CREB1 and Alzheimer disease: Given these data, and the finding that synaptic deficits are the strongest correlates of cognitive dysfunction in AD (Terry et al., 1991), some have argued that therapeutic approaches directed at CREB signaling pathways constitute our best chance for treating AD (Teich et al., 2015), given the diverse role of CREB in neuronal function and positive neurobehavioral ramifications of its upregulation in AD models (De Felice et al., 2007; Saura and Valero, 2011; Teich et al., 2015).