Recognizing that disSOD1 pathology may result from either the disruption of these modifications or the introduction of atypical PTMs, we employed proteomic mass spectrometry to profile the post-translational fingerprint of SOD1 protein immunoprecipitated from the post-mortem SNc and OCx of Parkinson disease patients and age-matched controls [87]. This evidence concerns the gene SOD1 and Parkinson disease.