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At a conference in New York in 2017, Richard Faragher, professor of biogerontology at the University of Brighton, screened a slide on the screen behind him. "It's not a sight test," he joked, pointing to a graph showing declining columns. The highest represented the British budget: £ 715 billion. The next one was the share allocated to the National Health Service – 106 billion pounds – alongside the sums spent for people 65 years and over: 42 billion pounds, or nearly 40% of the total budget. Nobody could see the last column, which was not bigger than a complete stop. "It's research on the basic biology of aging," he said. "£ 0.2 billion. Three times for everything.
For Faragher, this is an inexcusable lapse of time. It is part of a group of scientists around the world who hope to reconfigure our understanding of old age and popularize a controversial idea: the aging process is itself a disease. Many people in academic and secular circles are reluctant to this suggestion. According to them, aging is a natural and inevitable process; to clbadify this disease as a disease is an economic opportunism, or even a narcissistic denial of mortality.
And yet, the most important risk factor for many of the conditions we badociate over the years – from stiffening joints to bone thinning to heart failure, cancer, stroke, dementia – is old age itself. So, if we accepted the notion of aging as a disease, we would attack the roots of the infirmity tree rather than its individual branches – the current goal of geriatrics.
"One of the great peculiarities of aging is that it is considered do not a disease, "says David Gems, professor of biology of aging at University College London. According to Gems, our state of mind is "a relic concept" rooted in the writings of Roman physician Claudius Galen in the second century AD, whereas the only way to tolerate the progressive infirmities of old age was to accept them. with philosophy. But this is no longer the case. In the field of genetics, Gems scientists have discovered genes related to longevity and have been able to manipulate them to prolong the lifespan of model organisms such as worms, flies and mice – in the case of C elegans worm, up to ten times.
The most compelling message from this work, says Gems, is that "aging is not static; it can be modified. The study of "senescent cells" is at the forefront of the effort. Our body grows, develops and repairs itself through a process of cell division in which the genetic material of a cell is copied to produce a clone. As DNA copy errors spread over time, dividing cells have a limited life span as part of a strategy to protect us from potentially harmful mutations. But cells that have reached the end of their replicative life do not die; they simply "senesce".
As our immune system weakens with age, senescent cells accumulate and begin to damage body tissues. They secrete substances that eat away at collagen, a substance that keeps our cells together. as it degrades, it leaves wrinkles and sagging pieces. Ironically, the degraded collagen also leaves spaces leaving enough room for the proliferation of precancerous cells, previously controlled by a young and firm tissue. And the secretions of these cells that no longer divide themselves promote inflammation – the constant and low-intensity excitation of the immune system, considered one of the major driving forces of aging.
Scientists are studying strategies to treat senescent cells. They have discovered drugs that can eliminate them – and they have also found a way to rejuvenate them by going back in time so that they can divide again and return to normal functioning. However, each of these strategies has serious drawbacks. It turns out that senescent cells have certain beneficial attributes. They secrete substances that promote effective healing of wounds. Their elimination prevents the repair of the tissues. The disadvantage of allowing senescent cells to divide again is that it takes precedence over the anticancer mechanism of our body, eventually giving way to corrupted DNA.
Researchers are working to refine drugs and techniques to the point of controlling senescent cells and making real progress. Likewise, exciting work is underway in other areas of gerontology: from immunology and genetics to stem cells and neuroscience.
However, efforts to translate recent discoveries made in laboratories around the world into clinically useful services are facing a huge hurdle. As long as drug regulatory authorities, policy makers and health care officials do not recognize aging as an editable process, it is not perceived as a legitimate intervention target. In the absence of a defined market, Big Pharma has little incentive to participate in drug development.
Today, however, a group of eminent international gerontologists is seeking to break this stalemate by using a drug already present in the drug compartment. Metformin – the most widely used anti-diabetic drug in the world – has recently been discovered, by chance, to have a marked protective effect against other age-related diseases. In 2015, a team led by Nir Barzilai of the Albert Einstein College of Medicine in New York got approval from the US Food and Drug Administration to use this drug in the very first trial of an anti-aging treatment .
Known as Tame (Targeting Metformin Aging), the trial involves approximately 3,000 people aged 65 to 79 and is expected to last until 2021. It will measure the speed – if any – of the individual taking the active drug to develop geriatric disease compared with those taking a placebo. Metformin, they say, is not necessarily the most effective anti-aging candidate, but it's safe, well-tolerated and no longer patented, so it's very cheap. And its main purpose is simply to prove the principle that aging can be slowed down and trigger a paradigm shift in the way we treat it in the future.
The World Health Organization is already involved, with a specific mention of "old age" in the latest issue of International clbadifications of diseases, published at the end of last year.
"This little line of text could be one of the most important documents in the history of humanity," commented Barzilai. As he wrote in a blog for TedMed a year earlier: "Today, the opportunity to live longer and healthier is no longer science fiction, it's science."
Sue Armstrong is the author of "The Time Borrowed: The Science of How and Why We Aged" (Bloomsbury)
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