Tag: longevity

Categories : AgeingTags :

Humans are Approaching a Hard Limit in Life Expectancy Gains

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Photo by Matteo Vistocco on Unsplash

Life expectancy increased dramatically over the 19th and 20th centuries, thanks to improvements such as healthier diets and medical advances. But after nearly doubling over the course of the 20th century, the rate of increase has slowed considerably in the last three decades, according to a new study led by the University of Illinois Chicago.

Despite frequent breakthroughs in medicine and public health, life expectancy at birth in the world’s longest-living populations has increased only an average of six and a half years since 1990, the analysis found. That rate of improvement falls far short of some scientists’ expectations that life expectancy would increase at an accelerated pace in this century and that most people born today will live past 100 years.

The Nature Aging paper offers new evidence that humans are approaching a biologically based limit to life. The biggest boosts to longevity have already occurred through successful efforts to combat disease, said lead author S. Jay Olshansky of the UIC School of Public Health. That leaves the damaging effects of aging as the main obstacle to further extension.

“Most people alive today at older ages are living on time that was manufactured by medicine,” said Olshansky, a professor of epidemiology and biostatistics. “But these medical Band-Aids are producing fewer years of life even though they’re occurring at an accelerated pace, implying that the period of rapid increases in life expectancy is now documented to be over.”

That also means extending life expectancy even more by reducing disease could be harmful, if those additional years aren’t healthy years, Olshansky added. “We should now shift our focus to efforts that slow aging and extend healthspan,” he said. Healthspan is a relatively new metric that measures the number of years a person is healthy, not just alive.

Life expectancy increased rapidly through the 19th century and first half of the 20th century. In 1990, some scientists predicted those rapid gains would continue, leading to “radical life extension.” But a new analysis proposes that we may be nearing the limit of human longevity. (Strategic Marketing and Communications / UIC)

The analysis, conducted with researchers from the University of Hawaii, Harvard and UCLA, is the latest chapter in a three-decade debate over the potential limits of human longevity.

In 1990, Olshansky published a paper in Science that argued humans were approaching a ceiling for life expectancy of around 85 years of age and that the most significant gains had already been made. Others predicted that advances in medicine and public health would accelerate 20th-century trends upward into the 21st century.

Thirty-four years later, the evidence reported in the 2024 Nature Aging study supports the idea that life expectancy gains will continue to slow as more people become exposed to the detrimental and immutable effects of aging. The study looked at data from the eight longest-living countries and Hong Kong, as well as the United States – one of only a handful of countries that has seen a decrease in life expectancy in the period studied.

“Our result overturns the conventional wisdom that the natural longevity endowment for our species is somewhere on the horizon ahead of us – a life expectancy beyond where we are today,” Olshansky said. “Instead, it’s behind us – somewhere in the 30- to 60-year range. We’ve now proven that modern medicine is yielding incrementally smaller improvements in longevity even though medical advances are occurring at breakneck speed.”

While more people may reach 100 years and beyond in this century, those cases will remain outliers that won’t move average life expectancy significantly higher, Olshansky said.

That conclusion pushes back against products and industries, such as insurance and wealth-management businesses, which increasingly make calculations based on assumptions that most people will live to be 100.

“This is profoundly bad advice because only a small percentage of the population will live that long in this century,” Olshansky said. 

But the finding doesn’t rule out that medicine and science can produce further benefits, he said. There may be more immediate potential in improving quality of life at older ages instead of extending life, the authors argue. More investment should be made in geroscience – the biology of aging, which may hold the seeds of the next wave of health and life extension.

“This is a glass ceiling, not a brick wall,” Olshansky said. “There’s plenty of room for improvement: for reducing risk factors, working to eliminate disparities and encouraging people to adopt healthier lifestyles – all of which can enable people to live longer and healthier. We can push through this glass health and longevity ceiling with geroscience and efforts to slow the effects of aging.”

Source: University of Illinois Chicago

Categories : AgeingTags :

Can Being More Flexible Help People to Live Longer?

