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Pathways to neuronal injury and apoptosis in HIV-associated dementia

Author

Listed:
  • Marcus Kaul

    (Center for Neuroscience and Aging Research, The Burnham Institute)

  • Gwenn A. Garden

    (University of Washington)

  • Stuart A. Lipton

    (Center for Neuroscience and Aging Research, The Burnham Institute)

Abstract

Human immunodeficiency virus-1 (HIV-1) can induce dementia with alarming occurrence worldwide. The mechanism remains poorly understood, but discovery in brain of HIV-1-binding sites (chemokine receptors) provides new insights. HIV-1 infects macrophages and microglia, but not neurons, although neurons are injured and die by apoptosis. The predominant pathway to neuronal injury is indirect through release of macrophage, microglial and astrocyte toxins, although direct injury by viral proteins might also contribute. These toxins overstimulate neurons, resulting in the formation of free radicals and excitotoxicity, similar to other neurodegenerative diseases. Recent advances in understanding the signalling pathways mediating these events offer hope for therapeutic intervention.

Suggested Citation

  • Marcus Kaul & Gwenn A. Garden & Stuart A. Lipton, 2001. "Pathways to neuronal injury and apoptosis in HIV-associated dementia," Nature, Nature, vol. 410(6831), pages 988-994, April.
    • Handle: RePEc:nat:nature:v:410:y:2001:i:6831:d:10.1038_35073667
    DOI: 10.1038/35073667
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    Cited by:

    1. Romain Volmer & Céline Monnet & Daniel Gonzalez-Dunia, 2006. "Borna Disease Virus Blocks Potentiation of Presynaptic Activity through Inhibition of Protein Kinase C Signaling," PLOS Pathogens, Public Library of Science, vol. 2(3), pages 1-9, March.
    2. Cristina Granziera & Alessandro Daducci & Samanta Simioni & Matthias Cavassini & Alexis Roche & Djalel Meskaldji & Tobias Kober & Melanie Metral & Alexandra Calmy & Gunther Helms & Bernard Hirschel & , 2013. "Micro-Structural Brain Alterations in Aviremic HIV+ Patients with Minor Neurocognitive Disorders: A Multi-Contrast Study at High Field," PLOS ONE, Public Library of Science, vol. 8(9), pages 1-10, September.

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