Kynurenic acid

A breakdown product of the kynurenine pathway – an NMDA receptor antagonist. Is looked at with questions about concentration and drive.

What kynurenic acid does in the body

Kynurenic acid is formed when the kynurenine aminotransferases (KAT) convert kynurenine with vitamin B6. In the brain this happens mainly in the astrocytes, which take up kynurenine from the blood. At the NMDA receptor, kynurenic acid occupies the binding site for the co-agonist glycine and thereby dampens the effect of glutamate; in higher amounts it also inhibits other glutamate receptors. Whether it additionally inhibits the α7 nicotinic receptor and thereby slows the release of glutamate and acetylcholine is assessed differently in research. It also acts on immune cells and the gut lining via the receptors GPR35 and AhR. Kynurenic acid is excreted via the kidneys.

Low kynurenic acid – what happens in the body?

When little kynurenic acid is present, part of the natural brake on glutamate signalling is missing: NMDA receptors respond more easily, especially when a lot of quinolinic acid is formed at the same time. Less kynurenic acid is formed when vitamin B6 is scarce or when a large share of kynurenine flows via KMO into the branch towards quinolinic acid. Low values have been observed in studies in some neurodegenerative diseases and in migraine.

High kynurenic acid – what happens in the body?

More kynurenic acid is formed when, with inflammation, a lot of kynurenine is produced via IDO and astrocytes convert it, or when KMO works little and kynurenine is diverted into this branch. The stronger dampening of NMDA receptors and the reduced release of glutamate and acetylcholine affect signalling pathways that are needed for learning, memory and attention. Raised values in the cerebrospinal fluid have been observed in studies in schizophrenia and bipolar disorder. Because kynurenic acid is excreted via the kidneys, it also rises with reduced kidney function.

The interpretation is given in your report.