Interestingly, rodent models of PD that overexpress human α-syn by mutations in the SNCA gene (e.g. the M83 strain, overexpressing mutant human A53T α-syn) do develop inclusions but the anatomical distribution is widely variable among animals and often coincides with areas of substantial neuroinflammation (Sacino et al., 2014; Lee et al., 2002; Dawson et al., 2011; Fares et al., 2016). This evidence concerns the gene SNCA and Parkinson disease.