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A clam lived 507 years and you can also

A book tells how scientists work so that we live much more and better.
The oldest animal in the world lived 507 years. It was an Icelandic clam that had been born in 1499, before Miguel de Cervantes. He died in 2006 after being collected by scientists. A year later, in 2007, a boreal whale appeared in Alaska with a harpoon nailed since the 19th century, suggesting that this mammal can live two centuries. And monarch butterflies, which normally only live for a few weeks, produce a Methuselah generation once a year that reaches six months to migrate from Canada to the temperate forests of Mexico.

Aging in living beings is surprising. A rat lives three years, while a squirrel reaches 25. There are seemingly capricious mechanisms that regulate the process. And what happens in humans? “In the future we will die young. At 140 “, he proclaims a new book about how scientists work to make us live more and better. It is entitled, precisely, Die young, at 140 (editorial Paidós). The volume defends that aging is not obligatory and that scientists will soon be able to prolong youth. And it is not a butade. Its authors are Monica G. Salomone, journalist specializing in science, and molecular biologist Maria Blasco, director of the National Center for Oncological Research (CNIO) in Madrid and, without exaggeration, one of the leading experts in aging in the world.

Blasco’s hypothesis is that aging is the common cause of diseases associated with aging: cancer, Alzheimer’s, diabetes, cardiovascular disease, and so on. If aging were attacked as if it were a pathology, the youth would be prolonged and the rest of the ailments would disappear. You could die young, at 140 years old. “It’s not about living 120 years as a person of 120 years lives today; it’s about being 70 years old with the appearance, health and vitality of the 40 “, explains Blasco.

The molecular biologist believes that this brake to old age exists and is called telomerase, one of the tens of thousands of proteins that make up the human body. Salomone, tanned in national and international media, masterfully explains the role of this macromolecule in aging and the history of its discovery, interviewing almost all the scientists who have painted something on this journey.

The journalist travels to the nucleus of the cell, on scales of millionths of a millimeter, until it reaches DNA, our instruction book, packaged in chromosomes. Our cells are constantly dividing. The face of a person, for example, is completely renewed every month. And every time a cell divides it duplicates its DNA packets, but in such a way that the ends of the chromosomes are not copied until the end. After each division, the chromosomes are a tad shorter.

What is shortened, says Salomone, is “a structure of DNA and proteins called a telomere, a protective cap that forms the end of each chromosome.” The older the cell is, the more divisions it has suffered and the shorter its telomeres. And that’s where the telomerase protein comes in, which naturally stops this biological clock in stem cells. It makes the telomeres grow back. It makes the cells immortal. The trouble is that, in most of the cells of an adult being, the gene that produces telomerase is deactivated.

Our cells are going to die, with their tiny telomeres, and we with them. Or not. Maria Blasco returned to Spain in 1997, after spending four years in the USA in the laboratory of biochemistry Carol Greider, Nobel Prize in Medicine for discovering telomerase. The objective of the Spanish scientist was to verify if increasing telomerase could delay the aging of a mouse. The problem is that the protein makes immortal both healthy cells and those that have mutations that cause tumors. So telomerase favors cancer.

Blasco came up with an ingenious solution. His colleague Manuel Serrano had created a transgenic mouse with three genes that protected against cancer by eliminating cells with dangerous mutations. Blasco crossed his rodents with telomerase with mice resistant to Serrano cancer. The result was Triple, a lineage of superratons born in 2008 who lived 40% more than normal, without diseases. “In worms it has been possible to multiply by 10 the normal life expectancy in the species, but in mammals, which do develop diseases associated with aging like those of humans, Triple still holds today the record of longevity”, highlights Salomone in Morir young, at 140.

The future is promising. The investigation of aging is boiling. At the end of 2014, María Blasco’s laboratory at the CNIO managed to use telomerase to treat myocardial infarction in mice, which is lethal in people in rich countries. The team, led by the young German researcher Christian Bär, treated the mice with telomerase and then caused a heart attack. The protein rejuvenated the heart tissue of rodents and increased their survival after attack by 17%.

Researchers from the Blasco team have four other experiments under way with the same strategy: activate the telomerase gene in specific parts of the body and temporarily, to avoid the risk of cancer. They get it through modified viruses. The technique is underway against Alzheimer’s, Parkinson’s, idiopathic pulmonary fibrosis and aplastic anemia, a disease caused by the malfunctioning of blood stem cells.

At the moment, everything is promising in mice, but Maria Blasco is optimistic. “The origin of Parkinson’s and cancer is the same, the deterioration of our cells, and this occurs associated with the passage of time, which goes hand in hand with alterations in the cell division process, tissue regeneration, exposure to environmental stress, etc. It’s what I think. If I have to put all the eggs in a basket, I would put them in this one. That is why we are with an idea to fixed gear: if we aim at the aging processes will be not one, but many, the diseases that we will understand and delay. In our case, the way to aim at aging to end it is through the activation of telomerase and the rejuvenation of telomeres. ” To die young, at 140 years old.

An article written by: https://elpais.com/elpais/2016/05/06/ciencia/1462535288_701160.html

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