Our previous in vitro studies showed that LM11A-31 inhibited Aβ-induced degenerative signaling (including excess activation of GSK3β, cdk5 and JNK), activated survival signaling that is compromised in AD (AKT and NFκB), and prevented excess tau phosphorylation in a p75NTR-dependent manner [13]. This evidence concerns the gene NGFR and Alzheimer disease.