Category: Ageing

Categories : Ageing Neurodegenerative DiseasesTags :

Hearing Loss Linked to Dementia Risk

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A nationally representative study published in JAMA found that older adults with greater severity of hearing loss were more likely to have dementia, but the likelihood of dementia was lower among hearing aid users compared to non-users.

The findings are consistent with prior studies showing that hearing loss might be a contributing factor to dementia risk over time, and that treating hearing loss may lower dementia risk.

“This study refines what we’ve observed about the link between hearing loss and dementia, and builds support for public health action to improve hearing care access,” says lead author Alison Huang, PhD, MPH, a senior research associate in the Bloomberg School’s Department of Epidemiology and at the Cochlear Center for Hearing and Public Health, also at the Bloomberg School.

Hearing loss is a critical public health issue affecting two-thirds of Americans over 70. The growing understanding that hearing loss might be linked to the risk of dementia, which impacts millions, and other adverse outcomes has called attention to implementing possible strategies to treat hearing loss.

For the new study, Huang and colleagues analysed a nationally representative dataset from the National Health and Aging Trends Study (NHATS). Funded by the National Institute on Aging, the NHATS has been ongoing since 2011, and uses a nationwide sample of Medicare beneficiaries over age 65, with a focus on the 90-and-over group as well as Black individuals.

The analysis covered 2413 individuals, about half of whom were over 80 and showed a clear association between severity of hearing loss and dementia. Prevalence of dementia among the participants with moderate/severe hearing loss was 61% higher than prevalence among participants who had normal hearing. Hearing aid use was associated with a 32% lower prevalence of dementia in the 853 participants who had moderate/severe hearing loss.

The authors note that many past studies were limited in that they relied on in-clinic data collection, leaving out vulnerable populations that did not have the means or capacity to get to a clinic. For their study, the researchers collected data from participants through in-home testing and interviews.

How hearing loss is linked to dementia isn’t yet clear, and studies point to several possible mechanisms. Huang’s research adds to a body of work by the Cochlear Center for Hearing and Public Health examining the relationship between hearing loss and dementia.

Source: Johns Hopkins Bloomberg School of Public Health

Categories : Ageing ExerciseTags :

How to Stop Losing Exercise Recovery Capacity as We Age

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Although exercise is well-known to protect against many ageing-related diseases, it is not known the beneficial effects of exercise diminish with age. Now, in a paper published in the Proceedings of the National Academy of Sciences, researchers investigated how a mitochondrial mechanism improves physical fitness by exercise training and identified one anti-ageing intervention that delayed the declines that occur with ageing in the model organism. These findings may lead to new strategies for promoting muscle function during ageing.

“Exercise has been widely employed to improve quality of life and to protect against degenerative diseases, and in humans, a long-term exercise regimen reduces overall mortality,” said co-corresponding author T. Keith Blackwell, MD, PhD, a senior investigator at Joslin. “Our data identify an essential mediator of exercise responsiveness and an entry point for interventions to maintain muscle function during ageing.”

That essential mediator is the cycle of fragmentation and repair of the mitochondria. Disruption of mitochondrial dynamics the cycle of repairing dysfunctional mitochondria and restoring the connectivity among the energy-producing organelles has been linked to the development and progression of chronic, age-related diseases, such as heart disease and type 2 diabetes.

“As we perceive that our muscles undergo a pattern of fatigue and restoration after an exercise session, they are undergoing this mitochondrial dynamic cycle,” said Blackwell. “In this process, muscles manage the aftermath of the metabolic demand of exercise and restore their functional capability.”

Blackwell and colleagues investigated the role of mitochondrial dynamics during exercise in the model organism C. elegans, a simple, well-studied microscopic worm species frequently used in metabolic and aging research.

Recording wild type C. elegans worms as they swam or crawled, the investigators observed a typical age-related decline in physical fitness over the animals’ 15 days of adulthood. The scientists also showed a significant and progressive shift toward fragmented and/or disorganised mitochondria in the ageing animals. For example, they observed in young worms on day 1 of adulthood, a single bout of exercise induced fatigue after one hour. The 60-minute session also caused an increase in mitochondrial fragmentation in the animals’ muscle cells, but a period of 24 hours was sufficient to restore both performance and mitochondrial function.

