plays a key role in neuronal responses to physiological conditions and resistance to degeneration. The team suggested that enhancing mitochondrial functions and resistance to stress in neurons, through an increase in the levels of SIRT3 via gene therapy technology, could be a promising therapeutic approach for the treatment of neurodegenerative diseases and age-related cognitive decline.