A research group led by Professor Toru Yamamoto of Kagawa University School of Medicine has elucidated the mechanism that regulates the connections (synapses) between nerve cells so that they are not created too much.In addition, when this mechanism does not work properly, nerve cells in the brain become overexcited, causing changes in social behavior similar to autism spectrum disorder (ASD), and the research results are published in the US scientific journal `` Published in "Neurons".
Autism spectrum disorder (ASD) is said to have an adult prevalence of 1%, and it is sometimes diagnosed with social difficulties after adulthood, so there is a strong demand for elucidation of the pathology and development of treatment methods. There is.
In the brain, two commands are sent, "excitatory input" that excites nerve cells via connections (synapses) and "inhibitory input" that calms the excitement, and the balance is usually maintained properly. In ASD, there are many cases of epilepsy caused by excessive excitement of the cranial nerves, so it is speculated that this imbalance in balance may cause excessive excitement of nerve cells in the brain and contribute to ASD. ..
One of the causes of excessive excitement is that "excitatory synapses" that perform excitatory inputs are created too much, but the mechanism that controls the generation of synapses in the brain was unknown.
While studying the process of formation of neural networks in the brain, the research group binds to specific substances that are important in synaptic formation, inhibits their function, and works to prevent over-creation of synapses, "MDGA2". I found a membrane protein called. Analysis in mice genetically modified to reduce the amount of MDGA2 revealed that excitatory synapses were overformed and nerve cells in the brain were overexcited.
When the behavior of this mouse was continuously observed, behavior similar to ASD was observed, such as repeating the same behavior and having little interest in not communicating with other mice.These results suggest that MDGA2 suppresses the excessive excitement of nerve cells in the brain by controlling excitatory synapses.
Although there is more than one pathophysiology and onset factor of ASD, this study reveals a part of the pathology and is useful for further elucidation of the pathology and treatment policy.In addition, similar imbalances in balance have been confirmed in neuropsychiatric disorders such as schizophrenia, and are expected to be applied to the understanding and treatment of these disorders in the future.
