Notably, recent studies have shown that stimulation of synaptic activity can protect against pathological Tau accumulation/aggregation via autophagy-lysosomal degradation by enhancing nuclear translocation of TFEB in cellular and mouse models of tauopathies, which provides encouraging support for the use of synaptic stimulation against autophagy and lysosomal defects in AD and other tauopathies [378,379]. The gene discussed is TFEB; the disease is tauopathy.