Schizophrenics found lack of protein in synapses

–

For the first time, scientists were able to study one of the markers of schizophrenia – the SV2A protein, which is involved in the formation of synaptic connections – in the brain of living people. To do this, they introduced 18 patients with schizophrenia and 18 healthy people with a radioactive tracer that binds to SV2A and checked its concentration using positron emission tomography: it turned out that with schizophrenia the concentration of this protein in the cingulate cortex and frontal lobes of the brain is much lower. Additional experiments on rats showed that the use of antipsychotic drugs did not affect SV2A levels. Article published in Nature communications.

One of the alleged causes of schizophrenia is the pathology of neural development, which leads to disruption of the synapses (the contact points of two neurons): due to the fact that the transmission of signals in the nervous system is disturbed, apparently, occur pathological disorders of perception, cognitive functions and behavior. This is confirmed by genetic studies: for example, it is known that in patients with schizophrenia observed specific gene polymorphism SV2A, which encodes one of the synaptic vesicle glycoproteins – SV2A.

So far, however, the association of a lack of SV2A protein in the brain and schizophrenia has been established in humans only post mortem. Scientists led by Oliver Howes from Imperial College London decided to fix this: they conducted an experiment involving 18 patients with schizophrenia and 18 healthy people. They suggested that SV2A levels would be lower in some brain structures of schizophrenics.

The experiment was carried out using positron emission tomography, and a tracer was used as an indicator substance ^elevenC-UCB-J, which specifically binds specifically to SV2A. It turned out that in the brain of patients the protein was significantly (p <0.00001) less than in healthy patients. Deficiency was observed in the cingulate cortex and frontal lobes, but not in the hippocampus.

All patients who participated in the study took antipsychotic drugs: haloperidol and olanzapine. In order to exclude the effect of drugs on protein deficiency, scientists conducted an additional experiment on laboratory rats that were injected with haloperidol or olanzapine for four weeks. The concentration of SV2A in their brain has not changed – from this, scientists concluded that protein loss is not the result of taking antipsychotics.

Thus, the authors were able to show that a reduced concentration of SV2A protein in synapses can serve as a marker of schizophrenia, and is not caused by the use of antipsychotic drugs. Scientists believe that the protein found may be the goal in treating the disease, but for this it is also necessary to study how its concentration changes with age.

About schizophrenia – one of the most difficult in the study of mental disorders – we wrote quite a lot. You can read a brief history of the study of the disease in one of our latest materials – The Reaver of the Mind.

Elizabeth Ivtushok

–
–