On the other hand, we also found pathophysiological components of T2DM that could lead to PD such as metabolic inflammation [31], downregulation of dopamine in the nigrostriatal pathway [32–34], long-term hyperglycemia condition [35], decrease in the expression of PGC-1α (peroxisome proliferator-activated receptor-gamma coactivator-1α) [36–39], increase in the expression of PED/PEA-15 (phosphoprotein enriched in diabetes/phosphoprotein enriched in astrocytes 15 protein) [40], increased methylglyoxal levels [41, 42], and the formation of alpha-synuclein amyloid fibrils [17]. This evidence concerns the gene SNCA and Parkinson disease.