COX6A2 and miR137 Two Schizophrenia Biomarkers Identified by Swiss Researchers

Approximately 2.6 million Americans suffer from schizophrenia. Worldwide, the disease is estimated to affect between 0.7 and 1% of the population. It is a psychiatric disorder that generally appears between the ages of 15 and 25. The symptoms (social withdrawal, cognitive difficulties, hallucinations, delusions, etc.) are very diverse, which makes the diagnosis more complex. Better understanding and early detection of this disorder will allow for more effective treatment and earlier intervention to limit the severity of the disease. To that end, several researchers are attempting to identify markers of this disorder. The ultimate goal is for physicians to be able to prescribe tests to their patients to see if these markers are present.



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Glutathione deficiency in patients with schizophrenia

A research team has just discovered two new blood markers for schizophrenia. Their findings have been published in the journal Molecular Psychiatry. A blood marker is a molecule whose presence in the blood indicates the presence of a condition or disease. To identify markers of schizophrenia, the researchers examined parvalbumin interneurons and the mitochondria. Mitochondria are organelles within cells. They are sources of energy and cellular respiration. They are therefore important for the good health of these neurons.

“One molecule of the antioxidant system, glutathione, is deficient in schizophrenic patients. Its deficiency leads to impaired parvalbumin interneurons, which are directly involved in all cognitive functions of the brain and thus in thinking,” explains Kim Q. Do, professor of neuroscience at the University of Geneva. Do, is a professor of neuroscience at the Center for Psychiatric Neuroscience (CNP) in Switzerland and one of the authors of this study.

The role of dysfunctional mitochondria

Researchers noticed those dysfunctional mitochondria accumulated in the brains of some patients with schizophrenia because they were no longer being eliminated or recycled. This accumulation of dysfunctional mitochondria increases oxidative stress, which can be defined as an attack on cells by reactive oxygen species (ROS).

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Normally ROS are destroyed by antioxidant molecules, but their production is reduced during oxidative stress. They can therefore easily destroy our neuronal cells. In the long term, oxidative stress can partly cause neuron death.

In their experiments, the researchers observed that miR137 and COX6A2, two molecules, were particularly sensitive to oxidative stress. In patients with schizophrenia, the amount of miR137 was particularly high, which, according to the researchers, indicates that the dysfunctional mitochondria cleaning system was not sufficiently activated. In other words, dysfunctional mitochondria were accumulating because miR137 molecules were present in high amounts. In contrast, COX6A2 levels were very low in the study participants, explaining poor cellular respiration, which is one of the roles of mitochondria. Because this mitochondrial function was impaired in these schizophrenic patients, it is a marker.

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Improving the treatment of patients with mitochondrial abnormalities

The researchers, therefore, thought that miR137 and COX6A2 might be markers for schizophrenia and looked for them in the blood of patients with this disease. Two categories of patients were found: those with mitochondrial problems and those without. “Patients with a mitochondrial defect have more severe clinical symptoms than the others,” says Ines Khadimallah, author of the study. These patients had a greater loss of autonomy. The researchers concluded that miR137 and COX6A2 were two blood markers in schizophrenic patients with mitochondrial defects.

In the long term, this work could lead to the development of new treatments. Patients with mitochondrial abnormalities could benefit from antioxidant treatment, which would improve the status of their parvalbumin interneurons and their disease symptoms.

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Mitochondrial, exosomal miR137-COX6A2 and gamma synchrony as biomarkers of parvalbumin interneurons, psychopathology, and neurocognition in schizophrenia



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