A new study suggests biochemical changes associated with schizophrenia aren’t limited to the central nervous system and that the disease could have more encompassing effects throughout the body than previously thought. The findings, scheduled for publication in the January 2007 issue of the American Chemical Society’s Journal of Proteome Research, could lead to better diagnostic testing for the disease and could help explain why those afflicted with it are more prone to type II diabetes, cardiovascular diseases and other chronic health problems.
Researcher Sabine Bahn, M.D., Ph.D., and her colleagues at Cambridge University in England and the University of Cologne in Germany, detected abnormal proteins linked to schizophrenia in the liver and red blood cells of people who have the disorder. It is the first time the same altered proteins have been detected both within brain tissue as well as in non-brain tissue, according to Bahn.
In time, Bahn says, these protein “biomarkers” could be used to trace the progression of the disease throughout the body.
“If changes in the rest of the body can be observed, and if these changes reflect what is going wrong in the brain, we can use these (findings) to learn about the cellular dysfunction that causes schizophrenia and this will allow us to develop better drugs and diagnostics,” Bahn says.
About 1 percent of the world’s population — including 2.4 million Americans — has schizophrenia, a complex and puzzling mental illness that can lead to delusions, hallucinations and disordered thinking. It is one of the world’s most common causes of psychosis, according to Bahn. Since it was first described more than 100 years ago, scientists have made little progress in unraveling the causes of the disease, and no definitive test is available to diagnosis it, she says.
“We desperately need a better understanding of this illness. It is, however, difficult to study the disease, as the brain can’t easily be investigated. We can’t take multiple biopsies from patients to look at the disease-related changes,” Bahn says. “We need a new concept.”
While most scientists investigating the disease believe it only affects the brain, Bahn notes that researchers have long known that people who have schizophrenia are at higher risk than the general population for a number of chronic diseases. Some evidence suggests these health problems might be somehow tied to schizophrenia, she adds, but most studies have been inconclusive. Bahn’s latest discovery could help bridge this gap.
Recently, Bahn and her colleagues discovered a set of abnormal proteins in post-mortem brains of people who had schizophrenia. In this new study, they sought to detect similarly altered proteins in other organs and tissues of individuals living with the disease. After looking at thousands of proteins, they found that people with schizophrenia had 14 liver proteins and eight red blood cell proteins that were significantly altered compared to individuals who didn’t have the disease. These altered proteins were strikingly like those found in the post-mortem brains.
Several of these abnormal proteins appear to promote oxidative stress and disrupt energy metabolism in cells, Bahn says. She theorizes that schizophrenia is caused, at least in part, by these two problems. In her earlier work, for instance, Bahn found evidence that schizophrenic brains might have difficulty producing or using energy properly and are more susceptible to cell-damaging free radicals than healthy brains. The new findings, she says, suggest that the same sort of energy starvation, increased free-radical damage cycle could be occurring in other tissue and, in addition to schizophrenia, possibly be contributing to the onset of other chronic diseases.
— Doug Dollemore
2-D DIGE Analysis of Liver and Red Blood Cells Provides Further Evidence for Oxidative Stress in Schizophrenia (pr060308a)
The online version of this research paper was initially published Dec. 9 2006 on the journal’s Web site. Journalists can arrange access to this site by e-mailing the ACS Newsroom or calling the contact person for this release.