Although overexpression of IL-6 or IL-1β produced inconclusive results in terms of amyloid load and tau accumulation in mouse AD models [3, 4], two recent studies in mice showed that IL-12 and IL-23 was upregulated in the senescent/AD brain, and experimentally induced inactivation of the common IL-12 and IL-23 subunit p40 reduced amyloid load and improved cognitive functions [5, 6]. This evidence concerns the gene IL6 and Alzheimer disease.