Next, typical pro‐inflammatory mediators, including cluster of differentiation 86 (CD86), interleukin‐1β (IL‐1β), and tumor necrosis factor‐α (TNF‐α), were examined by RT‐PCR, CatE deficiency significantly reduced the expression of CD86, IL‐1β, and TNF‐α mRNA in the cortex of AD mice (Figure 4d‐f). This evidence concerns the gene CTSE and Alzheimer disease.