In addition, recent studies implicate AMPK activity in the pathogenesis of AD as a regulator of both tau phosphorylation and amyloidogenesis (Thornton et al., 2011; Vingtdeux et al., 2011), and the contribution of AMPKα activation has been assessed in mouse primary neurons where an increase of tau phosphorylation at multiple sites upon endogenous AMPK activation has been reported, whereas AMPK inhibition led to a rapid decrease of tau phosphorylation (Domise et al., 2016). The gene discussed is PRKAA1; the disease is Alzheimer disease.