Administration of an antioxidant or p38 MAP kinase inhibitor to Tg Sh3gl2/mAPP mice or hippocampal neurons alleviated LTP decline and synaptic loss, increased synaptic vesicle recycling, and improved learning and memory; these results indicate that blocking EP-involved ROS production and p38 MAP kinase activation restores synaptic and cognitive function in an model of AD-expressing EP/Aβ. This evidence concerns the gene MAPK14 and Alzheimer disease.