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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:

What are telomeres, one of the keys studied by scientists to understand aging.

What are telomeres, one of the keys studied by scientists to understand aging

WritingBBC Mundo
    March 27, 2018

Telomeres are like the protective shields of our cells’ DNA.
Its name, of Greek origin, literally means “final part”, and that is that the telomeres are that: the ends of the chromosomes, something similar to the plastic tips of the shoelaces.
But they are very repetitive and non-coding parts of DNA: their main function is to protect the genetic material that carries the rest of the chromosome.
As our cells divide to multiply and to regenerate the tissues and organs of our body, the length of the telomeres is reduced, and therefore they become shorter over time.
When finally the telomeres are so small that they can no longer protect the DNA, the cells stop reproducing: they reach a state of old age or old age.

Therefore, the length of telomeres is considered a key “biomarker of aging” at the molecular level, although it is not the only one, and in recent years it has attracted the attention of numerous researches.
How much do our telomeres measure and how fast do they deteriorate?
The length of the telomeres is measured in “base pairs”, which are the opposite and complementary nucleotide pairs that are connected by hydrogen bonds in the DNA chain.
The length of telomeres varies widely among different species.
In the case of humans, the length of the telomeres deteriorates from an average of 11 kilobases at birth to about 4 kilobases in old age.
Can you “intervene” on telomeres?
In 2009, three American researchers won the Nobel Prize in medicine for their work on cell aging and its relationship to cancer.
Elizabeth Blackburn, Carol Greider and Jack Szostak investigated the telomeres and discovered that the telomerase enzyme can protect the chromosomes from aging: it can cause the telomeres to regenerate, it can prolong them.
This enzyme helps prevent telomeres from shrinking with cell division, which helps maintain the biological youth of cells.
Much of the research on telomeres has nothing to do with an aesthetic aspiration of longevity, but with the potential cure of diseases.
The Spanish María Blasco, who worked in the United States with Greider, is now the director of the Telomeres and Telomerase Group of the National Center for Oncological Research of Spain.
Blasco led the development of a new technique that blocks the ability of glioblastoma, one of the most aggressive brain cancers, to regenerate and reproduce, precisely by attacking the telomeres of cancer cells.
In tests with mice, his team managed to reduce the growth of the tumors and increase the survival of the animals, something that could open the doors to potential treatment alternatives in humans.
But Blasco and his team are still investigating with strategies in reverse, according to Gabriela Torres, of BBC Mundo.
They aspire to activate telomerase in such a way that they can cure people who are dying of rare diseases due to genetic mutations associated with very short telomeres.
Do they keep the secret to make us younger?
But stopping the aging of cells does not necessarily have an anti-aging effect on the whole body.
According to Dr. Carmen Martin-Ruiz, researcher on aging at the Institute of Neuroscience at the University of Newcastle, in England, the longer a person’s telomeres can be said, the “stronger is biologically”.

When a person has the longest telomeres, it is because they have metabolic mechanisms that protect them, “the specialist told BBC Mundo.
“It’s like your body had better defense systems,” he explained.
But one of the current problems of scientific research in this field, according to this expert, is that there is no standardized and universal method to measure telomeres.
A recent study from the United States concluded that maternity shortened women’s telomeres more than tobacco or obesity, while another fact among Mayan women, smaller but with a “more robust” methodology, according to Martin-Ruiz, reached the opposite conclusion: that motherhood made women biologically younger, since their cells had longer telomeres.
Martin-Ruiz says that each laboratory uses different techniques and methodologies, which makes it difficult to compare studies and results because the calculations can be interpreted in many different ways.
So “the technical solidity of measuring telomeres is not as much as when you go to the hospital and they measure your glucose”, concludes the expert.

In any case, there is a large community of scientists who are investigating different aspects of human aging, including telomeres, mitochondria, the shape of proteins and many other aspects of that process.
According to the BBC, Gordon Lithgow, a scientist at the Buck Institute, aging is all these things, it affects all the systems of our body.

    An article of the BBC:

Elizabeth Parrish, the woman who rejuvenates every day.

He has skipped all the rules to try an anti-aging treatment. Today she is the only patient of a pioneering method. She is 45 years old and is determined to overcome aging and convince science that it is possible.

Science claims that astronauts, when on a mission, age more slowly. Just microseconds, but they return to Earth more “young”. Maybe Elizabeth Parrish tries to imitate them with so much travel. In the last two weeks he has traveled tens of thousands of kilometers flying between the United States and Germany (twice), a flight to South America, another to Russia, an air excursion to London and several transfers between Washington, where he has his headquarters, and other American cities. That’s why finding it has been so complex, but by combining phone and email in different continents we have managed to land and explain to Quo how he plans to cure aging. Because for Liz, as she prefers to be called, getting old is a disease, not a process. She is the zero patient of a therapy that she has designed so that time is more benevolent with her body. And, judging from the first results, he’s getting it. Although it is facing governments, regulatory agencies and scientific colleagues, with the aim of testing in humans a therapy whose side effects are unknown.

