The discovery that gives hope

A revolutionary medical advance offers new hope to paralyzed people. Swiss researchers have identified the VSX2 neurons, a real conductor of motor recovery after a spinal cord lesion. How does this discovery transform our approach to paralysis? Nine patients are already testifying to the promising results of this innovative therapy.

Medicine takes a decisive step in the treatment of spinal cord lesions. Swiss scientists have just identified a specific type of neurons, the VSX2, which play a crucial role in recovery of walking after paralysis. This discovery, which combines electrical stimulation and in -depth neurological understanding, opens up unprecedented therapeutic perspectives for millions of people in the world.

Electrical stimulation, first step to restart

The research team led by the neurosurgeon Jocelyne Bloch from the Vaud University Hospital Center (CHUV) has developed a revolutionary technique. It consists of implement An electronic device at the lumbar level of the spinal cord, a region controlling the leg muscles.

This device emits precise electrical impulses which reactivate the damaged neural circuits. “” We place the implant at the bottom of the of thethen send electrical stimulation via an external case “Explains Dr Bloch. The results are remarkable: a patient who had lost any sensation in his legs can now walk up to three consecutive hours.

The most intriguing observation? Improvements persisted even after stopping electrical stimulation. This phenomenon suggested real regeneration and reorganization of nerve fiberspushing researchers to deepen their investigations.

VSX2 neurons, orchestrators of motor recovery

In collaboration with Grégoire Courtine, neuroscientist at the Federal Polytechnic School in Lausanne, Dr Bloch conducted a study whose results were published in the journal Nature In November 2022. Their central discovery: identification of VSX2 neurons as key players in motor recovery.

To achieve this breakthrough, the researchers developed a detailed atlas of the murine spinal cord, listing almost every neuron. Their experiences on damaged mice revealed that VSX2 neurons are specifically activated during the recovery of walking.

« After a spinal trauma, we first observe a cell chaos where all neurons are expressed simultaneously. Gradually, VSX2 take control and regulate the activity of other neurons “, Specifies the Dr Bloch. This regulation explains the paradoxical decrease in neural activity during functional recovery.

Scientific validation and therapeutic perspectives

To confirm their discovery, scientists used theoptogenetica technique to control neural activity by the light. The results are unequivocal:

  • The deactivation of VSX2 neurons in injured mice causes immediate stopping of walking;
  • This same deactivation does not affect healthy mice;
  • VSX2 are little involved in normal locomotion;
  • These neurons become essential only during the post-traumatic recovery phase.

The research team has confirmed the presence of VSX2 neurons in humans, suggesting mechanisms similar to those observed in rodent. « We are now working to better understand these neurons to optimize their stimulation », it emphasizes Dr Bloch.

Towards a democratization of innovative treatments

Despite these promising advances, only a dozen patients around the world have benefited from the electrical stimulation of the spinal cord developed by the Swiss team. Researchers plead for a diffusion wider of this technology while they are continuing their work on VSX2 neurons.

THE applications potential exceeds the framework of accidents road or sports. This therapy could also benefit the victims ofAVC or certain neurodegenerative diseases affecting mobility. The future promises to be promising for millions of people faced with severe motor handicaps.

The path between this fundamental discovery and its large -scale clinical application remains to be traveled, but the identification of VSX2 neurons undeniably constitutes a major turning point in our fight against paralysis.

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