In older (day 5 and day 10) worms, the animals’ performance did not return to baseline within 24 hours. Likewise, the older animals’ mitochondria underwent a cycle of fragmentation and repair, but the network reorganization that occurred was reduced compared to that of the younger animals.

“We determined that a single exercise session induces a cycle of fatigue and physical fitness recovery that is paralleled by a cycle of the mitochondrial network rebuilding,” said first author Juliane Cruz Campos, a postdoctoral fellow at Joslin Diabetes Center. “Ageing dampened the extent to which this occurred and induced a parallel decline in physical fitness. That suggested that mitochondrial dynamics might be important for maintaining physical fitness and possibly for physical fitness to be enhanced by a bout of exercise.”

In a second set of experiments, the scientists allowed wild type worms to swim for one hour per day for 10 consecutive days, starting at the onset of adulthood. As in humans, the long-term training programme significantly improved the animals’ middle-aged fitness at day 10, and mitigated the impairment of mitochondrial dynamics typically seen during ageing.

Finally, the researchers tested known, lifespan-extending interventions for their ability to improve exercise capacity during ageing. Worms with increased AMPK – a “guardian” of metabolism and mitochondrial homeostasis – exhibited improved physical fitness. They also demonstrated maintenance of exercise performance during ageing – but not enhancement. Worms engineered to lack AMPK exhibited reduced physical fitness during ageing as well as impairment of the recovery cycle. They also did not receive the age-delaying benefits of exercise over the course of the lifespan.

“An important goal of the ageing field is to identify interventions that not only extend lifespan but also enhance health and quality of life,” said Blackwell, who is also a professor of genetics at Harvard Medical School. “In ageing humans, a decline in muscle function and exercise tolerance is a major concern that leads to substantial morbidity. Our data point towards potentially fruitful intervention points for forestalling this decline – most likely along with other aspects of ageing. It will be of great interest to determine how mitochondrial network plasticity influences physical fitness along with longevity and ageing-associated diseases in humans.”

Source: Joslin Diabetes Center

Categories : Ageing NeurologyTags :

Memory Loss and Confusion More Common among Middle-aged Smokers

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Middle-aged smokers are much more likely to report having memory loss and confusion than nonsmokers, and the likelihood of cognitive decline is lower for those who have quit, even recently, according to a new study appearing in the Journal of Alzheimer’s Disease.

The study is the first to examine the relationship between smoking and cognitive decline using a one-question self-assessment asking people if they’ve experienced worsening or more frequent memory loss and/or confusion.

The findings build on previous research that established relationships between smoking and Alzheimer’s Disease and other forms of dementia, and could point to an opportunity to identify signs of trouble earlier in life, said Jenna Rajczyk, lead author of the study.

It’s also one more piece of evidence that quitting smoking is good not just for respiratory and cardiovascular reasons, but to preserve neurological health, said Rajczyk, a PhD student in Ohio State’s College of Public Health, and senior author Jeffrey Wing, assistant professor of epidemiology.

“The association we saw was most significant in the 45–59 age group, suggesting that quitting at that stage of life may have a benefit for cognitive health,” Wing said. A similar difference wasn’t found in the oldest group in the study, which could mean that quitting earlier affords people greater benefits, he said.

Researchers used data from the 2019 Behavioral Risk Factor Surveillance System Survey to compare subjective cognitive decline (SCD) measures for current smokers, recent former smokers, and those who had quit years earlier. The analysis included 136 018 people 45 and older, and about 11% reported SCD.

The prevalence of SCD among smokers in the study was almost 1.9 times that of nonsmokers. The prevalence among those who had quit less than 10 years ago was 1.5 times that of nonsmokers. Those who quit more than a decade before the survey had an SCD prevalence just slightly above the nonsmoking group.

“These findings could imply that the time since smoking cessation does matter, and may be linked to cognitive outcomes,” Rajczyk said.

