Our collective data clearly demonstrate that upregulation of O-GlcNAcylation through GlcN supplementation or virus-mediated OGT overexpression rescues both functional and pathological PD phenotypes induced by 6-OHDA, supporting the emerging concept that O-GlcNAcylation plays a beneficial role in promoting cell survival and protecting neurons from various cellular stresses [39]. This evidence concerns the gene OGT and Parkinson disease.