SOD1 and Parkinson disease: Among physiological SOD1 PTMs, we observed a striking decrease in SOD1 O- and N-glycosylation and acetylglucosamination across 4 serine and asparagine residues (1.6-to-79.1-fold decrease) in the SNc of Parkinson disease patients compared with controls (Fig. 1e, f; Supplementary Table 6), which would be expected to negatively impact nascent SOD1 protein folding and trafficking in this region [68].