SOD1 and Parkinson disease: On the contrary, SOD1 glycosylation (13 residues; 1.9-to-6.7-fold increase) and deamidation (5 residues; 1.6-to-2.9-fold elevation) were upregulated in the OCx of Parkinson disease patients compared with controls (Supplementary Fig. 3; Supplementary Table 7), which likely act to suppress the accumulation of disSOD1 in this brain region by improving protein folding, trafficking and turnover [71, 97].