This development may open new pathways to schizophrenia diagnosis and treatment. An antibody that targets the body's own cells could be responsible for some schizophrenia cases, according to new research. The findings suggest an autoantibody that targets a molecule involved in brain cell communication could be an underlying cause after mice injected with it began displaying schizophrenia-like symptoms. “The results were impressive,” says Hidehiko Takahashi, senior author, in a statement. “Even though the mice only had these autoantibodies in their brains for a short time, they had changes in their behavior and synapses that were similar to what is seen in humans with schizophrenia.” The research was published in the journal Cell Reports Medicine. Autoantibodies are created by the immune system and target the body's own cells. They are implicated in a number of autoimmune diseases, such as Grave’s disease. Previous research has implicated the protein neural cell adhesion molecule (NCAM1) in the development of schizophrenia, owing to its integral role in communication between neurons in the brain. If something were to prevent NCAM1 from doing its job, the result may look a lot like schizophrenia. Researchers from Tokyo Medical and Dental University (TMDU) examined around 200 control patients without schizophrenia and 200 with schizophrenia, looking for autoantibodies against NCAM1. They discovered that a small but not insignificant number of schizophrenia patients had these autoantibodies circulating in their bodies. “We only found these autoantibodies in 12 patients, suggesting that they may be associated with the disorder in just a small subset of schizophrenia cases,” explained Hiroki Shiwaku, lead author of the study. To test their hypothesis about the action of anti-NCAM1 autoantibodies, the researchers took them from schizophrenia patients and injected a purified solution into the brains of healthy mice. Not long after, the mice began exhibiting changes in behavior in line with schizophrenia symptoms, plus reduced structures in their brains involved in signal communication. Together, the results suggest these autoantibodies could play a causal role in some schizophrenia patients. While the number of patients with anti-NCAM1 autoantibodies sounds small, schizophrenia is a complex disorder that often presents differently for each individual case. Such conditions likely have multiple causes, and identifying each will enable scientists to develop a comprehensive set of treatments. This development may open new pathways to schizophrenia diagnosis and treatment, which are large strides in taking on a complex mental disorder. Source
