Serum from Parkinson’s disease patients presents excess of protein halogenation and nitrosylation, with anomalous nitrosylation of serum α-synuclein as potentially etiological factor

Background Halogenative and nitrosative stress are two types of oxidative stress that have been proposed as pathogenic mechanisms in Parkinson’s disease (PD). They can be caused by over-stimulation of phagocytes. We hypothesize that maintained phagocyte overstimulation leads to both halogenative and nitrosative stress in Parkinson’s disease, which are present in serum and cerebrospinal fluid of patients. These types of oxidative stress could modify proteins related to the pathogenesis of Parkinson’s disease.