However, in the later neurotoxic stages of AD, microglial activation promotes the release of proinflammatory cytokines such as interleuking-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α), which in turn induce astrocyte transformation into a neurotoxic A1 phenotype [47,48] (Figure 2). This evidence concerns the gene IL1B and Alzheimer disease.