Here we found that GEE significantly activated IGF1R with an upregulation of CaMKIV/ERK/HAT/BDNF signaling in the offspring of AD mice, while simultaneous inhibition of IGF1R by intraperitoneal injection of BMS-536924 (BMS) abolished the GEE-induced upregulation of CaMKIV and ERK activity, histone acetylation and BDNF expression (Fig. 5a,b). This evidence concerns the gene TMPRSS11D and Alzheimer disease.