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Photo by Mikhail Nilov: https://www.pexels.com/photo/a-couple-doing-yoga-at-home-7500701/

Flexibility exercises are often included in the exercise regimens of athletes and exercisers. New research in the Scandinavian Journal of Medicine & Science in Sports suggests that levels of flexibility may affect survival in middle-aged individuals.

After analysing data on 3,139 people (66% men) aged 46–65 years, investigators obtained a body flexibility score, termed Flexindex. This score was derived from a combination of the passive range of motion in 20 movements (each scored 0–4) involving 7 different joints, resulting in a score range of 0–80.

Flexindex was 35% higher in women compared with men. During an average follow-up of 12.9 years, 302 individuals (9.6%) comprising 224 men and 78 women died. Flexindex exhibited an inverse relationship with mortality risk and was nearly 10% higher for survivors compared with non-survivors in both men and women.

After taking age, body mass index, and health status into account, men and women with a low Flexindex had a 1.87- and 4.78-times higher risk of dying, respectively, than those with a high Flexindex.

“Being aerobically fit and strong and having good balance have been previously associated with low mortality. We were able to show that reduced body flexibility is also related to poor survival in middle-aged men and women,” said corresponding author Claudio Gil S. Araújo, MD, PhD, of the Exercise Medicine Clinic – CLINIMEX, in Rio de Janeiro, Brazil.

He added that as flexibility tends to decrease with aging, it may be worth paying more attention to flexibility exercises and routinely including assessments of body flexibility as part of all health-related physical fitness evaluations.

Source: Wiley

Categories : Ageing GeneticsTags :

A Breakthrough Discovery of Gene that may Extend Longevity

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Source: CC0

Researchers from the Center for Healthy Aging, Department of Cellular and Molecular Medicine at the University of Copenhagen have made a breakthrough in lifespan research. They have discovered that a particular protein known as OSER1 has a great influence on longevity.

”We identified this protein that can extend longevity. It is a novel pro-longevity factor, and it is a protein that exists in various animals, such as fruit flies, nematodes, silkworms, and in humans,” says Professor Lene Juel Rasmussen, senior author behind the new study.

Because the protein is present in various animals, the researchers conclude that new results also apply to humans:

”We identified a protein commonly present in different animal models and humans. We screened the proteins and linked the data from the animals to the human cohort also used in the study. This allows us to understand whether it is translatable into humans or not,” says Zhiquan Li, who is a first author behind the new study and adds:

“If the gene only exists in animal models, it can be hard to translate to human health, which is why we, in the beginning, screened the potential longevity proteins that exist in many organisms, including humans. Because at the end of the day we are interested in identifying human longevity genes for possible interventions and drug discoveries.”

Paves the way for new treatment

The researchers discovered OSER1 when they studied a larger group of proteins regulated by the major transcription factor FOXO, known as a longevity regulatory hub.

“We found 10 genes that, when – we manipulated their expression – longevity changed. We decided to focus on one of these genes that affected longevity most, called the OSER1 gene,” says Zhiquan Li.

When a gene is associated with shorter a life span, the risk of premature aging and age-associated diseases increases. Therefore, knowledge of how OSER1 functions in the cells and preclinical animal models is vital to our overall knowledge of human aging and human health in general.

“We are currently focused on uncovering the role of OSER1 in humans, but the lack of existing literature presents a challenge, as very little has been published on this topic to date. This study is the first to demonstrate that OSER1 is a significant regulator of aging and longevity. In the future, we hope to provide insights into the specific age-related diseases and aging processes that OSER1 influences,” says Zhiquan Li.

The researchers also hope that the identification and characterization of OSER1 will provide new drug targets for age-related diseases such as metabolic diseases, cardiovascular and neuro degenerative diseases.

“Thus, the discovery of this new pro-longevity factor allows us to understand longevity in humans better,” says Zhiquan Li.

Source: University of Copenhagen – The Faculty of Health and Medical Sciences

Categories : AgeingTags :

Turning off Pro-inflammatory Cytokine IL-11 Extends Healthy Lifespan in Mice

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Credit: MRC LMS, Duke-NUS Medical School

Scientists have discovered that ‘turning off’ the cytokine IL-11 can significantly increase the healthy lifespan of mice by almost 25%.