The simplicity of SCD, a relatively new measure, could lend itself to wider applications, she said.

“This is a simple assessment that could be easily done routinely, and at younger ages than we typically start to see cognitive declines that rise to the level of a diagnosis of Alzheimer’s Disease or dementia,” Rajczyk said. “It’s not an intensive battery of questions. It’s more a personal reflection of your cognitive status to determine if you’re feeling like you’re not as sharp as you once were.”

Many people don’t have access to more in-depth screenings, or to specialists, making the potential applications for measuring SCD even greater, she said.

Wing said it’s important to note that these self-reported experiences don’t amount to a diagnosis, nor do they confirm independently that a person is experiencing decline out of the normal ageing process. But, he said, they could be a low-cost, simple tool to consider employing more broadly.

Source: Ohio State University

Categories : AgeingTags :

Adults Get the Least Sleep From Their 30s to 50s

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People sleep less in mid-adulthood than they do in early and late adulthood, according to a large study published in Nature Communications. The study investigators found that sleep duration declines in early adulthood until age 33, and then picks up again at age 53.

The study, involving 730 187 participants spread over 63 countries, revealed how sleep patterns change across the lifespan, and how they were largely the same across countries.

Study participants were playing the Sea Hero Quest mobile game, a citizen science venture designed for neuroscience research, which was designed to aid Alzheimer’s research by shedding light on differences in spatial navigational abilities. Thus far, over four million people have played Sea Hero Quest, contributing to numerous studies across the project as a whole.

In addition to completing tasks testing navigational ability, anyone playing the game is asked to answer questions about demographic characteristics as well as other questions that can be useful to neuroscience research, such as on sleep patterns.

The researchers, led by Professor Hugo Spiers (UCL Psychology & Language Sciences) and Dr Antoine Coutrot (CNRS, University of Lyon) found that across the study sample, people sleep an average of 7.01 hours per night, with women sleeping 7.5 minutes longer than men on average. They found that the youngest participants in the sample (age 19) slept the most, and sleep duration declined throughout people’s 20s and early 30s before plateauing until their early 50s and increasing again. The pattern, including the newly-identified key time points of age 33 when declining sleep plateaus and 53 for sleep to increase again, was the same for men and women, and across countries and education levels.

The researchers suggest the decline in sleep during mid-life may be from the demands of childcare and working life.

Professor Spiers said: “Previous studies have found associations between age and sleep duration, but ours is the first large study to identify these three distinct phases across the life course. We found that across the globe, people sleep less during mid-adulthood, but average sleep duration varies between regions and between countries.”

People who report sleeping the most are in Eastern European countries such as Albania, Slovakia, Romania and the Czech Republic, reporting 20–40 minutes extra sleep per night and the least in South East Asian countries including the Philippines, Malaysia and Indonesia. People in the United Kingdom reported sleeping slightly less than the average. People tended to sleep a bit less in countries closer to the equator.

The researchers found that navigational ability was unaffected by sleep duration for most of the sample, except for among older adults (aged 54–70) whose optimal sleep duration was seven hours, although they caution that the findings among older adults might be impacted by underlying health conditions.

Source: University College London

Categories : AgeingTags :

Good Hydration may be Key to Healthy Ageing

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Adults who stay well-hydrated appear to be healthier, develop fewer chronic conditions, such as heart and lung disease, and live longer than those who may not get sufficient fluids, according to a study published in eBioMedicine.

Using health data gathered from 11 255 adults over a 30-year period, researchers analysed links between serum sodium levels (which increase with reduced fluid intake) and various indicators of health. They found that adults with serum sodium levels at the higher end of a normal range were more likely to develop chronic conditions and show signs of advanced biological aging than those with serum sodium levels in the medium ranges. Adults with higher levels were also more likely to die at a younger age.

“The results suggest that proper hydration may slow down aging and prolong a disease-free life,” said Natalia Dmitrieva, PhD, a study author and researcher at the National Heart, Lung, and Blood Institute (NHLBI).

The study expands on previous research from the scientists, which found links between high-normal serum sodium levels and increased risks for heart failure. Both findings came from the Atherosclerosis Risk in Communities (ARIC) study, which started in 1987.

