OBJECTIVES: Both genetic and environmental risk factors for Alzheimer's disease have been identified. The best established environmental risk factor, head trauma, is thought to act through the triggering of an inflammatory response. Another stimulus to an inflammatory response in the brain is AIDS. Whether there is an increased prevalence of beta/A4 amyloid deposits in the form of argyrophilic plaques in the brains of patients with AIDS has therefore been investigated. METHODS: The prevalence of argyrophilic amyloid plaques in the cerebral cortex of frontal and temporal lobes was compared in 97 cases of AIDS dying at ages 30-69 years with that in 125 age matched, non-HIV infected controls. RESULTS: In the control group, and in AIDS, the prevalence of plaques increased with age (p=0.005 and 0.048 respectively). There was a significantly greater prevalence of argyrophilic plaques in the AIDS group as a whole (29%) (p < 0.004) and in those in the fourth decade (18%) (p < 0.014) than in control subjects (13% and 0% respectively). CONCLUSION: There is a predisposition to argyrophilic plaque formation in the brain in AIDS. The findings support the view that a stimulus to an inflammatory response in the brain favours argyrophilic plaque formation. The clinical relevance of our findings is, as yet, unclear.
OBJECTIVES: Both genetic and environmental risk factors for Alzheimer's disease have been identified. The best established environmental risk factor, head trauma, is thought to act through the triggering of an inflammatory response. Another stimulus to an inflammatory response in the brain is AIDS. Whether there is an increased prevalence of beta/A4 amyloid deposits in the form of argyrophilic plaques in the brains of patients with AIDS has therefore been investigated. METHODS: The prevalence of argyrophilic amyloid plaques in the cerebral cortex of frontal and temporal lobes was compared in 97 cases of AIDS dying at ages 30-69 years with that in 125 age matched, non-HIV infected controls. RESULTS: In the control group, and in AIDS, the prevalence of plaques increased with age (p=0.005 and 0.048 respectively). There was a significantly greater prevalence of argyrophilic plaques in the AIDS group as a whole (29%) (p < 0.004) and in those in the fourth decade (18%) (p < 0.014) than in control subjects (13% and 0% respectively). CONCLUSION: There is a predisposition to argyrophilic plaque formation in the brain in AIDS. The findings support the view that a stimulus to an inflammatory response in the brain favours argyrophilic plaque formation. The clinical relevance of our findings is, as yet, unclear.
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