According to a new study, published in the journal Biological Psychiatry, in mice, modifying levels of a compound known as kynurenic acid could effectively treat symptoms of schizophrenia. Kynurenic acid is a product of the standard metabolism of amino acid L-tryptophan. However, it could soon consume a significant role in treating schizophrenia.
In the past, researchers have suggested that kynurenic acid played a prominent role in schizophrenia. Essentially, researchers found that patients with schizophrenia were more likely to carry abnormal levels of kynurenic acid in the brain. Also known as KYNA, kynurenic acid reduces glutamate; research has shown that people with schizophrenia also have fewer levels of glutamate.
The lower levels of glutamate, combined with higher KYNA levels, could altogether be associated with a range of symptoms seen in people with schizophrenia, including cognitive issues.
One of the key researchers, Robert Schwarcz, Ph.D., a Professor at the University of Maryland School of Medicine, was the first to discovery KYNA, back in 1988. And since then, Dr. Schwarcz has been studying and finding the link between KYNA in schizophrenia and other neuropsychiatric diseases.
In this study, however, Dr. Schwarcz collaborated with researchers from Sweden, the United Kingdom, and the United States. The study is giving researchers a fresh look at an old hypothesis, in regards to how the KYNA system can cause dysfunction during schizophrenia. Researchers examined mice that were deficient in kynurenine 3-monooxygenase, or KMO, an enzyme associated with the levels of KYNA.
Based on the findings, researchers noticed that lower KMO resulted in higher levels of KYNA. Interestingly enough, people with schizophrenia who had lower levels of KMO may be linked to low levels of glutamate as well.
Contextual memory impairment was observed in the mice with low levels of KMO; it also spent less time interacting in a social environment with an unfamiliar mouse. Additionally, researchers also found high levels of anxiety when the mice were put into challenging settings such as a maze.
As a result, researchers concluded that the behavioral traits exhibited by the mice, which is similar to that of schizophrenia, is linked to the levels of KMO and KYNA in the brain. Although the discovery covered a lot of ground, there are still clinical implications. For instance, boosting glutamate can cause seizures and nerve cell death.
With the new findings, researchers aren’t getting ready to hang their lab coats just yet. More clinical trials are next, according to Dr. Schwarcz.