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Research Communications |
plus IFN
induce the production of Alzheimer ß-amyloid peptides and decrease the secretion of APPs
a Institute for Biomedical Aging Research of the Austrian Academy of Sciences, Innsbruck, Austria
b Department of Surgery, `Bezirkskrankenhaus' Hall, Austria
c Center for Molecular Biology Heidelberg (ZMBH), University of Heidelberg, Heidelberg, Germany
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 ß-amyloid precursor protein (ßAPP). We show that the combination of tumor necrosis factor and interferon triggers the production of ß-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. TNF plus IFN induce the production of Alzheimer ß-amyloid peptides and decrease the secretion of APPs. FASEB J. 13, 63–68 (1999)
Key Words: tumor necrosis factor • interferon • ßAPP • amyloid beta • Alzheimer's disease • glycosylation
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