THE ESSENTIAL
- A third of patients with schizophrenia go into lasting remission thanks to pharmacological and psychosocial treatments.
- One in two patients with schizophrenia makes at least one suicide attempt.
In France, 600,000 people suffer from schizophrenia. Globally, this disease affects around 0.7 to 1% of the population, according to Inserm. It is a psychiatric pathology which generally manifests between 15 and 25 years. Its symptoms (social withdrawal, cognitive difficulties, hallucinations, delusions …) are very different, which complicates the diagnosis. Better understanding and detecting this disease would thus make it possible to treat it more effectively and to intervene earlier in order to limit its severity. For this, several scientists are trying to identify markers of this pathology. The ultimate goal is for doctors to be able to order tests for their patients to see if these markers are present.
A lack of glutathione in patients with schizophrenia
A team of researchers has just discovered two new blood markers for schizophrenia. Their results were published in the journal Molecular Psychiatry. A blood marker is a molecule whose presence in the blood expresses the presence of a condition or disease. To identify those of schizophrenia, scientists looked at parvalbumin neurons and the mitochondria of these neurons. Mitochondria are organelles found in cells. These are sources of energy and cellular respiration. They are therefore important for the good health of parvalbumin neurons.
“A molecule of the antioxidant system, glutathione, is deficient in patients with schizophrenia. Its lack leads to an alteration of parvalbumin neurons, a type of neuron directly involved in all cognitive functions of the brain, and therefore of thought”explained Kim Q. Do, professor of neuroscience at the Center for Psychiatric Neuroscience (CNP) in Switzerland and one of the authors of this study.
The role of sometimes dysfunctional mitochondria
The researchers noted that dysfunctional mitochondria accumulated in the brains of some patients with schizophrenia because they were no longer removed or recycled. This accumulation of dysfunctional mitochondria increases oxidative stress, which can be defined as an attack on cells by reactive oxygen species (ROS). Usually, ROS are destroyed by antioxidant molecules, but their production is impaired under oxidative stress. They can therefore easily destroy our neuronal cells. Eventually, oxidative stress, in part, can cause neuron death.
During their experiments, the scientists observed that miR137 and COX6A2, two molecules, were more particularly sensitive to oxidative stress. In patients with schizophrenia, the amount of miR137 was particularly high, indicating, according to the researchers, that the dysfunctional mitochondrial cleansing system was not activated sufficiently. In other words, dysfunctional mitochondria accumulated because miR137 molecules were present in large quantities. In contrast, the level of COX6A2 was very low in the study participants, which explains the poor cellular respiration, one of the roles of mitochondria. As this function of the mitochondria was altered in these schizophrenic patients, it is therefore indeed a marker.
Improve the treatment of patients with mitochondrial abnormalities
The researchers estimated that miR137 and COX6A2 might therefore be markers of schizophrenia and looked for it in the blood of patients with this pathology. Thus, two categories of patients were discovered: those who had mitochondrial problems and those who did not. “Patients with a mitochondrial defect have more severe clinical symptoms than others”, developed Inès Khadimallah, author of the study. These patients had a greater loss of autonomy. The scientists concluded that miR137 and COX6A2 were two blood markers in schizophrenic patients with mitochondrial abnormalities.
Ultimately, this work might lead to the development of new treatments. Patients with mitochondrial abnormalities may benefit from antioxidant therapy, which would improve the condition of their parvalbumin neurons and the symptoms of their disease.
