The results exhibited that in both primary neurons and NGF-stimulated PC-12 cells, FOXQ1 expression was reduced, whereas PTGS2 and CDK5 expressions were elevated in AD models (with Aβ1−42 treatment) compared with normal cells (without Aβ1−42 treatment), which indicated that Aβ1−42 treatment indeed decreased FOXQ1 expression but increased PTGS2 and CDK5 expressions. Here, FOXQ1 is linked to Alzheimer disease.