May you have a healthy life with plentiful TTAGGG
These nubby bits of DNA and the enzyme that control them are a key ingredient in longevity, according to research unlocked by a trio of scientists honoured with the Nobel Prize for Medicine.Paris -- What do Peter Pan and Methuselah have in common?
How about... long telomeres?
These nubby bits of DNA and the enzyme that control them are a key ingredient in longevity, according to research unlocked by a trio of scientists honoured on Monday with the Nobel Prize for Medicine.
Telomeres are caps at the end of chromosomes, protecting the precious strands of genetic code that contain the chemical recipe for life.
Australian-American cell biologist Elizabeth Blackburn, one of the co-laureates, likens them to "tips of shoelaces" -- when you lose the little plastic end, the lace starts to fray.
The length of your telomeres, a repetitive sequence of the chemical code TTAGGG, and the repair job played by the enzyme telomerase, are unseen yet vital players in the ageing business.
"Telomerase is one of the basic mechanisms of life," Maria Blasco, a specialist at Spain's National Cancer Research Centre in Madrid, told AFP.
"In the last 10 years, it has been seen as a promise for cancer and ageing pathologies... and it seems that telomerase could be the key to the longevity of the species."
Every time a cell divides, the telomeres get worn down. Telomerase's job is to partially rebuild them. Eventually, when the telomeres are worn beyond a certain point, known as the Hayflick limit, cell death is triggered.
Low levels of telomerase are associated with early cell death and premature ageing. Malfunctioning telomerase also causes mercifully rare but devastating conditions, including a chronic form of anaemia.
Early discoveries into telomerase led to frenzied speculation that boosting the human lifespan lay just around the corner, in pumping up the enzyme.
Now the mood is more cautious, for at high levels telomerase can also be a curse.
In cancer, activated telomerase allows disease cells to divide endlessly and achieve what scientists call "cellular immortality," a hallmark of cancer.
This finding is both grim and compelling, for it has unlocked a decade-long search for drugs to inhibit telomerase or attack cells that express it. The first clinical trials are underway in the United States and Europe.
Telomerase "is an ideal target for chemotherapy because it is active in almost all human cancer tumours, but inactive in most normal cells," Emmanuel Skordalakes, a professor at the Wistar Institute in Philadelphia, told AFP last year.
"That means that a drug that deactivates telomerase would likely work against all cancers, with few side effects."
Another emerging belief is that telomeres are a biomarker of vulnerability to disease.
A British study among 1,500 middle-aged men in 2007 found that those with the shortest telomeres were twice as likely to develop heart disease within five years as those with the longest telomeres.
The reason for this is unclear. One idea is that worn telomeres impede cell repair on damaged parts of the arterial wall.
In 2004, Blackburn plunged into the so-called "mind-body connection," a hazy and sometimes criticised theory whereby emotional strain can have physical outcomes.
Her team found that the longer a woman had been caring for a sick child, the shorter her telomeres, the lower her levels of telomerase and the higher her levels of oxidative stress -- a process by which rogue molecules damage DNA, including telomeres.
Blackburn became wrapped up in telomeres and telomerase through an organism called Tetrahymena -- better known as pond scum -- whose single cell replicates with apparently immortality.
The two other 2009 laureates are Jack Szotak, who with Blackburn found that telomeres protect the chromosome, and her former grad student Carol Greider, who jointly discovered the enzyme with Blackburn.