In addition, the pathogenesis of PD may involve redox pathways such as androgen receptor-induced neurodegeneration, increased aggregation of α-synuclein and production of its oxidatively modified forms, degradation of quinone oxidoreductase 1 (NQO1), reduced activity of deglycase DJ-1, activation of the leucine-rich repeat kinase 2 (LRRK2) gene and impairment of tetrahydrobiopterin and tyrosine hydroxylase (TH) metabolism [21]. Here, TH is linked to Parkinson disease.