New research has found one of the causes for schizophrenia, and genetic faults in the brain's glial cells seem to be responsible for the condition.
It is currently estimated that more than
For now, available treatments are limited to eliminating the symptoms of the disease rather than "curing" it, as the causes of the condition remain largely unknown.
New research, however, moves closer to understanding what causes schizophrenia, as scientists foray into its genetic background and examine the brain cells involved.
The new findings, which are published in the journal Cell, suggest that genetic defects may affect the brain's so-called glial cells. Dysfunction in these cells may cause the symptoms of childhood-onset schizophrenia, say the researchers.
Dr. Goldman, a neurologist at the University of Rochester Medical Center in New York, led the study.
What are glial cells?
The brain's glial cells are neurons that make up the supportive tissue in the brain. Their main role is to facilitate the communication between other neurons located not only in the central nervous system, but also in the peripheral one.
Glial cells are of two main types: astrocytes and oligodendrocytes. The former surround the synapses and facilitate interneuronal communication and make sure that any waste between the cells is eliminated, while the latter are responsible for producing myelin - that is, the fatty tissue that forms a protective sheath around the axons of the neurons.
During the fetal development of the brain, glial cells form from "glial progenitor cells," which are a type of pluripotent stem cell - namely, an embryonic cell that can turn into any other kind of cell.
Scientists believe that genetic faults in these glial progenitor cells may lead to dysfunctional cell activity, thus causing schizophrenia.
The basis for schizophrenia
Dr. Goldman and team developed a mouse model and implanted human glial cells into the rodents' brain, which allowed them to create a human brain network in mice. These glial cells were formed from the progenitor cells of human patients with childhood-onset schizophrenia.
The researchers could see that the glial cells taken from patients with schizophrenia were abnormal. The dysfunctional progenitor cells did not create enough oligodendrocytes, so not enough myelin was produced. This damaged the signaling between the neurons.
Additionally, astrocytes did not develop properly either. This resulted in poor interneuronal connections as well as dysfunctional, underdeveloped cells. The white matter in the brain of the rodents was also underdeveloped.
"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," explains first author Martha Windrem, Ph.D. "As a result, the neural networks in the animals became desynchronized and uncoordinated."
Finally, the scientists examined the genetic aspect of schizophrenia-related behavior. To do so, they performed a series of tests that examined the rodents' cognitive and social skills.
Mice with cells from schizophrenia patients displayed higher levels of anxiety and fear. They were more socially reclusive and had sleep disorders, deficient sensory-motor coordination, and other cognitive impairments.
All of the aforementioned behavioral traits characterize human patients with schizophrenia.
"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."
Dr. Steve Goldman
"This is an important discovery because it will now enable us to develop methods that can counteract the unwanted development of progenitor cells," he adds.
The authors also note that the animal model they designed can be used to speed up drug testing in rodents.
Importantly, the study identified potential targets for new therapies, such as the chemical imbalances triggered by dysfunctional glial cells.