OGT and tauopathy: Moreover, it has been suggested that O-GlcNAcylation modification, mediated by OGT, exerts a neuroprotective function in neurodegenerative diseases by interfering with the production of toxic aggregates formed with α-synuclein, tau, amyloid precursor protein (APP) or neurofilament M (NFM) [9,10,11], and the cycling of O-GlcNAcylation was shown to modulate neurodegenerative phenotypes in Caenorhabditis elegans, such as amyloid β-peptide, polyglutamine, and tauopathy expansion.