In a development towards finding a permanent and reliable cure to Schizophrenia, a mental illness which has its causes hidden for ages: Researchers study the brain processes behind mental condition, via thorough investigation of kynurenic acid (KYNA) which plays a key role in the pathophysiology of schizophrenia.
Earlier studies have shown people with Schizophrenia to posses higher levels of KYNA than healthy individuals.
From existing research, findings show that kynurenic acid (KYNA) has both positive and negative effects: it helps to metabolize tryptophan, the amino acid that helps the body to produce happiness. Consequentially, kynurenic acid (KYNA) decreases glutamate, an important neurotransmitter for healthy brain functioning – which, in turn, explains the brain dysfunction in schizophrenia.
Base on this hypothesis, a team of scientists from the University of Maryland School of Medicine in Baltimore led by Robert Schwarcz, Ph.D., a professor in the Department of Psychiatry, decide investigating the link between the kynurenic acid (KYNA) and schizophrenia-like behavior in mice. Researchers found that, kynurenine 3-monooxygenase enzyme (KMO)-deficient mice with high KYNA show schizophrenia-like symptoms.
In the new study published in the journal Biological Psychiatry, researchers performed their experiment on mice that had their KMO deleted and characterized via the six schizophrenia-specific behavioral assays.
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As expected, researchers found higher levels of KYNA in KMO-deficient mice. Genetically modified mice with KMO-deficient displayed contextual memory problems with increased anxiety-like behavior, which are all typical symptoms of Schizophrenia when compared with control mice.
This study provides crucial new support for our longstanding hypothesis. It explains how the KYNA system may become dysfunctional in schizophrenia, concludes Prof. Robert Schwarcz.
Reference: Prof. Robert Schwarcz et al. Adaptive and Behavioral Changes in Kynurenine 3-Monooxygenase Knockout Mice: Relevance to Psychotic Disorders - http://dx.doi.org/10.1016/j.biopsych.2016.12.011
