Neurotoxicity Research

, Volume 7, Issue 1–2, pp 103–123 | Cite as

Involvement of quinolinic acid in aids dementia complex

  • Gilles J. Guillemin
  • Stephen J. Kerr
  • Bruce J. Brew
Article

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.

Keywords

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

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Copyright information

© Springer 2005

Authors and Affiliations

  • Gilles J. Guillemin
    • 1
    • 2
  • Stephen J. Kerr
    • 1
    • 4
    • 5
  • Bruce J. Brew
    • 1
    • 3
  1. 1.Centre for ImmunologySt Vincent’s HospitalSydneyAustralia
  2. 2.School of MedicineUniversity of New South WalesAustralia
  3. 3.Departments of Neurology and HIV MedicineSt Vincent’s HospitalSydneyAustralia
  4. 4.National Centre in HIV Epidemiology and Clinical ResearchSydneyAustralia
  5. 5.The HIV-Netherlands-Australia-Thailand Research CollaborationBangkokThailand

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