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Involvement of quinolinic acid in aids dementia complex

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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.

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Authors and Affiliations

  1. Centre for Immunology, St Vincent’s Hospital, Sydney, Australia

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

  2. School of Medicine, University of New South Wales, Australia

    Gilles J. Guillemin

  3. Departments of Neurology and HIV Medicine, St Vincent’s Hospital, Sydney, Australia

    Bruce J. Brew

  4. National Centre in HIV Epidemiology and Clinical Research, Sydney, Australia

    Stephen J. Kerr

  5. The HIV-Netherlands-Australia-Thailand Research Collaboration, Bangkok, Thailand

    Stephen J. Kerr

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  1. Gilles J. Guillemin
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Guillemin, G.J., Kerr, S.J. & Brew, B.J. Involvement of quinolinic acid in aids dementia complex. neurotox res 7, 103–123 (2005). https://doi.org/10.1007/BF03033781

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