In addition, investigations using transgenic mice and COX-2selective inhibitors have demonstrated that suppression of COX-2 activityin both AD and MS mouse models attenuates neuropathological hallmarksof these diseases such as Aβ plaque deposition, tau phosphorylation,and myelin degeneration, while also improving performance mice inmotor and cognitive tasks.13−18. The gene discussed is PTGS2; the disease is Alzheimer disease.