According to a recent study, people with schizophrenia may have deficits in the white matter. Ultimately, these results may lead to the development of new treatments, the researchers expect.
Schizophrenia is a psychiatric disease that affects 0.7% to 1% of the world’s population. The disease manifests itself worldwide through disturbed perception of reality, delusions, hallucinations or social and relational isolation. It is so disabling partly due to the fact that treatments are limited and have many side effects.
In fact, the generally prescribed antipsychotics can lead to significant weight gain, Blurred vision, fatigue, dry mouth, dizziness and restlessness. One study has even established a link between first-generation antipsychotics and the loss of brain tissue in patients suffering from schizophrenia. However, recent findings from the schizophrenia bulletin may lead to a new treatment. Here, researchers have observed that patients have deficits in the white matter, the part of the brain that includes the axons that transmit nerve impulses between neurons.
In the past, several studies on schizophrenics have shown differences in the levels of sphingolipids, fat molecules that play a role in the formation of myelin, which protects and isolates certain nerve fibers. Here, the researchers decided to analyze these levels in the post-mortem brain tissue of 15 patients. Using mass spectrometry, a technique used to identify particles in a sample by measuring their mass, they found that the levels of a sphingolipid called S1P were lower in people with schizophrenia.
A deficit that is specific schizophrenic
In detail, these values were lower in a region of the brain known as the corpus callosum. The abnormalities in this region, which is rich in white matter, can cause communication disorders between neurons.
“This was the first postmortem psychiatric study of the brain using mass spectroscopic analysis, and our discovery would not have been possible without our new comprehensive sphingolipid screening technique,” said Dr Takeo Yoshikawa, team leader at RIKEN CBS (Tokyo, Japan), who led the study.
To determine whether this dysfunction occurs in all mental disorders, the scientists also analyzed the brains of people with bipolar disorders and severe depression. They found that S1P levels were normal in these people. In summary, this deficit is specific to schizophrenia.
Stop the breakdown of the S1P sphingolipid
Subsequent experiments then showed that the problem could be caused by abnormal degradation of S1P rather than by impaired production. In this case, drugs could be developed to stop the degradation of S1P and treat schizophrenia. An existing treatment could also work: Fingolimod (Gilenya), which is used to treat multiple sclerosis. In fact, it targets S1P, the researchers recall. However, further research is needed to better understand the exact role of S1P in schizophrenia.
“Because we have no other perspective on the causes of schizophrenia, many pharmaceutical companies are withdrawing from developing drugs related to schizophrenia,” says Dr. Takeo Yoshikawa. We hope that our results will provide a new approach and a new target for drug development.
According to mentalhelp.net 3.2 million people in the US suffer from schizophrenia. Since the disease most commonly occurs between the ages of 15 and 25, it is important to control it as early as possible to bring it under control. Although patients never really recover from schizophrenia, about a third of them manage to return to a normal social, emotional and professional life after a few years of treatment.