The scientists, at the Medical Research Council Laboratory of Medical Science (MRC LMS), Imperial College London and Duke-NUS Medical School in Singapore, tested the effects of IL-11 by creating mice with the gene for IL-11 (interleukin 11) deleted. This extended the lives of the mice by over 20% on average. The cytokine has for years been misidentified as an anti-inflammatory and anti-fibrotic.

They also treated 75-week-old mice, equivalent to the age of about 55 years in humans, with an injection of an anti-IL-11 antibody, a drug that stops the effects of the IL-11 in the body.

Median lifespan extended

The results, published in Nature, were dramatic, with mice given the anti-IL-11 drug from 75 weeks of age until death having their median lifespan extended by 22.4% in males and 25% in females. The mice lived for an average of 155 weeks, compared with 120 weeks in untreated mice.

The treatment largely reduced deaths from cancer in the animals, as well as reducing the many diseases caused by fibrosis, chronic inflammation and poor metabolism, which are hallmarks of ageing. There were very few side effects observed.

Fewer cancers and free from the usual signs of ageing and frailty

Professor Stuart Cook, who was co-corresponding author, from MRC LMS, Imperial College London and Duke-NUS Medical School in Singapore, said:

These findings are very exciting. The treated mice had fewer cancers, and were free from the usual signs of ageing and frailty, but we also saw reduced muscle wasting and improvement in muscle strength. In other words, the old mice receiving anti-IL11 were healthier.

Previously proposed life-extending drugs and treatments have either had poor side-effect profiles, or don’t work in both sexes, or could extend life, but not healthy life, however this does not appear to be the case for IL-11.

While these findings are only in mice, it raises the tantalising possibility that the drugs could have a similar effect in elderly humans. Anti-IL-11 treatments are currently in human clinical trials for other conditions, potentially providing exciting opportunities to study its effects in ageing humans in the future.

The researchers have been investigating IL-11 for many years and in 2018 they were the first to show that IL-11 is a pro-fibrotic and pro-inflammatory protein, overturning years of incorrect characterisation as anti-fibrotic and anti-inflammatory.

Levels of IL-11 increases with age

Assistant Professor Anissa Widjaja, who was co-corresponding author, from Duke-NUS Medical School, Singapore, said:

This project started back in 2017 when a collaborator of ours sent us some tissue samples for another project. Out of curiosity, I ran some experiments to check for IL-11 levels. From the readings, we could clearly see that the levels of IL-11 increased with age and that’s when we got really excited!

We found these rising levels contribute to negative effects in the body, such as inflammation and preventing organs from healing and regenerating after injury. Although our work was done in mice, we hope that these findings will be highly relevant to human health, given that we have seen similar effects in studies of human cells and tissues.

This research is an important step toward better understanding ageing and we have demonstrated, in mice, a therapy that could potentially extend healthy ageing, by reducing frailty and the physiological manifestations of ageing.

Previously, scientists have posited that IL-11 is an evolutionary hangover in humans, as while it is vital for limb regeneration in some animal species, it is thought to be largely redundant in humans.

IL-11 linked to chronic inflammation and frailty

However, after about the age of 55 in humans, more IL-11 is produced and past research has linked this to chronic inflammation, fibrosis in organs, disorders of metabolism, muscle wasting (sarcopaenia), frailty, and cardiac fibrosis. These conditions are many of the signs we associate with ageing.

When two or more such conditions occur in an individual, it is known as multimorbidity, which encompasses a range of conditions including lung disease, cardiovascular disease, diabetes, vision and hearing decline and a host of other conditions.

Professor Cook said:

The IL-11 gene activity increases in all tissues in the mouse with age. When it gets turned on it causes multimorbidity, which is diseases of ageing and loss of function across the whole body, ranging from eyesight to hearing, from muscle to hair, and from the pump function of the heart to the kidneys.

Multimorbidity among biggest global healthcare challenges

Multimorbidity and frailty are acknowledged to be among the biggest global healthcare challenges of the 21st century, according to many leading health bodies, including the NHS and the World Health Organization.

