Abstract
Besides the positive and negative symptoms, the cognitive deficits are now recognized as a core domain of schizophrenia (SZ). Here, we introduce recent advances in “The kynurenic acid (KYNA)hypothesis of SZ” based especially on the abnormally elevated levels of KYNA, a tryptophan metabolite on the kynurenine pathway, in the SZ prefrontal cortex and the cerebrospinal fluid possibly due to the decreased activity of kynurenine 3 -monooxygenase (KMO) . KYNA modulates glutamate, dopamine, and acetylcholine (Ach) signaling via NMDA- Receptor and α 7nAch-Receptor. The regulation of the kynurenine pathway by inflammatory mediators suggests immunological alterations and neuroinflammation-mediated dysregulation of kynurenine pathway which pertains partly to psychiatric disorders including SZ. Novel therapeutic targets for SZ are discussed according to this hypothesis, regarding especially the cognitive deficits in SZ.
