The "germ theory" of schizophrenia got a mild boost this week as scientists discover that recently afflicted schizophrenics show higher levels of inflammatory proteins in the brain.

As reported in the December issue of Molecular Psychiatry, researchers in Sweden and Germany found that recent-onset schizophrenics-- those first showing symptoms, usually young adults-- had elevated amounts of interleukin-1beta in their spinal fluid. In normal controls, IL-1beta levels were nearly undetectable.

The researchers looked at around 10 common cytokines, proteins used by the body's defenses to communicate with immune cells, but only IL-1beta was unusually expressed in the mentally ill patients.

"This cytokine has been implicated in a variety of brain function[s], in particular IL-1beta appears to induce [the] 'sickness behavior' all of us experience during a virus infection," Goran Engberg, professor of physiology and pharmacology at Karolinska Institutet in Stockholm, Sweden and lead author of the study, tells DOTmed News by email.

While Engberg says that fever and lack of sleep are known to increase IL-1beta levels slightly, it's unlikely for those to account for the levels seen in these patients.

Germ theory

As early as the 1970s, some scientists have suggested that schizophrenia, which afflicts about 1 percent of the U.S. population, could be triggered by an infection.

A popular candidate has been the protozoan Toxoplasma gondii, transmitted from cat feces or uncooked meats. Engberg says infection from the toxoplasma parasite more than doubles one's risk for schizophrenia. "Toxoplasma gondii appears to be one of several micro-organisms that can trigger [the] brain immune system," he says.

Still, the jury's out on whether T. gondii or another infection could lead to schizophrenia, or even whether an infection, or some other cause, is boosting IL-1beta levels in the brains of schizophrenics. Nonetheless, Engberg has some ideas as to how IL-1beta, or other cytokines, could, in part, bring about symptoms.

It appears that cytokines directly affect the brain's dopamine systems, chemical-signaling systems long implicated in schizophrenia. However, Engberg suggests a more likely immediate trigger could be increases in brain kynurenic acid, "an angel dust-like endogenous substance that produces psychotic symptoms in healthy individuals," he says, and which also affects dopamine activity.

Currently, Engberg is collecting evidence from older schizophrenics to see if the inflammatory condition persists. And so far, it seems it does.

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