Since autophagy is the sole mechanism of the cell for the bulk degradation of organelles and long-lived proteins (Dunn, 1994; Klionsky and Emr, 2000; Kuma et al., 2004), and since AD and tauopathies are deficient in this function (Cataldo et al., 1996; Funderburk et al., 2010), we were interested to test whether TFEB, as a master regulator of lysosome biogenesis, could ameliorate the pathological hallmarks of paired-helical filament (PHF)-tau in a mouse model. Here, MAPT is linked to Alzheimer disease.