. 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.


    . Beta-amyloid-stimulated microglia induce neuron death via synergistic stimulation of tumor necrosis factor alpha and NMDA receptors. J Neurosci. 2005 Mar 9;25(10):2566-75. PubMed.

    . Abnormality of G-protein-coupled receptor kinases at prodromal and early stages of Alzheimer's disease: an association with early beta-amyloid accumulation. J Neurosci. 2004 Mar 31;24(13):3444-52. PubMed.

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    . TNF-alpha modulation for treatment of Alzheimer's disease: a 6-month pilot study. MedGenMed. 2006;8(2):25. PubMed.

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