Several mechanisms are proposed to induce the BACE1 elevation associated with AD; for example, caspase-3-dependent inactivation of GGA3 leading to decreased lysosomal degradation of BACE1 [38], [39], increased phosphorylation of the translation initiation factor eIF2α [33], transcriptional upregulation mediated by p25/cyclin-dependent kinase 5 [40], [41] and changes in microRNA expression profiles [42], [43]. This evidence concerns the gene EIF2A and Alzheimer disease.