Figure 5.

A schematic representation of the selected mechanisms in the pathogenesis of PD. The higher levels of α-synuclein (SNCA) can accumulate to form oligomers, insoluble fibrils, and ultimately “Lewy bodies”, triggering apoptosis within the neural cells. α-synuclein can relocate DNMT1 from the nucleus into the cytoplasm of neural cells and depletes the nuclear reservoir of this DNMT, thereby leading to the hypomethylation and associated with the upregulation of many PD-related genes, including SNCA and CYP2E1. The increased activity of the CYP2E1 gene may contribute to the degeneration of dopaminergic neurons by the formation of toxic metabolites. The light green colors highlighted hypomethylated genes. CYP2E1: cytochrome P450 2E1; SNCA (α-Syn): synuclein alpha.