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Study identifies psychosis as a quantifiable neurological autoimmune disease.

Antibodies defend the body against bacterial, viral, and other invaders. But sometimes the body makes antibodies that attack healthy cells. In these cases, autoimmune disorders develop.  Immune abnormalities in patients with psychosis have been recognized for over a century, but it has been only relatively recently that scientists have identified specific immune mechanisms that seem to directly produce symptoms of psychosis, including hallucinations and delusions.

This ‘immune hypothesis’ is supported by a new study from researchers at The Children’s Hospital at Westmead. They detected antibodies to the dopamine D2 receptor and the N-methyl-D-aspartate (NMDA) glutamate receptor in a subgroup of children experiencing their first episode of psychosis, but no such antibodies in healthy children. Both are key neural signaling proteins that have previously been implicated in psychosis.

In the current study the antibodies 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.

For decades psychiatrists have administered drugs that stimulate dopamine D2 receptors or block NMDA receptors. These drugs may briefly produce side effects that resemble symptoms of psychotic disorders, including changes in perception, delusions, and disorganization of thought processes. The current findings suggest that people may develop antibodies that affect the brain in ways that are similar to these psychosis-producing drugs.

The team state that the current study adds fuel to the growing discussions about the importance of antibodies targeting neural proteins and add that it raises many important questions for the field. Therefore, the researchers ask if 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?.

Importantly, work is advancing rapidly in this area. Less than a decade ago, anti-NMDA receptor encephalitis was first identified, a disease characterized by inflammation of the brain that causes acute psychiatric symptoms including psychosis. It is commonly misdiagnosed as schizophrenia or bipolar disorder, but is a form of treatable brain inflammation caused by antibodies that attack the brain’s NMDA receptors.

The team state that the findings suggest that better interventions are possible, providing hope that major disability can be prevented for the subset of children experiencing acute psychosis with antibodies.  These findings also contribute significantly to an emerging acceptance in the field of the involvement of autoimmune antibodies in neurological diseases.

The researchers summise that 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.

Source:  Elsevier B.V

Credit:  Ian Patrick Coyle, Dr. Barry Ganetzky Laboratory, Michael Gleicher.  UW-Madison Department of Genetics.
Credit: Ian Patrick Coyle, Dr. Barry Ganetzky Laboratory, Michael Gleicher. UW-Madison Department of Genetics.

Michelle Petersen View All

Michelle is a health industry veteran who taught and worked in the field before training as a science journalist.

Featured by numerous prestigious brands and publishers, she specializes in clinical trial innovation--expertise she gained while working in multiple positions within the private sector, the NHS, and Oxford University.

4 thoughts on “Study identifies psychosis as a quantifiable neurological autoimmune disease. Leave a comment

  1. Exellent article.
    I would ask if the dopamine D2 receptor and the N-methyl-D-aspartate (NMDA) glutamate receptor antibodies could be related to mother Thyroperoxidase Antibody detection ? Could it be triggered during fetal development ?


  2. I am curious if there is a link available to the study mentioned above? If it is not yet published, is there a projected date of when we can read the original study?


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