Using a blocking Ab specific for the p19 subunit of IL-23, we demonstrated that anti-IL-23p19 treatment significantly dampened the development of AAA (increase in AD = 94% or 0.48 mm, n = 8, SD = 14% or 0.07 mm in the IL-23p19 antagonist treatment group versus AD = 151% or 0.74 mm, n = 10, SD = 16% or 0.08 mm in the isotype control group, p < 0.001) (Fig. 3B,C). This evidence concerns the gene IL23A and Alzheimer disease.