In a mouse model of AD, microglia showed a reduction in N-AS generation, leading to decreased acetyl-S565 COX2 and SPMs production; mouse treatment with N-AS increases acetylated COX-2 and N-AS-triggered SPMs in microglia, leading to resolution of neuroinflammation, an increase in microglial phagocytosis, and improved memory [99]. This evidence concerns the gene PTGS2 and Alzheimer disease.