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- W1153204693 abstract "Publisher Summary This chapter reviews a series of experiments leading to a hypothesis that accounts at least in part for the neurotoxicity observed in the brains of AIDS patients. There is growing support for the idea of the existence of HIV- or immune-related toxins that lead indirectly to the injury or demise of neurons through a potentially complex web of interactions among macrophages (or microglia), astrocytes, and neurons. HIV-infected macrophages/ microglia or macrophages activated by HIV-1 envelope protein gp120 appear to secrete excitants/neurotoxins including plateletactivating factor, arachidonate, and its metabolites, and possibly cysteine, nitric oxide, and superoxide anion. In addition, interferon-γ (IFN-7) stimulation of macrophages induces release of the glutamate-like agonist quinolinate. Furthermore, HIV-infected macrophage production of cytokines, including TNF-α and ILl-β, contributes to astrogliosis. A final common pathway for neuronal susceptibility appears to be operative, similar to that observed in stroke, trauma, epilepsy, and several neurodegenerative diseases, possibly including Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis. This mechanism involves the activation of voltage-dependent Ca 2+ channels and N-methyl-D-aspartate (NMDA) receptor-operated channels. Therefore, it offers hope for future pharmacological intervention." @default.
- W1153204693 created "2016-06-24" @default.
- W1153204693 creator A5066753734 @default.
- W1153204693 date "1994-01-01" @default.
- W1153204693 modified "2023-10-09" @default.
- W1153204693 title "Ca2+, N-Methyl-d-Aspartate Receptors, and Aids-Related Neuronal Injury" @default.
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