The possible reasons for this phenomenon are as follows: (1) the inflammatory responses in AD brains are mainly regulated by the TLR-NF-κB signaling, not the TLR-TRIF-IRF-3 signaling; (2) the time point of detection was later; and (3) the Poly (I:C)-induced increase in IRF-3 in the early stage returned to normal levels, while NF-κB was persistently activated in AD brains. Here, NFKB1 is linked to Alzheimer disease.