Notably, NCT and Nup98 defects could be rescued in FTD-tau transgenic mice by reducing soluble transgenic tau, suggesting a new pathogenic mechanism, in which the somatodendritic accumulation of tau enables abnormal interactions of tau with components of the NPC and leads to NCT impairment, which is further accompanied by cytoplasmic aggregation of nucleoporins. This evidence concerns the gene MAPT and frontotemporal dementia.