Patients with schizophrenia disorder displayed a significantly low level of SV2A, a brain protein responsible for synaptic.
Cognitive dysfunction in patients with schizophrenia disorder
A team of UK researchers discovered that a specific type of brain protein is causing cognitive dysfunction in patients with schizophrenia disorder. Using a modern imaging tool, researchers found out that the brain protein SV2A is responsible for the communication between neurons in the brain.
According to lead researcher Oliver Howes,
The current treatment we have for schizophrenia disorders are focused on psychotic symptoms, never have we considered the impact on the cognitive part of the brain.
Cognitive dysfunction refers to the loss of certain abilities, such as planning and remembering. More often, this effect goes long-term and not curable.
A key brain protein
For decades, synaptic dysfunction was all left to theories and hypotheses. There was no actual testing in living human subjects.
According to studies, a genetic variation in SV2A has been found to contribute to the increased risk in schizophrenia cases. The gene is responsible for the production of a specific protein that aids in synaptic communication.
The discovery led to developing a modern imaging tool that can trace SV2A proteins in the brain. It is the first imagine tool to trace protein activity in patients with schizophrenia.
A random set of participants underwent the imaging procedure, 18 patients with schizophrenia, and another 18 without the disorder. Results showed patients with schizophrenia have lower levels of SV2A in the frontal cortex and the anterior cingulate cortex of the brain.
Based on the results, lower levels of synaptic protein could be an indication that a person is developing symptoms of schizophrenia. At the same time, antipsychotic treatments for schizophrenia do not affect brain connections in patients.
With the relation of brain proteins in the diseases’ development, researchers conclude that by boosting SV2A activity in the brain, schizophrenic patients can recover their synaptic functions.
What we are looking for in the future is to scan younger people to detect early stages of synaptic level changes that may lead to the development of the illness.
