More On Lamin A and "Normal" Aging

More on what researchers have learned from studying the biochemistry of progeria can be found at the Journal of Cell Biology: "Aging looks and feels like it is multifactorial: everything falls apart independently. ... [but] multiple hallmarks of cellular aging can be reversed by eliminating one aberrant splicing product of lamin A. The lamins form a structural cage on the interior surface of the nucleus. Lamin A has a long tail that is first farnesylated and then chopped off. In [progeria] an aberrant splicing event creates a lamin A that gets farnesylated but not cleaved. ... normal cells also have a small amount of this aberrant splice product. Although neither the splice product nor its protein product accumulate to higher levels with age, their effects do. As in [progeria] cells, older cells have decreased heterochromatin and other nuclear markers, and increased markers of unrepaired DNA damage. Many of these changes were reversed by an oligonucleotide that eliminated the aberrant splice product."



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