Nevertheless, the tissue damage due to the toxic age-related proinflammatory state may participate in the onset of Aβ agglomeration, which is consistent with the increased incidence of AD in patients with increased cytokines due to polymorphisms in genes of plaque associated cytokines, namely TNF-α, IL-1, IL-6, and acute phase proteins (α1-antichymotrypsin) [31,68,69,70]. Here, IL1B is linked to Alzheimer disease.