Mitochondria, the tiny energy-producing structures inside cells, are essential for keeping our bodies — and especially our brains — functioning.
A new study published in Nature Neuroscience by researchers from Inserm and the University of Bordeaux, in collaboration with the Université de Moncton in Canada, has for the first time shown a direct causal link between mitochondrial dysfunction and the cognitive symptoms seen in neurodegenerative diseases.
Using a unique and innovative tool, the researchers were able to increase mitochondrial activity in animal models of neurodegenerative diseases.
When they did this, the animals showed improved memory, suggesting that targeting mitochondria could be a promising new therapeutic approach. While the findings are still at an early stage, they represent an important step toward understanding the role of mitochondria in brain health.
Mitochondria provide the energy cells need to function, and neurons depend heavily on this energy to communicate effectively. In neurodegenerative diseases like Alzheimer’s, brain cells gradually lose their function and die.
Researchers have observed that even before neurons die, mitochondrial activity is often impaired. However, until now, it was unclear whether mitochondrial dysfunction was a cause of the disease or simply a byproduct.
In this study, the scientists developed a tool to temporarily stimulate mitochondrial activity. They reasoned that if boosting mitochondria improved symptoms, it would indicate that mitochondrial problems occur before neuron loss and may contribute directly to the disease process.
Building on earlier work showing the role of G proteins in controlling mitochondrial activity, the team created an artificial receptor called mitoDreadd-Gs.
This receptor activates G proteins directly inside mitochondria, increasing their activity. When mitoDreadd-Gs was activated in the brains of dementia mouse models, both mitochondrial function and memory performance returned to normal levels.
Giovanni Marsicano, Inserm research director and co-senior author, said the findings are the first to establish a cause-and-effect link between mitochondrial dysfunction and neurodegenerative symptoms. This suggests that mitochondrial impairment could be a trigger for neuronal degeneration rather than just a secondary effect.
Étienne Hébert Chatelain, professor at the Université de Moncton and co-senior author, noted that the new tool could help uncover the molecular and cellular mechanisms that cause dementia, making it easier to develop targeted treatments.
Luigi Bellocchio, Inserm researcher and co-senior author, added that the next step will be to test the effects of continuously stimulating mitochondrial activity to see if it can reduce symptoms, delay neuron loss, or even prevent it if activity is restored early enough.
This study opens an exciting new chapter in neurodegenerative disease research by identifying mitochondria as a potential root cause of cognitive decline. The creation of mitoDreadd-Gs provides a powerful experimental tool to test therapies aimed at restoring mitochondrial function.
If these findings can be replicated and translated into human studies, they could lead to treatments that address the underlying energy deficits in the brain, potentially slowing or halting diseases like Alzheimer’s at an earlier stage.
If you care about dementia, please read studies about Early heart rhythm problem linked to higher dementia risk and findings of Green leafy vegetables may help reduce Alzheimer’s risk.
For more information about dementia, please read studies about Research shows an important cause of frontotemporal dementia and findings of New way to detect Lewy body disease early, a leading cause of dementia.
The study is published in Nature Neuroscience.
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