IT鈥橲 not quite the elixir of life, but researchers may have found a way of keeping us younger for longer. In mice at least, increasing the production of two proteins called p53 and Arf enabled more of the animals to survive to old age while showing fewer signs of ageing.
Since its discovery in 1979, p53 has been a key therapeutic target for cancer research. When activated, it encourages damaged cancer cells to commit suicide 鈥� a process called apoptosis. 鈥減53 is the single most important tumour suppressor protein,鈥� says Ander Matheu of the in London. 鈥淚t鈥檚 inactivated in 30 to 50 per cent of human tumours.鈥� Arf helps to control the expression of p53 by binding to a gene that normally suppresses it. 鈥淲hen you have more Arf, you have a greater activation of p53 and a stronger tumour-suppressing effect,鈥� Matheu says.
Previous research has shown that mice with an extra copy of either the p53 or Arf gene are better protected from cancer. Now Matheu鈥檚 team has shown that an extra copy of both carries an additional benefit: living to a ripe old age without becoming frail (Nature, ). 鈥淎rf and p53 are antioxidants,鈥� says Matheu. 鈥淭he mice accumulate less oxidative stress, which is normally associated with ageing.鈥�
Advertisement
While the maximum age the mice survived to did not increase, adding extra copies of the genes did result in more of them reaching old age. The mice also appeared younger, showing reduced hair loss, for example. 鈥淭hey have a better quality of life,鈥� Matheu says.
鈥淲hile the maximum age the mice survived to did not increase, the genes did result in more of them reaching old age鈥�
Adding extra copies of genes to humans may be more complicated, although drugs that increase the activity of p53 and Arf already exist and could potentially benefit humans, Matheu says.
There is a catch, however. Too much of a good thing can be bad for you, and at times of stress p53 can damage rather than repair the body. In January, Issei Komuro of the Chiba University Graduate School of Medicine in Tokyo, Japan, showed that may increase the risk of further heart attacks once the heart has been damaged (Nature, ). 鈥淩apid and robust blood vessel formation is necessary when organs are injured, and p53 inhibits vessel formation,鈥� Komuro says. It may also increase the risk of damage to normal cells in patients undergoing radiotherapy for cancer.
This means age researchers must develop a drug that stimulates Arf and p53 to a very precise degree. That may take many years, Matheu admits. Kevin Ryan of the Beatson Institute for Cancer Research in Glasgow, UK, agrees. 鈥淎t present, it may still be best to try and reduce oxidation damage naturally by not smoking, by drinking alcohol in moderation and eating plenty of fruit and vegetables,鈥� he says.
