- Schizophrenia is an often misunderstood chronic mental illness that causes psychosis.
- The biological mechanism of schizophrenia is poorly understood, and current treatments have significant limitations.
- According to a new study, the imbalance of nerve cell activity responsible for the condition and its associated symptoms may result from the body trying to rebalance excitatory and inhibitory functions.
Schizophrenia is a debilitating, complicated mental disorder that affects
It is a psychotic condition. People with schizophrenia have a unique combination of symptoms or experiences, which may include :
- feeling disconnected
- hallucinations
- hearing voices
- delusions
- confused thinking or speech
People can manage the condition with medicine and psychosocial therapy. However, relapses can occur, affecting a person’s work or education.
Despite treatment, people with schizophrenia are 2-3 times more likely to die early than the general population.
The exact cause of schizophrenia is unknown. However, several
Researchers have long suspected differences in brain chemistry to be the cause of schizophrenia. People with the condition typically have differences in their neurotransmitters — chemicals that control communication within the brain.
Dr. Rick Adams, a Research Fellow at the Centre for Medical Image Computing at University College London (UCL), U.K., explained to Medical News Today that there is an enormous amount of indirect evidence that synaptic gain decreases in schizophrenia. This means that excitatory neurons have a reduced ability to stimulate one another.
It was this implicit theory that led to the recent study looking into synaptic disruption in schizophrenia. The paper appears as a Journal pre-proof in Biological Psychiatry.
In the study, Dr. Adams and colleagues used computational modeling of electroencephalography (EEG) to record brain activity and measure overall synaptic gain. They collected EEG data from 272 participants, which comprised 107 with diagnosed schizophrenia, 57 of their relatives, and 108 control participants.
Study co-author L.Elliot Hong, MD, Professor of Psychiatry at the University of Maryland School of Medicine, told MNT: “Participants were recruited from the Greater Baltimore area, and the racial proportions in the sample should be roughly consistent with those in this area. This area is racially diverse.”
Each participant underwent three EEGs and a
- mismatch negativity, where a rogue or different pitched sound or other stimulus interrupts a steady, repetitive noise
- 40Hz auditory steady-state response, where the stimulus is a frequent click-sound
Dynamic causal modeling of each of the EEG experiments and fMRI data showed changes in the group of people who had received a diagnosis of schizophrenia.
The altered brain waves in those with diagnosed schizophrenia occurred due to a loss of synaptic gain, or excitability. The hallucinations and other symptoms of schizophrenia were, however, associated with loss of neural inhibition.
“This might mean that the loss of excitation comes first, then the brain tries to compensate for this by reducing inhibition, but then this leads to hallucinations,” said Dr. Adams.
He went further to say, “Imagine you are trying to listen to someone speaking on the radio, but the signal is very weak: if you turn the volume right up, the speech is louder, but so is all the static and background noise, and so you may mistake some of this noise for actual speech.”
Despite a great deal of pharmaceutical investment, there is still not a targetted drug to treat schizophrenia by understanding the biology of the disease and identifying the receptors and processes involved.
Dr. Adams believes that “if future studies can establish this, it means we should be able to give treatments that change excitatory or inhibitory function at the right time and to the right people.”
Dr. Adams added:
“We need to try to replicate these findings in other datasets. In particular, we need to look at different stages of the disorder — not just at people with fairly long-established diagnoses. It would also be important to use animal models to investigate whether loss of synaptic gain on excitatory neurons is indeed compensated by the loss of inhibition — and how we might be able to intervene in this process.”