Scientists believe they have found the driving issue behind childhood-onset schizophrenia. The brain’s glial cells ensure communication between neurons, and scientists studying a possible cause of childhood-onset schizophrenia say that the culprit could be dysfunction in these glial cells. The scientists, who have published their new findings in the journal Cell, say that genetic defects might be the cause of the dysfunction in the brain’s glial cells.
Medical News Today reports that more than 21 million people on earth are living with schizophrenia and that the National Institute of Mental Health estimates more than one percent of adults in the United States are affected by schizophrenia. The new research was led by neurologist Dr. Goldman. Goldman works at the University of Rochester Medical Center and says that dysfunction in the brain’s glial cells are likely the cause of childhood-onset schizophrenia.
Glial cells make up the supportive tissue in the brain, Medical News Today reports. Their primary function is believed to be to facilitate communication between neurons, including neurons in the peripheral nervous system, not just the central nervous system.
Glial cells can be grouped into two main types. One type facilitates communication and eliminates waste and the other produces myelin, which is a protective fatty tissue found around the axons of the neurons. While still in utero, our glial cells are created out of a type of pluripotent stem cell known as “glial progenitor cells.” Pluripotent stem cells are special because they are is genetically modified to turn into any other kind of cell. The point when schizophrenia is caused is when glial progenitor cells fail. The researchers didn’t indicate in the press release what might cause the glial progenitor cells to be faulty and create dysfunctional glial cells.
What they did report though is that they created a mouse model and implanted human glial cells into the animals’ brains. The glial cells had formed from the progenitor cells of humans diagnosed with childhood-onset schizophrenia.
The researchers had known that the progenitor cells didn’t create enough myelin-producing glial cells. They could also see that the glial cells responsible for eliminating waste and facilitating communication didn’t mature properly either. The glial cells facilitated some synapses, but not others, according to first author Dr. Martha Windrem.
“The astrocytes didn’t fully mature, and their fibers did not fill out their normal domains, meaning that while they provided control to some synapses, others had no coverage. As a result, the neural networks in the animals became desynchronized and uncoordinated.”
Mice that had cells from patients with schizophrenia showed higher levels of anxiety, fear, social reclusiveness, and sleep disorders than the controls. They also had cognitive impairments and sensory-motor coordination issues.
“The findings of this study argue that glial cell dysfunction may be the basis of childhood-onset schizophrenia […] The inability of these cells to do their job, which is to help nerve cells build and maintain healthy and effective communication networks, appears to be a primary contributor to the disease.”
This research allowed the scientists to have a better idea of ways they may treat childhood-onset schizophrenia.
According to an article in Frontiers in Pediatrics, several recent studies have linked dysfunctional glial cells to other conditions like Autism Spectrum Disorders and Fetal Alcohol Spectrum Disorders (FASD).
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