Thus, accumulation of Aβ in DAM drives neuroinflammatory responses by producing a plethora of proinflammatory mediators (e.g., TNF-α, IL-1, and IL-6) and neurotoxic molecules (e.g., nitric oxide, superoxide), leading to accelerated AD progression (Block et al., 2007; Hickman et al., 2008; Smith et al., 2012; Deczkowska et al., 2018). Here, IL1B is linked to Alzheimer disease.