Currently, no treatment for multimorbidity is available, other than to try to treat the separate multiple underlying causes individually.

The scientists caution that the results in this study were in mice and the safety and effectiveness of these treatments in humans need further establishing in clinical trials before people consider using anti-IL-11 drugs for this purpose.

Source: UK Research & Innovation

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Activating Specific Neurons Extends the Lifespan of Mice

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Photo by Kanashi ZD on Unsplash

Studies have recently begun to reveal that the lines of communication between the body’s organs are key regulators of aging. When these lines are open, the body’s organs and systems work well together. But with age, communication lines deteriorate, and organs don’t get the molecular and electrical messages they need to function properly.

A new study from Washington University School of Medicine in St. Louis identifies, in mice, a critical communication pathway connecting the brain and fat tissue in a feedback loop that appears central to energy production throughout the body. The research suggests that the gradual deterioration of this feedback loop contributes to the increasing health problems that are typical of natural aging.

The study, which appears in Cell Metabolism, has implications for developing future interventions that could maintain the feedback loop longer and slow the effects of advancing age.

The researchers identified a specific set of neurons in the brain’s hypothalamus that, when active, sends signals to the body’s fat tissue to release energy. Using genetic and molecular methods, the researchers studied mice that were programmed to have this communication pathway constantly open after they reached a certain age. The scientists found that these mice were more physically active, showed signs of delayed aging, and lived longer than mice in which this same communication pathway gradually slowed down as part of normal aging.

“We demonstrated a way to delay aging and extend healthy life spans in mice by manipulating an important part of the brain,” said senior author Shin-ichiro Imai, MD, PhD, the Theodore and Bertha Bryan Distinguished Professor in Environmental Medicine and a professor in the Department of Developmental Biology at Washington University. “Showing this effect in a mammal is an important contribution to the field; past work demonstrating an extension of life span in this way has been conducted in less complex organisms, such as worms and fruit flies.”

These specific neurons, in a part of the brain called the dorsomedial hypothalamus, produce an important protein: Ppp1r17. When this protein is present in the nucleus, the neurons are active and stimulate the sympathetic nervous system, which governs the body’s fight or flight response.

The fight-or-flight response is well known for having broad effects throughout the body, including causing increased heart rate and slowed digestion. As part of this response, the researchers found that the neurons in the hypothalamus set off a chain of events that triggers neurons that govern white adipose tissue stored under the skin and in the abdominal area. The activated fat tissue releases fatty acids into the bloodstream for fuelling physical activity, as well as another important protein, an enzyme called eNAMPT, which returns to the hypothalamus and allows the brain to produce fuel for its functions.

This feedback loop is critical for fuelling the body and the brain, but it slows down over time. With age, the researchers found that the protein Ppp1r17 tends to leave the nucleus of the neurons, and when that happens, the neurons in the hypothalamus send weaker signals. With less use, the nervous system wiring throughout the white adipose tissue gradually retracts, and what was once a dense network of interconnecting nerves becomes sparse. The fat tissues no longer receive as many signals to release fatty acids and eNAMPT, leading to fat accumulation, weight gain and less energy for the brain and other tissues.

The researchers, including first author Kyohei Tokizane, PhD, a staff scientist and a former postdoctoral researcher in Imai’s lab, found that when they used genetic methods in old mice to keep Ppp1r17 in the nucleus of the neurons in the hypothalamus, the mice were more physically active, with increased wheel-running, and lived longer than control mice. They also used a technique to directly activate these specific neurons in the hypothalamus of old mice, and they observed similar anti-aging effects.

The high end of the life span of a typical laboratory mouse is generally about 900–1000 days. In this study, all of the control mice that had aged normally died by 1000 days of age. Those that underwent interventions to maintain the brain-fat tissue feedback loop lived 60 to 70 days longer than control mice. This is a roughly 7% increase in lifespan, which translates to a 75-year human lifespan being extended about five more years. The mice receiving the interventions also were more active and looked younger, with thicker and shinier coats, at later ages, suggesting more time with better health as well.

