In light of our previous data showing that reduced BVR-A levels or impaired BVR-A activity parallels the hyper-activation of mTOR in both human brain tissue [21,27,36] and in animal models of AD [12,19] or aging [23], the main goal of this study was to evaluate age-associated alterations of mTOR and autophagic flux in the cerebral cortex of a knock-out mouse model for BVR-A (BVR-A−/−). The gene discussed is BLVRA; the disease is Alzheimer disease.