Consistent withprevious observations in BV-2 cells (Figure 3F), we observed significant reduction inthe mRNA level of proinflammatory cytokines, such as TNF-α,IL-1β and IL-6, in the cortex and hippocampus of the 5xFAD mice(Figure 5C–D).Collectively, these data suggest that PRZ-18002 alleviates neuroinflammationand pathophysiological hallmarks of AD, such as cognitive impairmentand accumulation of Aβ, via inducing selective degradation ofp-p38 and thereby downregulating proinflammatory signaling pathway. The gene discussed is IL6; the disease is Alzheimer disease.