Using these animal α-synucleinopathy models, a variety of processes including phosphorylation and aggregation of α-synuclein (Chen and Feany, 2005; Lo Bianco et al., 2008; Chen et al., 2009; Kuwahara et al., 2012), mitochondrial dysfunction (Martin et al., 2006; Ordonez et al., 2018; Sarkar et al., 2020; Portz and Lee, 2021) and altered proteostasis (Auluck et al., 2002; Colla et al., 2012; Yan et al., 2019; Karim et al., 2020; Sarkar et al., 2021) have been implicated in α-synuclein neurotoxicity. This evidence concerns the gene SNCA and synucleinopathy.