034-33257301
info@autismkerman.ir

Prevention of autism and protein disorders

Prevention of autism and protein disorders

Prevention of autism and protein disorders

View Details

Prevention of autism and protein disorders

6 Apr 2020
According to Medical Express
 
 Brain connections are very important. The outer surface of a neuron must have certain proteins to hold the connections in the brain.
These protein molecules remain on the surface for a long time; As a result, they may break the connections between cells.
 
Researchers at Rockefeller University in the United States have shown in a new study that a protein called ASTN can help move proteins across the layer. The study, conducted in collaboration with Horinaz Beheshti, an Iranian student at the university, shows that ASTN protein deficiency leads to developmental neurological disorders such as autism and mental disabilities.
 
Neurons send messages to each other using chemicals or neurotransmitters that activate receptor proteins on the surface of adjacent cells. Chemical connections are very dynamic; As a result, the receivers must be dynamic. The receivers are constantly rotating around the layer, ensuring a rapid response to the received signals. This process requires the resistance of proteins called "traffickers" that encourage receptors to move.
 
Mary Hatten, a professor at Rockefeller University and one of the project's researchers, has shown that the ASTN protein acts as a traffic protein during the early stages of cell transfer.
 
Beheshti believed that ASTN may play an important role in human adulthood because it is found in the brains of adults. The ASTN is located in the adult cerebellum, which manages complex cognitive aspects in addition to regulating movement.
 
Hutton and Beheshti used a special microscopic method to determine the location of "ASTN" in the rat cerebellum. They found that the protein was present in the neuronal compounds responsible for moving proteins around. The two researchers were able to identify a set of molecules attached to the ASTN. These molecules contained proteins that are involved in the formation of synapses and traffic proteins.
 
When the researchers increased the expression of the "ASTN" protein in mouse neurons, the binding level of the molecules decreased. This caused ASTN to bind to them and transfer them from the surface of the cell layer.
 
Beheshti said: "Our data show that in the body of people with mutations in ASTN2, less amount of this protein is made; As a result, it leads to weaker synapses.
 
Researchers claim that proteins, without enough ASTN2, accumulate on the cell surface and destroy neuronal connections.
 
Beheshti added: Synapses are not fixed. They must respond to the dynamic stimulus in real time, and one way to do this is to change the expression of their surface protein.

Articles Related