A study that used a mixture of Aβ-based AD models, including hippocampal primary neurons, murine brain slices and monkeys, demonstrated that Exendin-4, in a GLP-1R-dependent manner, diminished the levels of phospho-Ser312/ Ser616/Ser636 IRS-1, enhanced the activating Tyr465 phosphorylation of IRS-1 and restored (JNK-associated) axonal transport deficiencies as well as spatial learning and memory retainment (Bomfim et al., 2012). This evidence concerns the gene GLP1R and Alzheimer disease.