Hutchinson-Gilford progeria syndrome (HPGS) is a very rare condition that causes an apparent rapid ageing of young children so that by the time they are about 10 years old, they have the respiratory, cardiovascular and arthritic health of a 70-year-old. They even look like miniature old people, with wrinkled skin and bald heads. 

The genetics of HGPS is known. It is a dominant condition: only one defective gene is required. This mutation is not inherited, as HGPS victims usually die as teenagers. Instead, it arises spontaneously and that is the reason it is very rare, affecting perhaps one child in eight million.

The defective gene in HGPS is known as lamin A. This gene is the code for a protein that forms part of the structural framework for the nucleus of cells in that spherical body where our chromosomes reside.

In HGPS sufferers a faulty lamin A protein is produced. Like warped timbers in a stud wall, it damages the integrity of the nucleus. In turn, that leads to damaged DNA.

However, scientists have so far been unable to work out how this specifically leads to the symptoms seen in HGPS and whether normal ageing is caused by the same defects occurring more mildly or slowly.

Researchers from the National Cancer Institute in the USA have just published a study in the journal Science that shows normal old people do indeed age in the way HGPS sufferers do and that the cause is essentially the same defective lamin A protein.

The researchers cultured cells from the skin of people aged 81-96 years and compared them to equivalent cells cultured from people aged 3-11 years and people suffering HGPS. They were immediately able to observe under the microscope that the old cells and the HGPS cells had similar-looking, poorly structured nuclei.

Next they investigated the role of lamin A. If normal ageing were due to a chance mutation in the lamin A gene, as occurs in HGPS, we might expect that some people would not get old and that some parts of their bodies would get old before others.

That is not the case. So if lamin A is involved, there must be some other, less fundamental way its production is compromised. To continue the timber stud analogy, if HGPS sufferers have a defective machine that constantly produces warped studs, old people might simply have an increasingly slack machine operator who feeds in timbers incorrectly and can't be bothered discarding warped ones.

That is just what the researchers found. Although normal old people don't have defective lamin A genes, there is an increase in sporadic production of defective lamin A protein.

To prove that causes elderliness, the researchers were able to show a chemical that could block production of defective lamin A made the old cells look young again. They had structurally sound nuclei and showed other molecular signs of not being just about to drop off.

It's possible that same chemical could be used in people to ward off not death but some of the visible symptoms of ageing.