Imai and his team are continuing to investigate ways to maintain the feedback loop between the hypothalamus and the fat tissue. One route they are studying involves supplementing mice with eNAMPT, the enzyme produced by the fat tissue that returns to the brain and fuels the hypothalamus, among other tissues. When released by the fat tissue into the bloodstream, the enzyme is packaged inside compartments called extracellular vesicles, which can be collected and isolated from blood.

“We can envision a possible anti-aging therapy that involves delivering eNAMPT in various ways,” Imai said. “We already have shown that administering eNAMPT in extracellular vesicles increases cellular energy levels in the hypothalamus and extends life span in mice. We look forward to continuing our work investigating ways to maintain this central feedback loop between the brain and the body’s fat tissues in ways that we hope will extend health and life span.”

Source: Washington University School of Medicine

Categories : Ageing GenderTags :

Women Who Reach Their 90s Tend to Have Maintained Stable Weight

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Reaching the age of 90, 95 or 100, known as exceptional longevity, was more likely for women who maintained their body weight after age 60, according to a multi-institutional study led by University of California San Diego. Older women who sustained a stable weight were 1.2 to 2 times more likely to achieve longevity compared to those who lost 5% of their weight or more.

In this study published in the Journal of Gerontology: Medical Sciences, researchers investigated the link between weight changes later in life with exceptional longevity among 54 437 women who enrolled in the Women’s Health Initiative, a prospective study investigating causes of chronic diseases among postmenopausal women. Throughout the follow up period, 30 647 (56%) of the participants survived to the age of 90 or beyond.

Women who lost at least 5% weight were less likely to achieve longevity compared to those who achieved stable weight. For example, women who unintentionally lost weight were 51% less likely to survive to the age of 90. However, gaining 5% or more weight, compared to stable weight, was not associated with exceptional longevity.

“It is very common for older women in the United States to experience overweight or obesity with a body mass index range of 25 to 35. Our findings support stable weight as a goal for longevity in older women,” said first author Aladdin H. Shadyab, PhD, MPH, associate professor at UC San Diego.

“If aging women find themselves losing weight when they are not trying to lose weight, this could be a warning sign of ill health and a predictor of decreased longevity.”

The findings suggest that general recommendations for weight loss in older women may not help them live longer. Nevertheless, the authors caution that women should heed medical advice if moderate weight loss is recommended to improve their health or quality of life.

The data adds to research connecting weight change and mortality and is notably the first large study to examine weight change later in life and its relation to exceptional longevity.

Source: University of California – San Diego

Categories : Ageing Diet and NutritionTags :

Yeast Studies Suggest that Early Diet may be Key for Lifelong Health

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Photo by Patrick Fore on Unsplash

Researchers at the Babraham Institute are proposing an alternative link between diet and ageing based on studies in yeast. In a study using yeast, a useful model organism to study ageing, researchers showed that a ‘healthier’ galactose diet in early life led to reduced senescence in those cells. The findings, published in PLOS Biology, suggest that dietary makeup at a young age may have a long-lasting impact on health throughout the lifespan.

Dr Jon Houseley and his team have published their experiments, showing that healthy ageing is achievable through dietary change without restriction by potentially optimising diet, and that ill-health is not an inevitable part of the ageing process.

Scientists have long known that caloric restriction improves health in later life and may even extend life. However, studies in mice show that caloric restriction really needs to be maintained throughout life to achieve this impact, and the health benefits disappear when a normal diet is resumed. Dr Houseley’s new research conducted in yeast suggests an alternative to calorie restriction can lead to improved health through the lifecycle.

“We show that diet in early life can switch yeast onto a healthier trajectory. By giving yeast a different diet without restricting calories we were able to suppress senescence, when cells no longer divide, and loss of fitness in aged cells.” Said Dr Dorottya Horkai, lead researcher on the study.

Rather than growing yeast on their usual glucose-rich diet, the researchers swapped their diet to galactose and observed that many molecular changes which normally accompany ageing did not occur. The cells grown on galactose remained just as fit as young cells even late in life, despite not living any longer, showing that the period of ill-health towards the end of life was dramatically reduced.

