A new study published in the journal Biological Psychiatry investigates the role antibodies may play in cases of psychosis, suggesting that psychosis symptoms such as hallucinations and delusions may be triggered by an antibody response to a protein in the brain.
It is well known that antibodies defend the body against bacteria and viruses, and that in some people antibodies also attack healthy cells, causing autoimmune disorders.
Less well known is the role autoimmune disorders may play in psychosis. However, scientists have been aware of a link between immune abnormalities and psychosis for over 100 years.
Only recently, though, have scientists been able to pinpoint the specific mechanisms in the immune system that appear to influence psychosis symptoms, such as the mechanism identified in the new study.
The authors of the new study found an antibody reaction to the dopamine D2 receptor or the N-methyl-D-aspartate (NMDA) glutamate receptor among a subgroup of children experiencing their first episode of psychosis, but no similar antibody response among healthy children.
Both of these receptors have been implicated in psychosis. In fact, psychiatrists commonly administer drugs that stimulate dopamine D2 receptors or block NMDA receptors.
These drugs have been associated with side effects that resemble psychosis symptoms – such as changes in perception, delusions and disorganized thought processes. The researchers believe that the antibodies described in the study may have a similar effect on the brain to these drug side effects.
“The antibodies we have detected in children having a first episode of acute psychosis suggest there is a distinct subgroup for whom autoimmunity plays a role in their illness,” says Dr. Fabienne Brilot, senior study author and head of the Neuroimmunology Group at The Children’s Hospital at Westmead in Sydney, Australia.
“The data from this study suggests that better interventions are possible, providing hope that major disability can be prevented for the subset of children experiencing acute psychosis with antibodies,” Dr. Brilot adds.
Within the last decade, similar research has identified anti-NMDA receptor encephalitis – an inflammation of the brain responsible for acute psychiatric symptoms including psychosis. Though commonly misdiagnosed as schizophrenia or bipolar disorder, the brain inflammation characterized by the disease is caused by an antibody attack on NMDA receptors and is treatable.
Dr. John Krystal, editor of Biological Psychiatry writes that the study fuels growing discussions on the importance of antibodies targeting neural proteins and raises many important questions for scientists working in this field: “Do these antibodies simply function like drugs in the brain or do they ‘attack’ and damage nerve cells in some ways? Also, are these antibodies producing symptoms in everyone or do they function as a probe of an underlying, perhaps genetic, vulnerability for psychosis?”
Dr. Brilot concludes of his team’s findings:
“These findings also contribute significantly to an emerging acceptance in the field of the involvement of autoimmune antibodies in neurological diseases. Combined, these investigations are providing a better understanding of the biology of psychiatric and neurological diseases, as well as pointing to novel treatment approaches for children with these debilitating illnesses.”
Last month, Medical News Today looked at a study published in The Lancet Psychiatry that found high-potency “skunk-like” cannabis increases risk of psychosis by fivefold.