Oxidative Medicine and Cellular Longevity / 2013 / Article / Tab 2

Review Article

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

Table 2

Alterations in QUIN levels presented in different neurodegenerative diseases and experimental models. Key references are shown in the quarter column.

Disease/modelQUIN levelsAssociated alterationsReference

Alzheimer↑ in demented patient
↑ in senile plaques
(i) IDO overexpression
(ii) KYNA
(iii) QUIN colocalizes with tau in cortical sections
(iv) ↑ QUIN/3-HK quotient in plasma
[25, 26, 91, 92]

A 1-42(i) IDO over-expression in microglia and macrophages[93]

Huntington(i) ↑ 3-HK[94]

Huntingtin transgenic mice↑ in YAC128 mice, HdhQ92/HdhQ111 knock-in mice(i) ↑ 3-HK[95]

Human immunodeficiency virus (HIV)↑ in CSF and serum of patients(i) Cytokines release
(ii) ↑ IDO
(iii) QUIN levels enhanced independent blood brain barrier breakdown

Suicide attempters↑ in CSF of suicide attempters(i) An increased QUIN/KYNA quotient[99]

Depression↑ QUIN expression in human brain during acute depressive episodes(i) Abnormal NMDA receptor function[100]

Autism↑ in CFS of patients(i) ↑ biopterin
(ii) neopterin

Amyotrophic lateral sclerosis↑ in CSF and serum of patients(i) ↑ TRP and L-KYN, human leukocyte antigen-DR
(ii) IDO over-expression

Experimental allergic encephalomyelitis, a model of multiple sclerosis↑ in the spinal cords of rats(i) ↑ in KMO activity and 3-HK levels[103, 104]

IDO: indolamine 2,3-dioxigenase, KYNA: kynurenic acid, QUIN: quinolinic acid, L-KYN: L-kynurenine, 3-HK: 3-hydroxykynurenine, TRP: tryptophan, and CSF: cerebrospinal fluid.

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