Quinolinic acid, the inescapable neurotoxin

Gilles J. Guillemin*

*Corresponding author for this work

Research output: Contribution to journalReview article

229 Citations (Scopus)

Abstract

Over the last two decades, evidence for the involvement of quinolinic acid (QUIN) in neuroinflammatory diseases has been exponentially increasing. Within the brain, QUIN is produced and released by infiltrating macrophages and activated microglia, the very cells that are prominent during neuroinflammation. QUIN acts as an agonist of the N-methyl-d-aspartate receptor and as such is considered to be a brain endogenous excitotoxin. Since the discovery of the excitotoxic activity of QUIN in the early 1980s, several other cytotoxic mechanisms have been identified. We know today that QUIN acts as a neurotoxin, gliotoxin, proinflammatory mediator, pro-oxidant molecule and can alter the integrity and cohesion of the blood-brain barrier. This paper aims to review some of the most recent findings about the effects of QUIN and its mode of action. Quinolinic acid (QUIN) is a brain endogenous excitotoxin produced by infiltrating macrophages and activated microglia during neuroinflammation. QUIN acts as a neurotoxin; gliotoxin, proinflammatory mediator, pro-oxidant molecule and can alter the integrity and cohesion of the blood-brain barrier. We review here some of the most recent findings about the effects of QUIN and its mode of action

Original languageEnglish
Pages (from-to)1356-1365
Number of pages10
JournalFEBS Journal
Volume279
Issue number8
DOIs
Publication statusPublished - Apr 2012
Externally publishedYes

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