In addition, increasing evidence points to prion-like transmission as a mechanism underlying the development of many proteinopathies, driven by α-syn, HTT, SOD1, Tau, TDP-43, which can be uptake by the cytoplasm of acceptor cells from the brain (i.e., phagocytic microglia; Bayer, 2015; Pearce et al., 2015; Jo et al., 2020; Holec et al., 2022; Trist et al., 2022). Here, TARDBP is linked to proteostasis deficiencies.