IngentaConnect Preventive actions of a synthetic antioxidant in a novel animal m...
IngentaConnect Preventive actions of a synthetic antioxidant in a novel animal m...: "Preventive actions of a synthetic antioxidant in a novel animal model of AIDS dementia
Authors: Bjugstad K.B.; Flitter W.D.; Garland W.A.; Su G.C.; Arendash G.W.1
Source: Brain Research, Volume 795, Number 1, 8 June 1998, pp. 349-357(9)
Publisher: Elsevier Science
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Abstract:
Accumulating evidence indicates that the mechanism for causing AIDS dementia complex (ADC) involves the release of damaging inflammatory-related agents by HIV-infected microglia in the brain resulting in CNS oxidative damage. One such agent, tumor necrosis factor alpha (TNF-alpha) is consistently elevated in the brains of ADC patients compared to non-demented HIV patients. To model this aspect of ADC in rats, chronic ventricular infusions of TNF-alpha were given and found to induce several aspects of ADC, including weight loss, learning/memory impairment, enlarged lateral ventricles, and increased apoptosis. Concurrent oral treatment with the antioxidant CPI-1189 prevented all of these TNF-alpha induced effects. The results support TNF-alpha as a key toxic agent in ADC and provide the first in vivo evidence that chronic treatment with a synthetic antioxidant may protect HIV-infected patients against ADC. Our findings may also have implications in other neurological diseases where brain TNF-alpha levels are elevated and inflammation/oxidative stress is suspected to be a contributing cause, such as Alzheimer's disease and Parkinson's disease.
Keywords: AIDS dementia complex; Inflammation; '>Tumor necrosis factor-alpha; Antioxidant; Apoptosis; Memory impairment"
Authors: Bjugstad K.B.; Flitter W.D.; Garland W.A.; Su G.C.; Arendash G.W.1
Source: Brain Research, Volume 795, Number 1, 8 June 1998, pp. 349-357(9)
Publisher: Elsevier Science
< previous article View Table of Contents
full text options
Abstract:
Accumulating evidence indicates that the mechanism for causing AIDS dementia complex (ADC) involves the release of damaging inflammatory-related agents by HIV-infected microglia in the brain resulting in CNS oxidative damage. One such agent, tumor necrosis factor alpha (TNF-alpha) is consistently elevated in the brains of ADC patients compared to non-demented HIV patients. To model this aspect of ADC in rats, chronic ventricular infusions of TNF-alpha were given and found to induce several aspects of ADC, including weight loss, learning/memory impairment, enlarged lateral ventricles, and increased apoptosis. Concurrent oral treatment with the antioxidant CPI-1189 prevented all of these TNF-alpha induced effects. The results support TNF-alpha as a key toxic agent in ADC and provide the first in vivo evidence that chronic treatment with a synthetic antioxidant may protect HIV-infected patients against ADC. Our findings may also have implications in other neurological diseases where brain TNF-alpha levels are elevated and inflammation/oxidative stress is suspected to be a contributing cause, such as Alzheimer's disease and Parkinson's disease.
Keywords: AIDS dementia complex; Inflammation; '>Tumor necrosis factor-alpha; Antioxidant; Apoptosis; Memory impairment"
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