Potentiation of excitotoxicity in HIV-1-associated Dementia and the significance of glutaminase

Nathan B. Erdmann, Nicholas P. Whitney, Jialin Zheng

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

HIV-1-associated Dementia (HAD) is a significant consequence of HIV infection. Although multiple inflammatory factors contribute to this chronic, progressive dementia, excitotoxic damage appears to be an underlying mechanism in the neurodegenerative process. Excitotoxicity is a cumulative effect of multiple processes occurring in the CNS during HAD. The overstimulation of glutamate receptors, an increased vulnerability of neurons, and disrupted astrocyte support each potentiate excitotoxic damage to neurons. Recent evidence suggests that poorly controlled generation of glutamate by phosphate-activated glutaminase may contribute to the neurotoxic state typical of HAD as well as other neurodegenerative disorders. Glutaminase converts glutamine, a widely available substrate throughout the CNS to glutamate. Inflammatory conditions may precipitate unregulated activity of glutaminase, a potentially important mechanism in HAD pathogenesis.

Original languageEnglish (US)
Pages (from-to)315-328
Number of pages14
JournalClinical Neuroscience Research
Volume6
Issue number5
DOIs
StatePublished - Dec 2006

Keywords

  • Excitotoxicity
  • Glutamate
  • Glutaminase
  • HIV-1-associated dementia
  • Macrophage
  • Neurodegeneration

ASJC Scopus subject areas

  • Neuropsychology and Physiological Psychology
  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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