Origin of schizophrenia in the brain revealed

Schizophrenia affects about 20 million people globally. Symptoms include hallucinations, delusions, flat affect (lack of emotional expression), loss of sense of personal identity, and memory loss.

A new study led by researchers at USC Dornsife College of Letters, Arts and Sciences and published in Nature Communicationsfocused on a protein called synaptic-associated protein 97, or SAP97, found in nerve cells in the brain.

The normal functionality of SAP97 remained elusive for many years. Not knowing how or where the protein works has also cast a veil on why mutations in SAP97 lead to schizophrenia.

Bruce Herring, associate professor of biological sciences at USC Dornsife, said: “Reduced SAP97 function most likely increases the risk of schizophrenia in humans as we know it, but SAP97 function remains a mystery. for decades,” said Bruce Herring, assistant professor of biological sciences at USC Dornsife.

SAP97 belongs to the family of proteins that regulate glutamatergic signaling between neurons and affect how memories are created and stored..

Glutamatergic signaling is an important way neurons communicate with each other that involves neurons releasing the neurotransmitter glutamate into neighboring neurons.

Experiments to date have not demonstrated that SAP97 plays any important role in the regulation of glutamatergic signaling in the brain.

The lack of evidence for SAP97’s function in regulating communication between neurons has frustrated scientists as there is growing evidence for the protein’s link to schizophrenia.

With no SAP97 activity evident in traditionally studied brain regions, the researchers chose to look at another brain region theoretically associated with schizophrenia, called the gyrus gyrus.

Studying mice with damaged SAP97 disease, the researchers looked for changes in jaw gyroscope activity — and they found them. Neurons in the jaw gyrus with reduced SAP97 function show an extremely large increase in glutamatergic signaling.

The increase in signal with mutant SAP97 suggests that the protein normally helps to reduce specific glutamatergic signaling in the gyrus.

The large increase in glutamatergic signaling in the jaw gyrus due to reduced SAP97 function also induces a significant deficit in contextual episodic memory in rodents – a hallmark of schizophrenia.

The results are the first to confirm the location in the brain SAP97 is active and directly links changes in jaw gyroscope function to the development of schizophrenia.

In future studies, the researchers plan to look for SAP97 activity in other areas of the brain. They will also determine whether schizophrenia-associated mutations in other proteins induce similar increases in glutamatergic signaling in the gyrus.

Their ongoing work will significantly aid the development of more effective treatment strategies for this historically mysterious disorder.

Source: Medindia

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