The FASEB Journal · 1999 · 281 citations · 23 references
Life SciencesNeurobiologyNeuroscienceInflammationNeurodegenerationNeuroimmunologyAlzheimer DiseaseAmyloid FormationCytokine-mediated PathologyNeurodegenerative DiseasesNeurodegenerative DisordersNeuroinflammationAlzheimer Disease NeuroimmunologyAmyloid Beta AggregationAmyloid Beta PeptidesAmyloid Beta PlaquesAmyloid PlaquesNeuroinflammation In Alzheimer DiseaseNeuroinflammatory CytokinesTumor Necrosis Factor Therapy
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 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)
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Amyloid β-peptide is produced by cultured cells during normal metabolism
Christian Haass, Michael G. Schlossmacher, Albert Y. Hung et al. · Nature · 1992 · 1.9K citations