It is remarkable (i) that human microbes that produce amyloids such as CsgA and curli, and the Aβ42 peptides that accumulate in AD, are recognized by the same TLR2/TLR1 immune sensor-receptor system of the 13 different TLR-type receptors available; and (ii) that they direct the same up-regulation of IL-17A- and IL-22-mediated pro-inflammatory-signaling (Rapsinski et al., 2013; Zhang et al., 2013; Yu and Ye, 2014). This evidence concerns the gene TLR1 and Alzheimer disease.