IL1B and Alzheimer disease: Overaccumulation of Aβ aggregates in DAM cells may also promote neuroinflammation through stimulating the expression of pro-inflammatory mediators (IL-1, IL-6, TNF-alfa) as well as other neurotoxic substances that can promote the progress of AD (e.g., nitric oxide and superoxide anion) (Block et al., 2007; Hickman et al., 2008; Smith et al., 2012; Deczkowska et al., 2018).