GRN and frontotemporal dementia: Given earlier evidence that GRN mutations interrupt lysosomal lipid catabolism, Marian et al. [124] compared lipid metabolism across GRN-FTD and C9orf72-FTD postmortem brains, revealing pronounced myelin lipid loss, cholesterol ester accumulation, and fatty acid metabolism disruption that was more pronounced in GRN-FTD, consistent with its more severe white matter pathology.