Notably, in PD, excessive O-GlcNAcylation can activate mTOR, impair autophagic flux, and exacerbate α-synuclein accumulation (140), whereas in AD, O-GlcNAcylation promotes neuronal autophagy via mTOR-independent pathways, facilitating the clearance of pathological tau (141, 142). This evidence concerns the gene MTOR and Alzheimer disease.