With the increase in levels of inflammatory biomarkers such as interleukin beta 1 (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) produced by overactivation of glial cells, including microglia, in the brains of AD patients, as well as the discovery of AD risk genes associated with innate immune function, neuroinflammation has become another crucial factor in the onset of AD [4]. This evidence concerns the gene IL6 and Alzheimer disease.