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TNFalpha plus IFNgamma induce the production of Alzheimer beta-amyloid peptides and decrease the secretion of APPs.

I Blasko·F Marx·E Steiner·T Hartmann·B Grubeck-Loebenstein
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Abstract

The appearance of inflammatory markers associated with amyloid plaques indicates a state of chronic inflammation in Alzheimer's disease (AD). Multiple epidemiological studies also suggest that patients taking anti-inflammatory drugs have a decreased risk of developing AD. Here we present evidence that inflammatory cytokines can alter the metabolism of the beta-amyloid precursor protein (betaAPP). We show that the combination of tumor necrosis factor alpha and interferon gamma triggers the production of beta-amyloid peptides and inhibits the secretion of soluble APPs by human neuronal and extraneuronal cells. The results demonstrate a new mechanism by which inflammatory components can exacerbate the fundamental pathology in AD.

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Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCells, CulturedHumansInterferon-gammaRecombinant ProteinsTime FactorsTumor Cells, CulturedTumor Necrosis Factor-alphaJournal ArticleResearch Support, Non-U.S. Gov't

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I Blasko, F Marx, E Steiner, T Hartmann, B Grubeck-Loebenstein. 1999. TNFalpha plus IFNgamma induce the production of Alzheimer beta-amyloid peptides and decrease the secretion of APPs.. https://doi.org/10.1096/fasebj.13.1.63

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