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Involvement of quinolinic acid in AIDS dementia complex.

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.
AuthorsGilles J Guillemin, Stephen J Kerr, Bruce J Brew
JournalNeurotoxicity research (Neurotox Res) Vol. 7 Issue 1-2 Pg. 103-23 ( 2005) ISSN: 1029-8428 [Print] United States
PMID15639803 (Publication Type: Journal Article, Review)
Chemical References
  • Quinolinic Acid
Topics
  • AIDS Dementia Complex (etiology, metabolism, pathology)
  • Animals
  • Humans
  • Quinolinic Acid (chemistry, physiology, toxicity)

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