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Schizophrenia is a severe neurodevelopmental disorder that makes people decline. Finding a causal relationship between electrone dysfunction and specific behavioral characteristics associated with schizophrenia is key to revealing the mechanisms of the disease. Recently, researchers from the University of Geneva in Switzerland made exciting progress in this regard by discovering a molecular mechanism that causes the desynotation of neural networks and successfully repairing this tissue defect in adult animal models, thereby suppressing abnormal behavior associated with schizophrenia.
researchers studied an animal model of human 22q11 removal syndrome, a genetic mutation that means the genetic risk of schizophrenia is highest. The researchers found that the non-synchronization of the accumulation of hema neurons was caused by a decrease in the excitability of neurons in the middle of the protein. Restoring the excitability of neurons in the middle of the protein by drug or genetic means is sufficient to restore CA1 network dynamics and sea mass dependence in adult animals to normal wild animal levels.
overall, the study provides new information on the causes of neural network abnormalities behind schizophrenia, suggesting that reversing the associated signaling path paths in animal models to restore physiological activity and behavior in animals is feasible. (Bio Valley)
