Information de reference pour ce titreAccession Number: | 00003653-200607000-00001.
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Author: | Brabers, N. A. C. H.; Nottet, H. S. L. M.
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Institution: | Department of Virology, University Medical Center, Utrecht, the Netherlands (N. A. C. H. Brabers, H. S. L. M. Nottet).
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Title: | |
Source: | European Journal of Clinical Investigation. 36(7):447-458, July 2006.
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Abstract: | Human immunodeficiency virus-1 (HIV-1)-infected and immune-activated macrophages and microglia secrete neurotoxins. Two of these neurotoxins are the pro-inflammatory cytokines tumour necrosis factor-[alpha] (TNF-[alpha]) and interleukin-1[beta] (IL-1[beta]), which are thought to play a major role in inducing neuronal death. Both TNF-[alpha] and IL-1[beta] increase the permeability of the blood-brain barrier, through which subsequently HIV-infected monocytes can enter the brain. They both induce over-stimulation of the NMDA-receptor via several pathways, resulting in a lethal neuronal increase in Ca2+ levels. Additionally, TNF-[alpha] co-operates with several other proinflammatory mediators to enhance their toxic effects. Although most research has focused on the neurotoxic effects of TNF-[alpha] and IL-1[beta] in HAD, there is also evidence that these cytokines can be neuroprotective. In this paper the effect of TNF-[alpha] and IL-1[beta] on neuronal life and death in HAD is discussed.
Copyright (C) 2006 Blackwell Publishing Ltd.
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Author Keywords: | AIDS; cytokines; HIV-1-associated dementia; HIV-1; neurotoxicity..
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Language: | English.
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Document Type: | Overview: Review.
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Journal Subset: | Clinical Medicine.
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ISSN: | 0014-2972
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NLM Journal Code: | en3, 0245331
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