An update to be younger
“I was not prepared to discover that biological aging is really a disease,” Parrish explains to Quo. I took the time to talk to many experts and discovered that some of the agents that cause diseases in children are accelerated aging processes. It was necessary to understand that the cells of the body are like a computer and much of the damage they cause over time is because they are programmed for it. Some people suffer from this deterioration at a young age, that is, some have programming problems, genetic. But we are all accumulating these damages that will eventually lead us to the symptoms of old age and cause us death. ” What Elizabeth Parris tries, continuing with the simile, is to update us.

“Exact!” Exclaims Liz. “For that, one of the most important things we need is to obtain information in humans. We have cured the cancer hundreds of times in mice, reverse the formation of arteriosclerosis plaques and biological aging with telomerase inducers. But we are not using those techniques in humans. So I decided to try them on myself. I’m going to show that it’s a safe therapy. ”

The first results indicate that Parrish has made his cells 20 years younger. But the scientific community demands more data
That therapy to which Parrish refers has two parts. On the one hand are the telomeres. In 2009, Elizabeth Blackburn won the Nobel Prize for her discovery of the “scissors” that divide cells: telomeres. These are repetitive sequences of DNA that protect them from degradation after each division. In a sense, they are like ink in a photocopier: they try to make the copy of the copy as close as possible to the original. The problem is that no matter how much ink you have, the copy of a copy of a copy (and so on) is not as good as the original: in cellular terms this amounts to saying that when a cell is divided, the two resulting have less telomeres than his “mother.”

And this is the reason for aging: the more our cells divide, the less similar they appear to the original, until they are so different that the differences could produce a risk and that branch of the family immolates itself for the sake of the rest. Thus, if we had a constant contribution of telomerase, the “nutritional supplement” of the telomeres, in charge of adding pieces of DNA so that there are no bad readings, aging would be much slower.

This has already been demonstrated by one of the pioneers in this field, María Blasco, director of the National Center for Oncological Research (CNIO) who has carried out a telomerase therapy in mice and managed to extend her life by 30%. But how has Parrish done it? Is there any way to explain it in a simple way?

“Surely, the patient responds zero to this treatment-. It is a gene therapy, but we did not put the genes directly, we use vectors through which we transmit the information we want. And these vectors are viruses. We know that viruses are essentially good at making us sick, but we use viruses that do not make us sick and we use them because they have the ability to connect with our cells and transmit their genetic material. In gene therapy, we remove viruses from the ability to get sick and put the information we want in our cells. In a certain sense it is very simple science. We are not creating molecules that you have to eat and go to a place in your body to create an effect. What we are doing is delivering a gene to the cell,

The risks of being the patient zero
There is only one small drawback. This therapy has not yet been tested in humans. When we consulted María Blasco about it, her answer was clear. “We do not know if in humans the extension (achieved in mice) would be the same or not. From the outset, humans are much more protected from aging than mice. While in humans up to 40 years it is very rare to suffer diseases associated with aging, such as heart attack, Alzheimer’s disease or cancer, in mice everything happens much faster and they begin to develop diseases at one year of age. At 2 years, most of the mice have already died. Therefore, something that extends life in mice by 30% could extend life in humans by 3% or 300%, we do not know … Anyway, The objective of understanding how to modulate longevity in mice or other model organisms is to understand which are the important molecular processes, determine the speed of aging to be able to intervene with the intention of preventing diseases linked to the passage of time or even treat them more efficiently. Right now there are many pathologies associated with old age that we neither know how to prevent nor how to cure, “says María Blasco.

And this is exactly what Parrish intends. What happens is that in the United States the trials with humans are regulated by the Food and Drug Administration (FDA) and until this agency does not approve, they can not be started … Unless it is in another country.

“If you manage to treat aging with this therapy, it will only be long-term,” predicts María Blasco
That’s why Parrish went to Colombia to start the first phase of the trial. Before starting, the Bioviva team, the company that Parrish runs, measured the length of the leukocyte telomeres and did it again after the therapy. The results show that their telomeres lengthened from 6.71 kb or kilobases (kb: a thousand DNA base pairs) to 7.33 kb. In a nutshell, your cells are 20 years younger.

