Nonetheless, AD patients showed a massive decline in the transcriptional levels of the autophagy initiator Beclin-1 during early stages of AD and strategies that have aimed to enhance the degree of autophagy, such as the lentivirus-mediated expression of Beclin 1 or the autophagy-inducing blockage of mTor by rapamycin, have been successful in the purging of Aβ and Tau pathology in in vitro and in vivo models of AD (Pickford et al., 2008; Jaeger et al., 2010; Spilman et al., 2010; Majumder et al., 2011). Here, BECN1 is linked to Alzheimer disease.