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Biomedical Engineering

The Biomedical Engineering blog is the place for conversation and discussion about topics related to engineering principles of the medical field. Here, you'll find everything from discussions about emerging medical technologies to advances in medical research. The blog's owner, Chelsey H, is a graduate of Rensselaer Polytechnic Institute (RPI) with a degree in Biomedical Engineering.

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Hope Springs from Schizophrenic Mice

Posted February 10, 2017 1:00 PM by MaggieMc

A recent study by the University of Maryland’s School of Medicine promises to shed some light on possible causes and solutions to schizophrenia symptoms (see: an in-depth description of the condition from the University of Maryland Medical Center). As someone who has witnessed schizophrenia outside the fog of Hollywood, this study—while preliminary—holds some hope.

The study considered mice deficient in kynurenine 3-monooxygenase (KMO), specifically noting how lower levels of the enzyme resulted in higher kynurenic acid (KYNA) levels. KYNA is a “metabolite of the amino acid tryptophan,” and high levels of KYNA correlate to low levels of glutamate activity, which has long been associated with symptoms of schizophrenia. Unfortunately, according to ScienceDaily, raising glutamate levels “on a large scale has serious side effects, including seizures and nerve cell death,” ruling it out pretty quickly as a method of treatment.

In summary, low KMO leads to high KYNA, which is correlated to low glutamate activity levels. This becomes even more significant when considering that lower levels of KYNA and higher levels of glutamate activity were associated with improved cognition in mice with cognitive defects, a classification the researchers compared to schizophrenia. In addition, low levels of KMO were associated with worse contextual memory, antisocial behavior, and increased anxiety during challenges.

After studying cognition in mice, and the effects of lower levels of KMO, researchers hope “modifying KYNA could adjust glutamate more precisely.… Because this mechanism is indirect, it does not seem to trigger the same side effects directly boosting glutamate does,” according to researchers.

Image Credit: The Patterson Lab

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Re: Hope Springs from Schizophrenic Mice

02/10/2017 1:44 PM

Thanks for the info, MaggieMc. I had always attributed the disorder to genetics/dopamine imbalance. Any positive advances, no matter how incremental, are welcome. (yes, there's a paranoid schizophrenic in my family. sigh)

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