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. Here, APP is linked to amyloidosis.