IL1B and Alzheimer disease: On the one hand, they activate many pro-inflammatory signaling networks, including the ubiquitous innate pro-inflammatory mediators, interleukin (IL)-1β and IL-6, which, along with tumor necrosis factor (TNF)-α, which are known to increase amyloidogenic pathology in AD (Erta et al., 2012; Brough and Denes, 2015; Su et al., 2016; Liu and Quan, 2018; Gonzalez Caldito, 2023).