“Crucially, the dietary change only works when cells are young, and actually diet makes little difference in old yeast. It is hard to translate what youth means between yeast and humans, but all these studies point to the same trend – to live a long and healthy life, a healthy diet from an early age makes a difference.” explains Dr Houseley.

Yeast are good model organisms for studying ageing as they share many of the same cellular machinery as animals and humans. This avenue of research in yeast helps us to seek a more achievable way to improve healthy ageing though diet compared to sustained and severe calorie restriction, although more research is needed.

Source: Babraham Institute

Categories : Ageing GeneticsTags :

Mice Live Longer when Given a Longevity Gene from Naked Mole Rats

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CRISPR-Cas9 is a customisable tool that lets scientists cut and insert small pieces of DNA at precise areas along a DNA strand. This lets scientists study our genes in a specific, targeted way. Credit: Ernesto del Aguila III, National Human Genome Research Institute, NIH

In a ground-breaking advance in aging research, scientists have successfully transferred a longevity gene from naked mole rats to mice, resulting in improved health and an extension of the mouse’s lifespan.

Naked mole rats are known for their long lifespans and exceptional resistance to age-related diseases. By introducing a specific gene responsible for enhanced cellular repair and protection into mice, the researchers have opened exciting possibilities for unlocking the secrets of aging and extending human lifespan.

“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, professor at Rochester University. Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, report in a study published in Nature that they successfully transferred a gene responsible for making high molecular weight hyaluronic acid (HMW-HA) from a naked mole rat to mice. This led to improved health and an approximate 4.4 percent increase in median lifespan for the mice.

A unique mechanism for cancer resistance

Naked mole rats are mouse-sized rodents that have exceptional longevity for rodents of their size; they can live up to 41 years, nearly ten times as long as similar-size rodents. Unlike many other species, naked mole rats do not often contract age-related diseases such neurodegeneration, cardiovascular disease, arthritis, and cancer. Gorbunova and Seluanov have devoted decades of research to understanding the unique mechanisms that naked mole rats use to protect themselves against aging and diseases.

The researchers previously discovered that HMW-HA is one mechanism responsible for naked mole rats’ unusual resistance to cancer. Compared to mice and humans, naked mole rats have about ten times more HMW-HA in their bodies. When the researchers removed HMW-HA from naked mole rat cells, the cells were more likely to form tumours.

Gorbunova, Seluanov, and their colleagues wanted to see if the positive effects of HMW-HA could also be reproduced in other animals.

Transferring an HMW-HA-producing gene

The team genetically modified a mouse model to produce the naked mole rat version of the hyaluronan synthase 2 gene, which is the gene responsible for making a protein that produces HMW-HA. While all mammals have the hyaluronan synthase 2 gene, the naked mole rat version seems to be enhanced to drive stronger gene expression.

The researchers found that the mice that had the naked mole rat version of the gene had better protection against both spontaneous tumors and chemically induced skin cancer. The mice also had improved overall health and lived longer compared to regular mice. As the mice with the naked mole rat version of the gene aged, they had less inflammation in different parts of their bodies — inflammation being a hallmark of aging — and maintained a healthier gut.

While more research is needed on exactly why HMW-HA has such beneficial effects, the researchers believe it is due to HMW-HA’s ability to directly regulate the immune system.

A fountain of youth for humans?

“It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice,” Gorbunova says. “Our next goal is to transfer this benefit to humans.”

They believe they can accomplish this through two routes: either by slowing down degradation of HMW-HA or by enhancing HMW-HA synthesis.

“We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials,” Seluanov says. “We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health.”

Source: University of Rochester

Categories : Ageing Cardiovascular DiseaseTags :

Common Hypertension Drug Extends Lifespan in Animal Studies

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Old man
Photo by Kindel Media on Pexels

Researchers have found that, in animal studies, the hypertension drug rilmenidine can extend lifespan and slow ageing. Published in Aging Cell, the findings show that animals treated with rilmenidine at young and older ages increases lifespan and improves health markers by mimicking the effects of caloric restriction.

They also demonstrate that the healthspan and lifespan benefits of rilmenidine treatment in the roundworm C. elegans are mediated by the I1-imidazoline receptor nish-1, identifying this receptor as a potential longevity target.

