TNF and Alzheimer disease: To further assess the contribution of Ast-AD when immunostimulated to the abnormal amyloid status and inflammatory signaling molecules, we compared the release of sAPPβ (a product of the amyloidogenic pathway) by Ast-AD and Ast-Ctrl cells in the absence and in the presence of C1q + IL-1α + TNF-α, as schematized in Figure 8A. The release of sAPPβ was markedly and exclusively enhanced upon immunostimulation in Ast-AD cells vs. the other conditions (Figure 8B,C; p < 0.05), thus potentially contributing to its dissemination and harmful consequences in AD.