Tau-FG-nucleoporin98 interaction and impaired nucleocytoplasmic transport in Alzheimer's disease

An emerging pathophysiology associated with the neurodegenerative Alzheimer's disease (AD) is the impairment of nucleocytoplasmic transport (NCT). The impairment can originate from damage to the nuclear pore complex (NPC) or other factors involved in NCT. The phenylalanine-glycine nucleoporins (FG-Nups) form a crucial component of the NPC, which is central to NCT. Recent discoveries have highlighted that the neuropathological protein tau is involved in direct interactions with the FG-Nups and impairment of the NCT process. Targeting such interactions may lead to the identification of novel interaction inhibitors and offer new therapeutic alternatives for the treatment of AD. This review highlights recent findings associated with impaired NCT in AD and the interaction between tau and the FG-Nups.

Automated summary

An emerging pathophysiology associated with Alzheimer's disease (AD) is the impairment of nucleocytoplasmic transport (NCT), which can result from damage to the nuclear pore complex (NPC) or other factors involved in NCT. Recent findings highlight the involvement of tau protein in direct interactions with phenylalanine-glycine nucleoporins (FG-Nups) and the resulting impairment of NCT in AD. Targeting these interactions may lead to the identification of novel inhibitors and offer new therapeutic alternatives for AD treatment.