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TNFα plus IFNγ induce the production of Alzheimer β‐amyloid peptides and decrease the secretion of APPs

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 β‐am‐yloid precursor protein (βAPP). We show that the combination of tumor necrosis factor α and interferon γ triggers the production of β‐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.—Blasko, I., Marx, F., Steiner, E., Hartmann, T., Grubeck‐Loebenstein, B. TNFα plus IFNγ induce the production of Alzheimer β‐amyloid peptides and decrease the secretion of APPs. FASEB J. 13, 63–68 (1999)