Kynurenic acid

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Kynurenic acid
2D structure for Kynurenic acid
Chemical Name	4-hydroxy-2-Quinolinecarboxylic acid
Chemical Formula	C₁₀H₇NO₃
CAS Number	492-27-3
Chemical Information	HMDB00715
Biochemical Taxonomy	Quinolines
Functional Taxonomy	Not Available
Nutritional Taxonomy	Not Available
Metabolic Pathways	Not Available
Biofluid Location	Blood Cerebrospinal Fluid (CSF) Urine
Tissue Location	Epidermis Fibroblasts Brain
Normal Biofluid Concentrations	Blood: 0.023 +/- 0.010 umol/L Cerebrospinal Fluid (CSF): 0.001 (0.0009-0.0011) uM Cerebrospinal Fluid (CSF): 0.0019 (0.0017-0.0021) uM Cerebrospinal Fluid (CSF): 0.0040 +/- 0.00014 uM Cerebrospinal Fluid (CSF): 0.07 (0.06-0.08) uM Urine: 1.34 +/- 0.30 umol/mmol creatinine
Normal Tissue Concentrations	Not Available
Diseases / Conditions Related to Nutrition	Anemia Cerebral malaria Convulsions Severe Malaria TB meningitis Uncomplicated malaria
Other (Monogenic Disorders)	Not Available
Abnormal Biofluid Concentrations	Cerebrospinal Fluid (CSF) (Anemia): 1.23 (0.18-8.40) uM Cerebrospinal Fluid (CSF) (Cerebral malaria): 0.21 (0.2-0.3) uM Cerebrospinal Fluid (CSF) (Convulsions): 0.05 (0.02-0.10) uM Cerebrospinal Fluid (CSF) (Severe Malaria): 0.06 (0.06-0.07) uM Cerebrospinal Fluid (CSF) (TB meningitis): 0.07 (0.0-34.1) uM Cerebrospinal Fluid (CSF) (Uncomplicated malaria): 0.05 (0.01-0.25) uM
Abnormal Tissue Concentrations	Not Available
Physiological Processes	Not Available

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Introduction

guidelines
Kynurenic acid (KYNA) is a well-known endogenous antagonist of the glutamate ionotropic excitatory amino acid receptors N-methyl-D-aspartate (NMDA), alphaamino-3-hydroxy-5-methylisoxazole-4-propionic acid and kainate and of the nicotine cholinergic subtype alpha 7 receptors, and KYNA neuroprotective and anticonvulsive activities have been demonstrated in animal models of neurodegenerative diseases. Because of KYNA's neuromodulatory character, its involvement has been speculatively linked to the pathogenesis of a number of neurological conditions including those in the ageing process. Different patterns of abnormalities in various stages of KYNA metabolism in the CNS have been reported in Alzheimer's disease, Parkinson's disease and Huntington's disease. In HIV-1-infected patients and in patients with Lyme neuroborreliosis a marked rise of KYNA metabolism was seen. In the ageing process KYNA metabolism in the CNS of rats shows a characteristic pattern of changes throughout the life span. A marked increase of the KYNA content in the CNS occurs before the birth, followed by a dramatic decline on the day of birth. A low activity was seen during ontogenesis, and a slow and progressive enhancement occurs during maturation and ageing. This remarkable profile of KYNA metabolism alterations in the mammalian brain has been suggested to result from the development of the organisation of neuronal connections and synaptic plasticity, development of receptor recognition sites, maturation and ageing. There is significant evidence that KYNA can improve cognition and memory, but it has also been demonstrated that it interferes with working memory. Impairment of cognitive function in various neurodegenerative disorders is accompanied by profound reduction and/or elevation of KYNA metabolism. The view that enhancement of CNS KYNA levels could underlie cognitive decline is supported by the increased KYNA metabolism in Alzheimer's disease, by the increased KYNA metabolism in down's syndrome and the enhancement of KYNA function during the early stage of Huntington's disease. Kynurenic acid is the only endogenous N-methyl-D-aspartate (NMDA) receptor antagonist identified up to now, that mediates glutamatergic hypofunction. Schizophrenia is a disorder of dopaminergic neurotransmission, but modulation of the dopaminergic system by glutamatergic neurotransmission seems to play a key role. Despite the NMDA receptor antagonism, kynurenic acid also blocks, in lower doses, the nicotinergic acetycholine receptor, i.e., increased kynurenic acid levels can explain psychotic symptoms and cognitive deterioration. Kynurenic acid levels are described to be higher in the cerebrospinal fluid (CSF) and in critical central nervous system (CNS) regions of schizophrenics as compared to controls. (PMID: 17062375, 16088227)