For the first time, a British team of researchers has demonstrated cognitive dysfunction in schizophrenia in a living human brain, possibly due to a lack of a known key protein that promotes communication between neurons in the brain. Lead researcher Oliver Howes explained: “Our current treatment for schizophrenia is only for the pathogenic symptoms of the disease. Patients generally have cognitive decline, such as the loss of planning and memory, resulting in more long-term disabilities.”
(Instagram via New Atlas)
There is no cure for these diseases, and for decades it has been thought that highlighting dysfunction is one of the key pathological features that cause schizophrenia attacks. The image above shows a comparison between the patient and the normal brain, with a cold color on the left indicating a lack of SV2A protein.
However, in addition to post-mortem brain tests and animal tests, it has not been possible to study this hypothesis in living human subjects.
Researchers generally suspect that genetic variation sinof symhttpation of the SV2A gene, which plays a role in the production of proteins and is thought to facilitate synaptic communication, is linked to the increased risk of schizophrenia.
In the new study, however, the team used a newly developed radioactive PET tracing agent designed to bind specifically to the SV2A protein, allowing researchers to image protein activity in the brains of living people for the first time.
Oliver Howes said: Our laboratory at the MRC London Institute of Medical Sciences is one of the few places in the world where research is carried out with this new tracer.
The new imaging technique scanned 18 patients with schizophrenia and compared the results with 18 control groups without the disease. The results showed that the patient’s SV2A levels in the two main areas of the frontal lobe of the brain (the frontal cortex and the front buckle back to the cortex) significantly reduced.
In other words, this means that for the first time we can demonstrate that the levels of important proteins associated with synaptic activity in patients with schizophrenia are low, indicating loss of synaptic function, or the basis for the development of schizophrenia.
The study also identified an important finding that the two most common antipsychotic drugs taken by people with schizophrenia were not the cause of such synaptic dysfunction.
In subsequent rat studies, the researchers determined that neither fluoroeoregium nor onopine levels affected SV2A protein levels.
“This reassuringly good news is that antipsychotic medication does not result in loss of brain connectivity,” oliver Howes said.
Finally, this finding sets the stage for future research into the treatment of new forms of schizophrenia, which can be used to improve SV2A activity to try to restore synaptic function in patients, thus providing new options for cognitive therapy.
Next, researchers will use this new imaging technique to reveal what happens to the human brain at the early stages of disease development. Oliver Howes says:
Next, we hope to scan the brains of young people at an early stage to see how synaptic levels change in the course of disease development and whether these changes are established early or over time.
Details of the study have been published in the recent journal Nature Communications. Originally published as:
Synaptic density marker SV2A is reduced in the vein a patient s and unaffected by antipsychotics in rats