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

According to a preprint abstract, researchers have found that the accumulation of Aβ, a protein associated with Alzheimer's disease, leads to dysfunction in the nuclear pore complex (NPC) in neurons. The NPC is responsible for regulating the movement of macromolecules across the nuclear envelope, and its impairment has been observed in various neurodegenerative disorders. The dysfunction of the NPC in Alzheimer's disease neurons makes them more susceptible to inflammation-induced necroptosis, a programmed cell death pathway. This research suggests that the NPC could be a potential therapeutic target for Alzheimer's disease. However, it is important to note that this preprint has not yet undergone peer review. [Extracted from the article]