This is the case for the amyloid-beta peptide and tau/phosphorylated tau for Alzheimer’s disease (Pérez et al., 2019), alpha-synuclein for Parkinson’s disease (Longoni et al., 2019), misfolded/mutant SOD1, TDP-43 and its pathological-related C-terminal fragments (of 35 kDa and 25 kDa) and FUS for ALS (Basso and Bonetto, 2016; Iguchi et al., 2016; Hanspal et al., 2017; Sproviero et al., 2018), and progranulin, TDP-43, and C9orf72 DPRs for FTD and ALS-FTD (Benussi et al., 2016; Iguchi et al., 2016; Westergard et al., 2016). This evidence concerns the gene C9orf72 and amyotrophic lateral sclerosis.