In Alzheimer’s disease (AD), mTORC1 overactivation and mitochondrial dysfunction contribute to neurodegeneration by impairing autophagy and mitophagy, increasing ROS production, reducing glucose utilization, disrupting energy metabolism, and promoting the accumulation of amyloid-beta oligomers as well as hyperphosphorylated and aggregated forms of pathological tau protein467 (Fig. 9). This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.