CREB1 and Alzheimer disease: Our findings revealed that SynCav1-transfected neurons exhibit enhanced phosphorylation of CaMKII (Thr-286) and CREB (Ser-133), both of which are downregulated in postmortem brains from AD patients and transgenic animal models.26–28 The temporal kinetics of CaMKII and CREB phosphorylation (i.e., activation) are transient cellular events,29–32 thus making it difficult to detect changes in expression of these signaling pathways in brain tissue in vivo several months after SynCav1 delivery.