Since I mentioned research into Werner's syndrome (a rare condition causing accelerated aging, or at least the appearance and consequences of accelerated aging) a couple of days ago, some interesting further work was drawn to my attention. It seems that gene expression changes due to Werner's syndrome closely resemble those accompanying normal aging:
Werner syndrome (WS) is a premature aging disorder, displaying defects in DNA replication, recombination, repair, and transcription. It has been hypothesized that several WS phenotypes are secondary consequences of aberrant gene expression and that a transcription defect may be crucial to the development of the syndrome.
Transcription alterations in WS were strikingly similar to those in normal aging: 91% of annotated genes displayed similar expression changes in WS and in normal aging, 3% were unique to WS, and 6% were unique to normal aging. We propose that a defect in the transcription of the genes as identified in this study could produce many of the complex clinical features of WS. The remarkable similarity between WS and normal aging suggests that WS causes the acceleration of a normal aging mechanism. This finding supports the use of WS as an aging model and implies that the transcription alterations common to WS and normal aging represent general events in the aging process.
Progeria, another accelerated aging condition, has already been confirmed to actually produce accelerated aging. If Werner's syndrome is also really accelerated aging, then understanding its mechanisms and finding a cure should help in the fight to defeat the normal aging process.