Maria Holtze

TL;DR: The results demonstrate increased levels of CSF KYN and KYNA in patients with schizophrenia and further support the hypothesis that KYNA is involved in the pathophysiology of schizophrenia.

TL;DR: The results suggest that the nonsynonymous KMO SNP rs1053230 influences CSF concentrations of KYNA, an end-metabolite of the kynurenine pathway, and the results are tentative until replication.

TL;DR: Subchronic elevation of rat brain KYNA may rationally serve as an animal model similar to a pathophysiological condition of schizophrenia and it is proposed that the reduced responsivity of VTA DA neurons to the inhibitory action of amphetamine observed in rats with subchronically elevated KYNA levels may partly account for the increase in terminal DA release.

TL;DR: The present data show that a neonatal infection targeting the brain can induce the kynurenine pathway and that such an infection can disrupt sensorimotor gating in adulthood in genetically vulnerable mice.

TL;DR: The present results indicate that central nervous system infections during early life can activate the entire kynurenine pathway and is likely to result in the generation of several bioactive metabolites, as supported by the finding of a transient increase of kynurenic acid.