However, cytosolic ubiquitinated TDP-43 inclusion was not observed in the core ischemic region [52,53], suggesting that the cytoplasmic redistribution of insoluble TDP-43 without the formation of TDP-43 inclusions is a hallmark of ischemic stroke and that TDP-43 pathology has a distinct molecular signature after stroke, compared to chronic neurodegenerative TDP-43 proteinopathies, such as FTLD and ALS. Here, TARDBP is linked to ischemic stroke.