Cell death in hiv dementia

M. P. Mattson, N. J. Haughey, A. Nath

Research output: Contribution to journalReview article

Abstract

Many patients infected with human immunodeficiency virus type-1 (HIV-1) suffer cognitive impairment ranging from mild to severe (HIV dementia), which may result from neuronal death in the basal ganglia, cerebral cortex and hippocampus. HIV-1 does not kill neurons by infecting them. Instead, viral proteins released from infected glial cells, macrophages and/ or stem cells may directly kill neurons or may increase their vulnerability to other cell death stimuli. By binding to and/or indirectly activating cell surface receptors such as CXCR4 and the N-methyl-D-aspartate receptor, the HIV-1 proteins gp120 and Tat may trigger neuronal apoptosis and excitotoxicity as a result of oxidative stress, perturbed cellular calcium homeostasis and mitochondrial alterations. Membrane lipid metabolism and inflammation may also play important roles in determining whether neurons live or die in HIV-1-infected patients. Drugs and diets that target oxidative stress, excitotoxicity, inflammation and lipid metabolism are in development for the treatment of HIV-1 patients.

Original languageEnglish (US)
Pages (from-to)893-904
Number of pages12
JournalCell death and differentiation
Volume12
DOIs
StatePublished - Jan 1 2005

Keywords

  • AIDS
  • Apoptosis
  • Cognitive impairment
  • Inflammation
  • Lipid rafts

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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