he researchers found.
The mice also had changes in the nerve cells that make and use dopamine, a key chemical in the brain that transmits messages from one nerve cell to another. The dopamine system has long been known to be altered in schizophrenia, and is the target of many antipsychotic drugs.
"Changing the white matter in the brain apparently unbalanced the dopamine system, something that also occurs in patients with neuropsychiatric disorders," says Corfas.
Finally, mice whose NRG1-erbB signaling was blocked showed behavioral changes that appeared to be consistent with mental illness. They explored their environment less than normal mice and had reduced social interaction, thought to be a manifestation of so-called "negative" schizophrenic symptoms such as decreased initiative and social withdrawal. The mice also showed behaviors suggestive of anxiety, a symptom seen in patients with schizophrenia and bipolar disorder, and increased sensitivity to amphetamine, also seen in many schizophrenia patients.
Is it possible to modify NRB1-erbB signaling with drugs, or otherwise protect oligodendrocytes (and white matter) as a way of treating or preventing schizophrenia?
"This is something that should be investigated," says Corfas. "People are thinking about ways to repair white matter as a treatment for multiple sclerosis, which is also a disease of white matter. That research could now be used in thinking about neuropsychiatric disorders."
Schizophrenia is typically diagnosed in late adolescence or early adulthood, but it is almost always preceded by subtle affective, cognitive or motor problems, Corfas adds. "We need to investigate whether the white-matter defects emerge early, before psychotic symptoms are evident," he says. "If they do, that raises the possibility of early diagnosis and preventive treatment."
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