The favorable drug development profile of LM11A-24 and -31, their low nanomolar potency and receptor selectivity, and their unprecedented ability to simultaneously inhibit Aβ-induced activation of calpain/cdk5, GSK3β and c-Jun and to block Aβ impairment of synaptic function, each of which are current pharmaceutical candidate targets for AD therapeutics, establish an important new class of candidate small molecule compounds for AD therapeutics. This evidence concerns the gene JUN and Alzheimer disease.