Recent experiments, using diabetes-induced MitoPark mice, showed that the acquisition of IR phenotype in these animals results in mitochondrial dysfunction by suppressing PGC-1α expression, promoting the upregulated ROS production and oxidative stress, as well as the upregulated expression of phosphorylated α-synuclein (SNCA) [41], a key constituent of Lewy bodies (LB) [42]. Here, SNCA is linked to diabetes mellitus.