September 9, 2003

MEDIA CONTACT: Jessica Collins
PHONE: 410-516-4570
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Similar Genetic Origins Possible for Schizophrenia and Bipolar Disorder

Findings may lead to childhood screening, early treatment A study by researchers at the Johns Hopkins Children's Center, University of Cambridge and the Stanley Medical Research Institute appears to offer the first hard evidence that schizophrenia and bipolar disorder, severe psychoses that affect 2 percent of the population, may have similar genetic roots.

The study's findings, reported in the Sept. 6 issue of The Lancet, trace the disorders to reduced expression of the genes responsible for myelin development in brain cells known as oligodendrocytes. Composed mostly of fats and proteins, myelin sheaths insulate nerve cells, enabling them to safely conduct electric signals between the brain and other parts of the body.

"Patients with schizophrenia and bipolar disorder differ in terms of their presentation and clinical course," says the study's co-author, Robert Yolken, M.D., a neurovirologist at the Children's Center. "However, there is some overlap in terms of symptoms and there are medications that have been used for the treatment of both disorders. Our findings suggest that there are similar mechanisms involved in both disorders and that they may be more closely related than previously thought."

In the study, researchers compared expression of myelin-associated genes in the preserved brains of 15 people with schizophrenia, 15 with manic-depressive illness (bipolar disorder), and 15 from a control group of individuals with neither disorder.

"The expression profiles of most known oligodendrocyte-specific and myelin-associated genes were greatly reduced, and several transcription factors known to coordinate myelin gene expression showed corresponding changes," says Yolken. "These results provide strong evidence for oligodendrocyte and myelin dysfunction in patients with schizophrenia and bipolar disorder."

Yolken says the reason for this dysfunction is not currently known, but may be related, in some cases, to infections of the central nervous system or other environmental issues. This possibility is consistent with previous studies which indicate that infections occurring early in infancy may be a risk factor for the development of schizophrenia and biopolar disorder later in life.

Because symptoms of both schizophrenia and bipolar disorder typically emerge only in late adolescence or early adulthood, Yolken says this current research may someday help physicians screen children whose family histories put them at potential risk for developing these disorders, and treat them before they exhibit symptoms.

"By looking for abnormalities in myelin, we might be able to identify children likely to develop these disorders as adults and begin treatment before symptoms become severe and debilitating," Yolken said.

Most of the laboratory work was conducted in the laboratory of Sabine Bahn at the Babraham Institute of the University of Cambridge. Additional authors of the study were Dmitri Tkachev, Michael L. Mimmack, and Margaret M. Ryan from the University of Cambridge and the Babraham Institute; Peter B. Jones from the University of Cambridge; Matt Wayland, Tom Freeman and Michael Starkey from the U.K. Human Genome Mapping Project Resource Centre; and Maree J. Webster from the Stanley Laboratory of Brain Research, Bethesda, MD.