Muscles for your stem cells
The other part of the treatment Parrish underwent involves the use of inhibitors of myostatin, a protein that obstructs muscle growth. In fact, sarcopenia (the loss of muscle mass from 30 years of age) kills 6% of the population. “So we block myostatin and our muscles keep growing,” says Parrish. But not only that. The benefits also include increased insulin sensitivity, decreased fat and an aid for the signals from the stem cells. Many people die looking very old, even if their stem cells are very healthy. That’s because they never received the signal to help the body regenerate. ”

A therapy to challenge them all
Is this enough information for FDA to approve human trials? Is there any context that justifies skipping the regulatory agencies and becoming “guinea pig”? For Maria Blasco is more than clear and her answer is Spartan: “None.” George Martin, pathologist, expert in genomic sciences and until a few weeks ago a member of the scientific board of BioViva, something similar happens. “Liz is an extremely hardworking and conscientious woman,” he explained to Quo in a telephone conversation, “but in my opinion the goal of the medical sciences is to cure and for that we must follow certain rules. That is the reason why I asked to leave the council. ”

Another member of the same council, which remains in him, is the well-known geneticist George Church. Church’s work is one more proof that BioViva investigates with diffuse ethical limits. He was the one who proposed to resuscitate a Neanderthal and came to look for a human who wanted to breed him. Church is aware that such work would be declared illegal in many countries, but this is something that does not stop him.

There is no controversy for Parrish either. “I think it’s a right to be able to do what you want with your own body and that we should be able to pay a doctor to do it as safely as possible. Initially, we kept the site where the trials were conducted and the people involved in it secret, because as the director of the company I wanted to protect my staff. Now that the results have proven to be positive, we have released the data. ”

The step has undoubtedly been risky. Not only because of the adverse effects that treatment could have on humans, but because when requesting approval from the FDA, the agency may not view this “insubordination” against the established order with good eyes, an act that could set precedents . The question then is, how do you plan to convince the FDA to approve this treatment and be able to begin the trials?

And Parrish already has it in mind. “Every day we lose close to 100,000 people because of aging,” he says in his conversation with Quo. And we are not facing this reality as the catastrophe that it is. We think that it is a normal process, but we must bear in mind that it is a very expensive one. In 2020 there will be more people over 65 who are under 5 years old. We have to think about how to make people work longer and be more active and healthy. There is no point in preventing the development of a technology that would allow us to save the billions of dollars spent on finding the cure for diseases related to aging, when we can directly treat what produces them. ”

If successful, Parrish’s commitment could not only extend our life expectancy, it would also have a huge impact on the economy, especially on pensions. At what age should we retire? How much would education extend? How would the pensions be paid if we live 20 more years? Have you thought about it? “The truth is that I do not ask myself those kinds of questions,” says Parrish. My job is to mitigate the diseases that we can cure. If we think we have a possible solution, it would be immoral not to share it. How long will we live? I do not know, but I would like it to be as long as possible and in the best conditions. ”

The therapy being carried out Elizabeth Parrish could have potential to treat diseases related to aging such as cancer, duchenne, Alzheimer’s, Parkinson’s, kidney problems, leukemia, esophagitis of Barret … The list is long. “The first people who should benefit from it,” Parrish explains, “are terminal patients. Then, if the data obtained are positive, we could start with patients with milder diagnoses and finally reach the area of ​​preventive care “. For this to happen, only one requirement will be necessary: ​​”That the regulatory agencies recognize old age as a disease”, concludes María Blasco.

Why do you add Miostatin?

From 50 years of age, muscle mass decreases between 1 and 2% and strength 1.5% annually and up to 3% from 60 years. Myostatin, also known as growth differentiation factor 8, not only solves this muscle loss. “He also works with telomerase,” says Parrish. This increases the supply of stem cells and myostatin would allow more stem cells to activate
and regenerate tissues. ”


Maria Blasco, director of the CNIO: Aging is not natural.

“It’s a laboratory like any other,” confesses modestly its director, Maria Blasco, as we walk between microscopes, test tubes, stills and retorts. It is nothing less than the laboratory of the Telomerase and Telomerase Group of the CNIO (National Center for Oncological Research), whose management also has Blasco. It will be like any other, but in other laboratories it has not been discovered how to significantly extend the life of small mammals, nor have deadly tumors been eliminated, nor has a gene therapy been developed that could extend our life, according to the most conservatives, up to 140 years. That is the figure that Maria Blasco ventures in the book she signs next to Mónica G. Salomone, Morir joven, at 140 (Paidós, 2016), of recent appearance. Disciple of the pioneers in their discipline, Molecular Biology, it is possible that Maria Blasco has found the exact distillation of the elixir of eternal youth. And yet modesty, once again, seems to be a distinctive feature of his character at the sight of his office, attached to the laboratory. Narrow, elongated and dominated by a large window from which you can see the treetops of this residential area in the vicinity of the Plaza de Castilla, there is barely room for the desk and the work chair. From this office Maria Blasco glimpses the future of human longevity and the fight against cancer, myocardial infarction and Alzheimer’s. On the wall, next to the computer, family photos. And in front, a horizon without mapping on which to blur the look.

Javier Redondo Jordán
this news has been extracted from:

At what point does the enzyme telomerase come into play?

Telomerase is the antidote that nature has to realarge telomeres. It is not present in the adult organism, but is activated in the embryonic development and resets the telomeres of the new individual. It is interesting that cancer cells are the only immortals that exist, and that is because they have telomerase and keep their telomeres long.