Via EurekAlert!: "We still have a very poor understanding of the mechanisms behind cell aging. It has been known for some time that the gene expression profile of an aging cell changes and somehow is linked to age-related diseases, but no one really knows why. Our work could provide an explanation for why we observe age-dependent defects in cells ... Like guards controlling access to a gated community, nuclear pore complexes are communication channels that regulate the passage of proteins and RNA to and from a cell's nucleus ... Do they turn over in nondividing cells, or do they remain in place for the life of the cell? Because most of the cells in our body are not actively dividing, the answer would have implications for aging and age-related diseases. ... Many of the neurons in the cortex area of the brain are as old as we are; they are nondividing for a very long time. ... What they found was that in aging cells, one of the proteins composing the scaffold structure becomes damaged, and the permeability barrier deteriorates; molecules that should be restricted to the cytoplasm invade the nucleus. ... Because some cells live for a long time, the accumulation of damage in the long-lived nuclear pore complexes can impair their function and have important consequences for cell homeostasis and survival. It may also play a significant role in the aging process."