Schizophrenia may be linked to inflammation: study

The key to schizophrenia may be found in a gene region thought to play a role in inflammation and autoimmune disorders, U.S. researchers said on Tuesday.

If confirmed, the finding could lead to a test and possibly new treatments for the mental disorder that affects about 1 percent of the world’s population, researchers said.

Schizophrenia, a disease marked by distorted thinking, hallucinations and reduced ability to feel normal emotions, has long been associated with heredity. But the link to inflammation might help explain why many patients with schizophrenia have autoimmune diseases.

In a study published in the journal Molecular Psychiatry scientists used a research technique called whole genome association to search the entire human genome of 178 patients with schizophrenia and 144 healthy volunteers.

Of 500,000 genetic variants studied, researchers zeroed in on a gene near the tip of both the X and Y chromosomes, which determine gender.

“That is a region that had not been looked at in schizophrenia so much,” said Todd Lencz, an investigator at the Feinstein Institute for Medical Research in Manhasset, New York, and lead author of the study.

Lencz said the variant was located near genes that produce receptors for two cytokines, which are involved in the body’s response to infection and may play a role in the brain’s response to injury.

Receptors are molecular doorways that cytokines use to attach to cells. Cytokines are immune system signaling chemicals and their production is a first step in causing inflammation.

Lencz and colleagues using gene sequencing technology on a separate group of 71 schizophrenia patients and 31 healthy volunteers.

That study turned up multiple gene abnormalities in patients with schizophrenia that were not found, or were found less often, in healthy patients.

Peter McGuffin, a professor of psychiatric genetics at Kings College London in Britain, said the study may have been too small to draw any conclusions about the genetic origins of schizophrenia.

“I’d worry that this will turn out to be a false positive,” McGuffin said in a statement.

Lencz said the findings need to be replicated in other studies. He said he and colleagues have obtained funding to test more patients.

The study was the result of an academic-industry collaboration involving a unit of the biotechnology company Clinical Data Inc., which is seeking a patent related to the findings.

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