Some of these mechanisms have been proposed to explain the increased accumulation of BACE1 observed in AD brains, including depletion of GGA3 [8], increased phosphorylation of translation factor eIF2α [40], increased expression of a non-coding anti-sense BACE1 transcript [41] and decreased expression of the BACE1 regulating microRNA’s, miR-29 and miR-107 [42, 43]. Here, GGA3 is linked to Alzheimer disease.