Growing evidence in murine models of AD have shown that rescuing brain GlcNAc levels, by OGA inhibition, reduces the levels of pathological tau [36, 106–108], limits APP amyloidogenic cleavage and Aβ accumulation [84, 85], boosts mitochondrial activity [28], and promotes the removal of toxic aggregates through macro-autophagy [90]. This evidence concerns the gene OGA and Alzheimer disease.