Based on the above reports (evidence which support the usage of celecoxib with mouse experiments and evidence how the normal physiological mechanism in human brain is perturbed upon administration of celecoxib), we can conclude that even though celecoxib modulates MTOR toward neuronal protection to limit the toxicity of Aβ and consequently neuroinflammation in AD, we may also require targeting TSC2, AKT, and AMPK simultaneously. This evidence concerns the gene AKT1 and Alzheimer disease.