Scientists believe the 'retirement' of a specific gene may go a long way to explaining why the human body deteriorates with age.

They have discovered that a gene called FoxM1B plays a crucial role in helping the body's tissues to heal and replenish themselves.

These results clearly link FoxM1B with the failure of tissues to mend Dr Robert Costa

This is a knack that we all gradually lose as we get older and leads, among other things, to progressive weakening of the muscles and bones, saggy skin and slower healing of wounds

A team from the University of Illinois at Chicago has shown that failure of the FoxM1B gene to work properly damages the body's ability to replicate its own cells.

And it seems that the older we get, the more likely are malfunctions in the gene.

Gene therapy

The researchers used gene therapy to created mice with liver cells lacking the FoxM1B gene.

They then measured how quickly the organ was able to regenerate itself following injury.

Regeneration was much faster in animals whose cells carried FoxM1B. Without the gene, regeneration was slow.

Cell division requires two basic steps: first a doubling of DNA, the genetic instructions inside a cell, and then a process called mitosis, in which the duplicated DNA is separated into two new daughter cells.

Lead researcher Dr Robert Costa said: "If the cells had no FoxM1B gene their DNA often failed to make a copy of itself, and they had trouble dividing."

Protein

The key appears to be the pile up of a specific protein - called p21Cip1 - in the cells which not only blocks DNA division, but also appears to trigger genes linked to diseases of old age, such as cancer and Alzheimer's.

Dr Costa believes that FoxM1B probably controls production of an enzyme that breaks down this protein and prevents it building up in the cell.

The researcher team also found that FoxM1B controls a key enzyme needed to help cells pull apart at the end of mitosis, the final step in cell division.

Dr Costa said: "These results clearly link FoxM1B with the failure of tissues to mend.

"And in old age, when the FoxM1B gene is essentially out of action, we see the results."

The research is published in the Proceedings of the National Academy of Sciences.