With side-effects being rare and non-severe, unlike other drugs previously studied for this purpose by the researchers, the widely-prescribed antihypertensive has potential for future translatability.

A caloric restriction diet has thus far proved to be the most robust anti-ageing intervention, promoting longevity across species. However, studies of caloric restriction in humans have had mixed results and side effects, meaning finding medications like rilmenidine that can mimic the benefits of caloric restriction is the most reasonable anti-ageing strategy.

Professor João Pedro Magalhães, who led the research whilst at the University of Liverpool and is now based at the University of Birmingham, said: “With a global ageing population, the benefits of delaying ageing, even if slightly, are immense. Repurposing drugs capable of extending lifespan and healthspan has a huge untapped potential in translational geroscience. For the first time, we have been able to show in animals that rilmenidine can increase lifespan. We are now keen to explore if rilmenidine may have other clinical applications.”

Source: University of Liverpool. 

Categories : AgeingTags :

Longevity Treatments Fail to Turn Back the Clock

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In a new study published in the journal Nature Communications, researchers have taken a close look at three treatment approaches that have been widely believed to slow the ageing process. However, when tested in mice, these treatments proved largely ineffective in their supposed impact on ageing.

“There is no internal clock of ageing that you can regulate with a simple switch – at least not in the form of the treatments studied here,” concludes Dr Dan Ehninger of the German Centre for Neurodegenerative Diseases (DZNE), the initiator of the study. The team has developed a new analytical approach to make influences on ageing processes measurable.

“We chose three regulators for our interventions that many experts believe slow down aging,” explains Prof Martin Hrab de Angelis, who also drove the project with his team. One of them is intermittent fasting, in which the calories consumed are reduced. Number two targets a central node of cell metabolism (mTOR), which is also the target of the supposed “anti-ageing drug” rapamycin. Number three, in turn, interferes with the release of growth hormone. Similar treatments are also used by humans, although their efficacy with regard to ageing has not been sufficiently proven.

For the assessment in mice, the scientists developed a new answer to the question of how to measure ageing. “Many researchers in recent decades have used lifespan as an indirect measure of ageing,” explains Dan Ehninger, who is a senior scientist at DZNE. So, for example, how old do mice get – and how can that lifespan be extended? “It is often assumed that if they just live longer, they will also age more slowly. But the problem is that mice, like many other organisms, do not die from general old age, but from very specific diseases,” says Ehninger. For example, up to 90 percent of mice die from tumors that form in their bodies at an advanced age. “So, if you were to look at the whole genome for factors that make mice become long-lived, you would like find many genes that suppress tumor development – and not necessarily genes that play a general role in aging.”

For their study, the scientists therefore chose an approach that does not emphasize lifespan, but rather focused on a comprehensive investigation of age-related changes in a wide range of bodily functions. “You can think of it as a complete health status survey,” says Martin Hrab de Angelis: “The health check results in a compendium of hundreds of factors covering many areas of physiology” – an exact description of the state of the animal at the moment of examination. That’s exactly the approach the researchers applied to the animals subjected to one of the three treatment approaches that supposedly slow ageing. Across different life stages, they were analysed and compared: How much does each parameter typically change at a given stage of life? And, do parameters change more slowly when the mice are given one of the three treatments? This study design makes it possible to determine precisely whether the natural aging process can be slowed, and with it the deterioration of important physiological functions.

The results were unambiguous: Although the researchers were able to identify individual cases in which old mice looked younger than they actually were, it was clear that “this effect was not due to slowing down aging, but rather due to age-independent factors,” says Dan Ehninger. “The fact that a treatment already has its effect in young mice – prior to the appearance of age-dependent change in health measures – proves that these are compensatory, general health-promoting effects, not a targeting of aging mechanisms.”

The DZNE and Helmholtz Diabetes Center teams have now set their sights on the next goal: They want to investigate other treatment approaches that experts believe can slow aging. The researchers hope that the new research method will provide a more comprehensive picture of possible treatment approaches and their effectiveness.

Source: DZNE – German Center for Neurodegenerative Diseases