Increased OPC proliferation has been observed in a mouse model of ALS expressing human mutant SOD1 and appears prevalent in ALS patient post mortem samples 3, 5. We, therefore, examined whether control and C9ORF72 patient‐derived OPCs differed in their rates of proliferation using proliferative markers EdU and Ki67. Analysis of PDGFRα+/EdU+ and PDGFRα+/EdU+/Ki67+ however showed no consistent difference between control and patient‐derived lines (Supporting Information Fig. 1D).
