These cells are involved in normal, beneficial, neuroinflammatory responses; however, their uncontrolled and sustained activation in AD can increase levels of pro-inflammatory cytokines (e.g., TNF-α and interleukins (ILs), such as IL-1b, IL-6), reactive oxygen species and oxidative stress, and lead to secondary neuronal injury and death, which further activate inflammatory processes in a positive feedback loop [81]. This evidence concerns the gene IL6 and Alzheimer disease.