Since patients with FTD-GRN and sporadic FTLD-TDP type A had similar lysosomal abnormalities that were generally limited to the degenerated frontal cortex and some of which were associated with levels of p-TDP-43 (Additional file 1: Fig. S2), we hypothesized that TDP-opathy, neurodegeneration, and/or neuroinflammation might be sufficient to drive these lysosomal abnormalities. The gene discussed is TARDBP; the disease is frontotemporal dementia.