Involvement of quinolinic acid in AIDS dementia complex

Gilles J. Guillemin, Stephen J. Kerr, Bruce J. Brew*

*Corresponding author for this work

Research output: Contribution to journalReview article

101 Citations (Scopus)

Abstract

Human immunodeficiency virus (HIV) infection is often complicated by the development of acquired immunodeficiency syndrome (AIDS) dementia complex (ADC). Quinolinic acid (QUIN) is an end product of tryptophan, metabolized through the kynurenine pathway (KP) that can act as an endogenous brain excitotoxin when produced and released by activated macrophages/microglia, the very cells that are prominent in the pathogenesis of ADC. This review examines QUIN's involvement in the features of ADC and its role in pathogenesis. We then synthesize these findings into a hypothetical model for the role played by QUIN in ADC, and discuss the implications of this model for ADC and other inflammatory brain diseases.

Original languageEnglish
Pages (from-to)103-123
Number of pages21
JournalNeurotoxicity Research
Volume7
Issue number1-2
DOIs
Publication statusPublished - 2005
Externally publishedYes

Keywords

  • AIDS
  • Chemokines
  • Cytokines
  • Dementia
  • HIV
  • Inflammatory brain disease
  • Kynurenic acid
  • Kynurenine
  • Macrophages
  • Microglia
  • N-methyl-D-aspartate
  • Quinolinic acid

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