The pathobiology we postulate in PD follows: FFAs promote PGC−1α promoter methylation, a decline in PGC−1α levels and consequent down-regulation of an array of genes involved in energy metabolism, mitochondrial biogenesis [46–48], respiratory function [49], anti-inflammation [7, 50] and anti-oxidant defense [7, 51]. This evidence concerns the gene PPARGC1A and Parkinson disease.