GRN and Alzheimer disease: Hence, there is strong genetic and cell biological support for the view that disturbances in lysosomal and autophagosomal function, leading to accumulations of unwanted, potentially neurotoxic proteins, may underpin the pathological changes which characterize FTLD‐TDP, and particularly so in those cases bearing mutations in GRN. With this in mind, we have investigated lysosomal and autophagosomal function in 60 cases of FTLD, and in others with Alzheimer's disease (AD) or without significant pathology, these acting as neurodegenerative and healthy controls respectively.