. Fibrillar beta-amyloid peptide Abeta1-40 activates microglial proliferation via stimulating TNF-alpha release and H2O2 derived from NADPH oxidase: a cell culture study. J Neuroinflammation. 2006;3:24. PubMed.

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  1. This article provides evidence implicating excess TNFα and microglial activation in the pathogenesis of Alzheimer disease, and specifically implicates Aβ1-40 in these mechanisms. This article, therefore, joins an increasing body of scientific evidence, including the work of Klegeris and McGeer in 1997, which suggests that amyloid-microglia-TNF interactions may be involved in the pathogenesis of AD. The authors conclude that their findings suggest that TNFα may be a potential target for AD treatment, which is, of course, concordant with our recent findings.

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