Mitochondrial dysfunction has been observed in α-Synucleinopathy animal models and post-mortem human brains consequent to a-Synuclein accumulation and Actin reorganization through Spectrin and altered Drp1 localization; Drp1 overexpression in animal models was sufficient to rescue motor deficit and mitochondrial homeostasis (Figure 6b) [201]. This evidence concerns the gene SNCA and synucleinopathy.