Aβ-driven nuclear pore complex dysfunction alters activation of necroptosis proteins in a mouse model of Alzheimer's disease.

ABSTRACT: The emergence of Aβ pathology is one of the hallmarks of Alzheimer's disease (AD), but the mechanisms and impact of Aβ in progression of the disease is unclear. The nuclear pore complex (NPC) is a multi-protein assembly in mammalian cells that regulates movement of macromolecules across the nuclear envelope; its function is shown to undergo age-dependent decline during normal aging and is also impaired in multiple neurodegenerative disorders. Yet not much is known about the impact of Aβ on NPC function in neurons. Here, we examined NPC and nucleoporin (NUP) distribution and nucleocytoplasmic transport using a mouse model of AD (App^{NL-G-F/NL-G-F}) that expresses Aβ in young animals. Our studies revealed that a time-dependent accumulation of intracellular Aβ corresponded wit

SUBMITTER: Bansal VA 

PROVIDER: S-EPMC11936419 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature