However, SCF’s mechanism appears to be more nuanced, as it prevented the pathological increase in COX-2 expression seen in the AD-Con group while preserving the constitutive COX-2 expression necessary for the prostaglandin E2/cAMP pathway and the p-PKA-p-CREB-BDNF axis, which are essential for neuronal survival and memory function [34]. This evidence concerns the gene KITLG and Alzheimer disease.