Two possible scenarios have been proposed to explain the origin of α-synuclein in oligodendrocytes and the mechanisms underlying α-synuclein accumulation in GCIs present in MSA brains: either oligodendrocytes pathologically overexpress α-synuclein in the context of MSA (Asi et al., 2014) or they take up neuronally derived protein from their environment (Kisos et al., 2012; Konno et al., 2012; Rockenstein et al., 2012; Ettle et al., 2014; Pukass and Richter-Landsberg, 2014; Reyes et al., 2014; Pukass et al., 2015; Kaji et al., 2018). The gene discussed is SNCA; the disease is multiple system atrophy.