BACE1 and amyloidosis: More recently, this finding was confirmed in an in vitro model of energy deficiency and in vivo, in two APP transgenic mouse models of AD-like amyloidosis (that is, Tg2576 and 5xFAD mice) in which pharmacological energy deprivation promoted amyloidogenesis via BACE-1-dependent mechanism.9 However, since these mice do not develop tau neuropathology it remained to be fully investigated whether energy deprivation was also capable to alter tau metabolism and phosphorylation.