Study Establishes A Causal Link Between Mitochondrial Dysfunction And Neurodegenerative Diseases

Mitochondria, nan mini organelles without which our bodies would beryllium deprived of energy, are gradually revealing their mysteries. In a caller study published successful Nature Neuroscience, researchers from Inserm and nan University of Bordeaux astatine nan NeuroCentre Magendie, successful collaboration pinch researchers from nan Université de Moncton successful Canada, person for nan first clip succeeded successful establishing a causal nexus betwixt mitochondrial dysfunction and nan cognitive symptoms associated pinch neurodegenerative diseases.

Thanks to nan creation of a circumstantial and unprecedented tool, they succeeded successful expanding mitochondrial activity successful animal models of neurodegenerative diseases, wherever they observed an betterment successful representation shortage symptoms. While these are only first results, they unfastened nan doorway to considering mitochondria arsenic a caller therapeutic target.

The mitochondrion is simply a mini intracellular organelle that provides nan power needed by nan compartment to usability properly. The encephalon is 1 of nan astir energy-demanding organs, and neurons trust connected nan power produced by mitochondria to pass pinch 1 another. Indeed, erstwhile mitochondrial activity is impaired, neurons do not person nan power required to usability correctly.

Neurodegenerative diseases are characterized by a progressive impairment of neuronal functions starring to nan decease of encephalon cells. In Alzheimer's disease, for example, it has been observed that neuronal degeneration, which precedes compartment death, is accompanied by impaired mitochondrial activity. However, owed to nan deficiency of suitable tools, it has been difficult successful nan past to find whether mitochondrial alterations play a causal domiciled successful these conditions aliases are simply a consequence of nan pathophysiological process.

In this caller study, researchers from Inserm and nan Université de Bordeaux, successful collaboration pinch researchers from nan Université de Moncton successful Canada, developed for nan first clip a instrumentality that allows to temporarily stimulate mitochondrial activity. They hypothesized that if this stimulation led to an betterment of symptoms successful animals, this would mean that nan impairment of mitochondrial activity precedes nan nonaccomplishment of neurons successful nan discourse of a neurodegenerative disease.

In erstwhile studies, nan investigation teams already described nan circumstantial domiciled of G proteins successful nan modulation of mitochondrial activity successful nan brain. In nan coming paper, nan researchers succeeded successful generating an artificial receptor, called mitoDreadd-Gs, capable to activate G proteins straight successful nan mitochondria, thereby stimulating mitochondrial activity. The stimulation of mitoDreadd-Gs successful nan encephalon led to nan normalisation of some mitochondrial activity and representation capacity of dementia rodent models.

"This activity is nan first to found a cause-and-effect nexus betwixt mitochondrial dysfunction and symptoms related to neurodegenerative diseases, suggesting that impaired mitochondrial activity could beryllium astatine nan root of nan onset of neuronal degeneration", explains Giovanni Marsicano, Inserm investigation head and co-senior writer of nan study.

"These results will request to beryllium extended, but they let america to amended understand nan important domiciled of mitochondria successful nan due functioning of our brain. Ultimately, nan instrumentality we developed could thief america place nan molecular and cellular mechanisms responsible for dementia and facilitate nan improvement of effective therapeutic targets", explains Étienne Hébert Chatelain, professor astatine nan Université de Moncton and co-senior writer of nan study.

"Our activity now consists of trying to measurement nan effects of continuous stimulation of mitochondrial activity to spot whether it impacts nan symptoms of neurodegenerative diseases and, ultimately, delays neuronal nonaccomplishment aliases moreover prevents it if mitochondrial activity is restored," added Luigi Bellocchio, Inserm interrogator and co-senior writer of nan study.