Scientists have clarified that new mechanisms of action for neurons in the brain promise to develop new therapies for rare immune diseases

Rasmussen's enitis is a rare autoimmune disease that mainly affects children and eventually leads to seizures, and because the disease is resistant to drug therapy, patients need frequent surgery to remove or cut off affected brain tissue.
In a recent study published in the international journal Cell, scientists from institutions such as the University of Geneva successfully described the mechanisms of neurons in the brains of mice or offered new hope for the treatment of Rasmussen encephalitis, after researchers believed that neurons were the target of immune cells that attack synapses ( synapses are connections between neurons) but found that neurons themselves may play a key role in inducing this process.
In Rasmussen encephalitis, the presence of antigens in affected neurons induces an immune response that causes synapses to change, and the researchers found that neurons may not be passive victims of this attack, playing an important role in inducing defense mechanisms that eventually lead to self-damage, and that neurons produce a special chemical signal to the devouring cells, which then induce attacks on synapses.double attack on synapses
is triggered by the antigen of the neuron, the CD8-T lymphocytes release the protein IFN-γ, which is captured by the corresponding neuron subject, which then activates the SATA1 signaling path, inducing The production of CCL2 molecules, which can spread into the neuron environment and activate the activity of other types of immune cells, such as phagocytosis cells, which are small glial cells present in the brain and macrophages from the blood circulation, which eventually attack synapses.
researcher Giovanni Di Liberto said that if we could manage to cut off the signals released by neurons, the series of signal reactions could be blocked; the researchers found similar signaling characteristics in a study of live tissue samples from more than 20 Rasmussen encephalitis patients, which the researchers believe may be the same as other forms of encephalitis; In mouse experiments, researchers were able to successfully block mechanisms at different levels, i.e. blocking the path of SATA1 and CCL2 molecular signaling, as well as blocking the migration and activation of phagocytosphages through drug intervention and genetic modification, thus avoiding synapse degradation and controlling the disease more effectively.
The researchers now hope to work with other researchers to develop treatments for Rasmussen encephalitis, and they hope to conduct the necessary clinical trials to shed light on the molecular mechanisms that trigger the disease; the mechanisms described by the researchers may also play a role in other diseases that induce a strong immune response, and may even play a key role in multiple sclerosis. (Bio Valley)