While the mechanism behind this dysregulation is still unclear, an overexpression of a mutant form of the gene encoding alpha-synuclein (A53T-SNCA) linked to familial cases of PD has been shown to increase triacylglycerol levels and associated with increased activity of acyl-CoA synthetase, which catalyzes fatty acyl-CoA formation as a substrate for β-oxidation47. This evidence concerns the gene SNCA and Parkinson disease.