What is noteworthy is that (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; (ii) that all of these amyloids similarly direct increases in IL-17A- and IL-22-mediated pro-inflammatory signaling; and (iii) that Aβ42 peptides and CsgA do not share any common sequences of amino-acid, only considerable structural similarity in their PAMPs [80,81]. This evidence concerns the gene TLR1 and Alzheimer disease.