Scientists identify glial cells as important factor in development of schizophrenia
The disease could develop due to damage to on a particular type of brain cell.
Scientists have taken another step towards a full understanding of how schizophrenia develops. And in doing so, they may also be moving closer towards a cure.
They have identified a connection between schizophrenia and damage to a particular group of brain cells—so-called glial cells—that allow neurons to communicate with each other.
Genetic defects that prevent the cells from developing properly can lead to schizophrenia, shows the new study. It is the first time that glial cells have been identified as a possible cause of schizophrenia.
“We now know that defects in glial cells play an important role in the development of schizophrenia. We also identified a substance that affects the cells, and we’re now testing possible candidates to develop a treatment for the disease,” says Professor Steven A. Goldman from the Center for Basic Translational Neuroscience at the University of Copenhagen, Denmark.
Fatty substance responsible for schizophrenia
In the new study, scientists have studied the role of glial cells in the development of schizophrenia.
Glial cells are responsible for maintaining brain function, which they do by protecting the neurons and allowing different parts of the brain to talk to one another.
They form a protective layer of fat around the neurons, called myelin.
But sometimes the cells do not produce enough myelin due to genetic defects. And this is one of the most important factors in the development of schizophrenia, according to the new research.
If not enough myelin is produced, the neural network responsible for communication between neurons does not develop as it should.
“Genetic mutations mean that it takes longer for the glial cells to develop. We think this is the reason why people develop schizophrenia. Previously it was thought that the cause of schizophrenia was found in the neurons, but our study shows something else. We see it both in mice and in patients with schizophrenia,” says Goldman.
Mice transplanted with human glial cells
In the study, scientists developed a special mouse with human glial cells.
Some mice received glial cells from schizophrenia patients with a number of genetic defects, and others received glial cells from people who did not suffer from the disease.
Mice transplanted with cells from schizophrenic patients were more nervous, antisocial, and anxious. Such traits indicate the same characteristics as those observed in schizophrenia in people, say the scientists behind the research.
The mice transplanted with glial cells from schizophrenic patients also had less myelin.
Does not solve all the mysteries of schizophrenia
The new study is definitely an important step forward in understanding schizophrenia and to developing a possible treatment, says Dr Mette Ødegaard Nielsen from the Centre for Neuropsychiatric and Schizophrenia Research at Glostrup Hospital, Denmark.
She was not involved in the new study but describes the results as “very exciting.”
“The study shows how the myelin defect can occur. Thereby the study suggests a primary mechanism that leads to specific changes that we see in some patients with schizophrenia,” says Nielsen
“It gives hope for new treatments for our patients. The new knowledge on the role of glial cells can lead to new treatments to correct the defect. As a clinician I can only welcome this, since many of our patients do not benefit from our current medical treatments,” she says.
Nielsen suggests however that a diagnosis of schizophrenia covers many disease mechanisms.
“Until now, we defined schizophrenia by the symptoms and not from a biological definition. Therefore this defect of the glial cells is probably only responsible for some of the cases of mental disorders that we today characterise as schizophrenia,” she says.
Read more in the Danish version of this story on Videnskab.dk
Translated by: Catherine Jex
- Human iPSC Glial Mouse Chimeras Reveal Glial Contributions to Schizophrenia, Cell Stem Cell (2017), doi: 10.1016/j.stem.2017.06.012 showArticle Info