Researchers from Inserm and the University of Bordeaux, in collaboration with the University of Moncton, have developed an innovative tool to specifically activate mitochondria in the brain. This technique, tested on animal models, has shown a notable improvement in cognitive functions, suggesting a direct link between mitochondrial dysfunction and dementia symptoms.
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The brain, a highly energy-consuming organ, depends closely on mitochondria for its proper functioning. These structures produce the energy necessary for communication between neurons. When they no longer fulfill their role correctly, neurons struggle to transmit signals, which can lead to their progressive degeneration.
The developed tool, named mitoDreadd-Gs, targets G proteins located in mitochondria to boost their activity. By acting directly on these mechanisms, scientists were able to reverse memory deficits in mouse models of neurodegenerative diseases, confirming the hypothesis of causality.
The authors emphasize that this discovery opens the way to new therapeutic approaches. By better understanding the molecular mechanisms at play, it may be possible to develop treatments specifically targeting mitochondria to prevent or slow neuronal loss.
Additional work is needed to evaluate the long-term effects of this continuous stimulation. Researchers now plan to study whether prolonged activation of mitochondria can not only improve symptoms but also delay or even prevent neuron death.
How do mitochondria produce cellular energy?
Mitochondria are often compared to power plants because they generate ATP, the molecule that serves as fuel for all cellular activities. This process, called oxidative phosphorylation, uses oxygen and nutrients to produce energy efficiently.
In nerve cells, this energy is essential to maintain membrane potential and allow neurotransmitter release. A mitochondrial energy deficit can thus alter neuronal communication and contribute to various neurological disorders.
Factors such as genetic mutations or oxidative stress can damage mitochondria, compromising their function. Understanding these mechanisms helps develop strategies to protect or restore their activity.
What is neurodegeneration and how does it progress?
Neurodegeneration refers to the progressive loss of neuron structure or function, often leading to diseases like Alzheimer's or Parkinson's. It usually begins with subtle alterations at the cellular level before evolving into visible clinical symptoms.
Early signs often include mitochondrial dysfunction, accumulation of misfolded proteins, and inflammation. These disruptions disturb cellular homeostasis, leading to oxidative stress and ultimately neuron death.
Progression varies depending on the disease, but it often follows a pattern where the most active brain regions are affected first. For example, in Alzheimer's, the hippocampus, crucial for memory, is often affected early.
Current research aims to identify the initiating events of neurodegeneration. Tools like mitoDreadd-Gs help establish causal links, offering targets for early interventions that could slow or stop progression.