Scientists find new cause of schizophrenia

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Researchers from Tokyo Medical and Dental University have made a significant discovery in the study of schizophrenia.

They identified an autoantibody—a protein made by the immune system that mistakenly targets the body’s own tissues instead of foreign invaders—in some patients with schizophrenia. This finding could offer new insights into the complex nature of this mental health condition.

Schizophrenia is a mental disorder that alters how individuals think, act, and perceive reality, often making it difficult for them to distinguish what is real. Treatment is challenging because the disorder varies greatly in its causes and manifestations.

The study, led by Hiroki Shiwaku and published in Cell Reports Medicine, focused on a particular protein called neural cell adhesion molecule (NCAM1), which is crucial for brain cells to form synapses.

Synapses are the connections through which cells communicate. Previous research has linked disruptions in this protein to schizophrenia, suggesting that it might play a role in the disorder’s development.

To explore this possibility, the researchers compared blood samples from 200 healthy individuals and 200 patients diagnosed with schizophrenia. They discovered the autoantibodies targeting NCAM1 in only 12 of the schizophrenia patients, indicating that these autoantibodies might only contribute to the disorder in a small fraction of cases.

To understand the impact of these autoantibodies, the team conducted an experiment where they isolated the autoantibodies from some of the patients and introduced them into the brains of mice.

Even with a short exposure, these mice began to exhibit changes similar to those observed in human schizophrenia. They showed cognitive impairments and altered responses in the startle reflex, which are typical features seen in schizophrenia.

Moreover, the treated mice had fewer synapses and dendritic spines, essential structures for neuronal connections that are also known to be compromised in schizophrenia.

These findings suggest that the presence of this specific autoantibody could be linked to some of the neurological and behavioral changes associated with schizophrenia, at least in a subset of patients.

This discovery is particularly promising because schizophrenia presents differently in each patient and is notoriously difficult to treat effectively with current therapies.

The identification of an autoantibody that might cause schizophrenia-like symptoms and brain changes offers a potential new target for understanding and eventually treating the disorder.

While only a small number of patients may have these autoantibodies, understanding their role could lead to more personalized approaches to treatment, potentially offering relief for those whose schizophrenia is linked to this immune system abnormality.

This research marks an important step toward unraveling the complex biological factors that contribute to schizophrenia and could pave the way for innovative treatments in the future.

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