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This is an interesting recent assessment of the change in the biophysical properties of the "nuclear lamina" in the cells of children that suffer from what the media commonly terms "Progeria". These findings are due to appear in the Proceedings of the National Academy of Science.

More specifically, the syndrome is known as "Hutchinson-Gilford Progeria Syndrome". There have been a succession of recent breakthroughs regarding this syndrome, as well as some interesting findings suggesting that what the individuals face in the course of this disease is what we all face in the course of aging, ableit on a significantly more protracted time scale.

In any case, the "pliability" of the nucleus is compromised in this disease, according to these findings, and this pathologic alteration will manifest itself in an acclerated aging process. They also found that the protein concentration drifted higher in HGPS, which may be another alteration that is contributing to the dramatic presentation of the disease.

I am sure there are some "normal" lab mice or rats, somewhere, that are currently being given farnesyltransferase inhibitors, with scientists dutifully monitoring their progress. These agents are thought to remedy some of the problems seen in HGPS, and, there is some evidence that the same problems seen with the "Lamin-A" protein in patients with HGPS are occurring in "normal aging". If this is the case, then the use of farnesyltransferase inhibitors could be beneficial in humans at advanced age.

However, a general heuristic of pharmacology that is best not forgotten is that you "don't get something for nothing", and so the downsides to this approach may not become manifest until extended follow-up of the first "phamacotherapeutic adventurers" is complete.

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