DNA can grow old

How old are we

Life expectancy is increasing steadily

Thanks to medical and technical progress, people's life expectancy has increased by an average of three months a year since industrialization. For people who are 30 years old or younger today, age over 90 will be the rule rather than the exception.

A child born in Germany today has a good chance of celebrating its 100th birthday. Researchers around the world are looking for the exact causes of longevity. Age should lose its apparent arbitrariness and become controllable.

Finding the Key to Aging: Genes or Environment?

One thing is certain: Nobody is born with a long life. Twin studies show that genes are about a quarter responsible for the differences in life spans. So longevity can only be inherited to a certain extent.

Another astonishing finding of age research shows that it is still worth looking for the genes for a long life: Studies on twins born between 1870 and 1910 showed that the influence of the genes on the life span before the age of 60. Life year is short, but clearly increases with increasing age.

At the center of research: the very old

Large-scale projects are running around the world in which scientists are studying the genes of very old people. Blood samples from voluntary donors who are approaching or have already passed their 100th birthday arrive at the institutes almost every day.

These samples are stored in so-called Methuselah biobanks. The isolated genetic material is analyzed in laboratories. The researchers hope to find and decipher the crucial genetic similarities.

However, the search turns out to be more difficult than expected. So far, only one thing is certain: there is no single gene that determines the length of our lives. Numerous genes play together. But how many of these age genes are there? And how do these genes have to work together to make us live longer?

Age genes: age-1, clock and Indy

Research into the aging process in humans has practical and ethical limits. Animal model organisms are therefore used in the search for age genes.

Mouse, fruit fly, roundworm and unicellular brewer's yeast are suitable candidates because their entire gene catalog is known, they have a relatively short lifespan and are easy to breed in large numbers.

The comparison with humans becomes possible because, despite the diversity of life, the genes of all living beings show an astonishing similarity in structure and function. Numerous age-influencing genes with nicknames such as "age-1", "clock" or "Indy" (from "I'm not dead yet") have already been found with the help of the model organisms.

Investigations on the tiny nematode led to a particularly great success. A gene was discovered in it, which apparently acts as a kind of regulator, controlling and slowing down the aging of the worm. The gene known as "daf-2" occurs in different variants and, depending on the variant, determines whether the worm has a shorter or longer life.

With this worm-like gene template, the researchers then went looking for humans and found what they were looking for. Humans also carry the genetic information of "daf-2", only that the information has been distributed over two genes in the course of evolution. It is assumed that "daf-2" has very similar functions in humans as in nematodes.

Genetic methods are used to search the genetic samples of very old donors for a human variant of "daf-2" that contains the command "age slowly" encoded in DNA.

A good repair is what counts

Some research groups take a different approach. They concentrate on the self-healing powers of the body cells. These self-healing powers are based on the repair mechanisms of our genetic make-up, the DNA.

Enzymes, which can generally be understood as tools of the body, are constantly busy repairing DNA that has been damaged by environmental influences. If this repair no longer works, our cells can no longer renew themselves. The body can no longer regenerate, it ages and ultimately dies.

An indication that aging and DNA repair are related is provided by a hereditary disease, the so-called "Werner Syndrome". The disease represents the best model for premature aging in humans. Those affected are confronted with typical characteristics of old age at a young age.

These include premature graying of hair, skin aging, diabetes, arteriosclerosis and osteoporosis. The cause of this disease is a defective gene. This gene normally carries the information for an enzyme that is responsible for winding up the spiral DNA in order to be able to repair it.

Model organisms show that there are significant differences in the quality of DNA repair. Naked mole rats, for example, are much older than house mice. According to the researchers, they can repair their DNA about three times more effectively than mice.

Humans also have good DNA repair mechanisms. The DNA of our skin cells is permanently damaged by UV radiation alone and, fortunately, is successfully repaired in most cases.

However, there are limits to this ability to be repaired, as shown by regular visitors to the solarium and sun worshipers. Their skin ages much faster.

In addition to UV radiation, there are numerous other factors that damage our DNA. And so the goal of this branch of research is to improve the ability to repair DNA and the protection of DNA in order to make our cells more durable.

Research cannot make any clear statements about the maximum life expectancy of humans. Some see the maximum at 130 years of age. Others are convinced that the upper limit is open and that age will at some point be controllable at will. What is certain, however, is that 100th birthdays will no longer be uncommon in the near future.