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"... a team has made a huge breakthrough, proving for the first time how mitochondrial dysfunction fuels neurodegenerative symptoms. Through this, they created a precision tool that restored memory function in several dementia models. ...
Researchers ... have for the first time identified a causal link between mitochondrial dysfunction and the debilitating symptoms that emerge and worsen in neurodegenerative diseases. ...
“This work is the first to establish a cause-and-effect link between mitochondrial dysfunction and symptoms related to neurodegenerative diseases, suggesting that impaired mitochondrial activity could be at the origin of the onset of neuronal degeneration,” ..."
"... In previous studies, the research teams have already described the specific role of G proteins in the modulation of mitochondrial activity in the brain. In the present paper, the researchers succeeded in generating an artificial receptor, called mitoDreadd-Gs, able to activate G proteins directly in the mitochondria, thereby stimulating mitochondrial activity.
The stimulation of mitoDreadd-Gs in the brain led to the normalization of both mitochondrial activity and memory performance of dementia mouse models. ..."
From the abstract:
"Many brain disorders involve mitochondrial alterations, but owing to the lack of suitable tools, the causal role of mitochondrial dysfunction in pathophysiological processes is difficult to establish.
Heterotrimeric guanine nucleotide-binding (G) proteins are key regulators of cell functions, and they can be found within mitochondria.
Therefore, we reasoned that the activation of stimulatory mitochondrial G proteins (Gs) could rapidly promote the activity of the organelle and possibly compensate for bioenergetic dysfunction.
Here, we show that a mitochondria-targeted recombinant designer receptor exclusively activated by designer drugs (mitoDREADD-Gs) can acutely trigger intramitochondrial signaling to increase mitochondrial membrane potential and oxygen consumption. In vivo activation of mitoDREADD-Gs abolished memory alterations in cannabinoid-treated mice and in two mouse models of Alzheimer’s disease and frontotemporal dementia.
Thus, mitoDREADD-Gs enables the establishment of causal relationships between mitochondria and biological or disease-related processes and represents an innovative potential therapeutic approach for disorders associated with mitochondrial impairment."
Neurodegenerative diseases: Research establishes causal link between mitochondrial dysfunction and cognitive symptoms
Potentiation of mitochondrial function by mitoDREADD-Gs reverses pharmacological and neurodegenerative cognitive impairment in mice (no public access)
Activation of mitoDREADD-Gs rescues cognitive impairment induced by cannabinoids.
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