For this latest analysis, researchers assessed information study participants shared during five medical visits – the first two when they were in their 50s, and the last between ages 70–90. Adults who had high levels of serum sodium at baseline check-ins or with underlying conditions, like obesity, that could affect serum sodium levels, were excluded.

The researchers then evaluated how serum sodium levels correlated with biological ageing, which was assessed through 15 health markers such as systolic blood pressure, cholesterol, and blood sugar. These provided insight about how well each person’s cardiovascular, respiratory, metabolic, renal, and immune system was functioning. They also adjusted for factors, like age, race, biological sex, smoking status, and hypertension.

They found that adults with higher levels of normal serum sodium, normallu between 135–146 milliequivalents per litre (mEq/L), were more likely to show signs of faster biological ageing. This was based on indictors like metabolic and cardiovascular health, lung function, and inflammation. For example, adults with serum sodium levels above 142mEq/L had a 10-15% associated increased odds of being biologically older than their chronological age compared to ranges between 137–142mEq/L, while levels above 144mEq/L correlated with a 50% increase. Likewise, levels of 144.5–146 mEq/L were associated with a 21% increased risk of premature death compared to ranges between 137–142mEq/L.

Similarly, adults with serum sodium levels above 142mEq/L had up to a 64% increased associated risk for developing chronic diseases like heart failure, stroke, atrial fibrillation and peripheral artery disease, as well as chronic lung disease, diabetes, and dementia. Conversely, adults with serum sodium levels between 138–140 mEq/L had the lowest risk of developing chronic disease.

The researchers caution that randomised, controlled trials are needed to prove an association between fluid intake and signs of ageing.

“People whose serum sodium is 142mEq/L or higher would benefit from evaluation of their fluid intake,” Dmitrieva said. She noted that most people can safely increase their fluid intake to meet recommended levels, which can be done with water as well as other fluids, like juices, or vegetables and fruits with a high water content. The National Academies of Medicine, for example, suggest that most women consume around 6-9 cups (1.5–2.2 litres) of fluids daily and for men, 8-12 cups (2–3 litres).

Others may need medical guidance due to underlying health conditions. “The goal is to ensure patients are taking in enough fluids, while assessing factors, like medications, that may lead to fluid loss,” said study author Manfred Boehm, MD, director of the Laboratory of Cardiovascular Regenerative Medicine at NHLBI. “Doctors may also need to defer to a patient’s current treatment plan, such as limiting fluid intake for heart failure.”

The authors also cited research that finds about half of people worldwide don’t meet recommendations for daily total water intake, which often starts at 6 cups (1.5 litres).

“On the global level, this can have a big impact,” Dmitrieva said. “Decreased body water content is the most common factor that increases serum sodium, which is why the results suggest that staying well hydrated may slow down the aging process and prevent or delay chronic disease.”

Source: NIH/National Heart, Lung and Blood Institute

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

Categories : AgeingTags :

Areas with Age Bias Associated with Greater Longevity

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Older adults living in areas with greater age bias had better health outcomes than those in areas with less bias, according to a study published in Social Science & Medicine. These findings came as a surprise to the researchers, who were expecting the reverse.

“Quite the opposite of what we expected emerged,” says senior author Allecia Reid, associate professor of social psychology and senior author of the paper published in the journal . “Rather than dying earlier in counties with more negative attitudes toward older adults, we found in fact that older adults were living longer in counties with more negative attitudes towards older adults.”

University of Massachusetts Amherst researcher Reid and colleagues had based their hypothesis on earlier research showing that minority groups, such as African Americans and sexual minorities, have worse health outcomes in counties with more negative attitudes toward their group.

“We were thinking, similar to those findings, that in counties with more negative attitudes towards older adults, we would see them being likely to die earlier than in counties with more positive attitudes toward residents 65 and older,” Reid says. “Contrary to what we thought, something positive is happening in these ageist communities that is helping them live longer, healthier lives.”

The only other study examining community-level age bias and older adults’ health found that explicit age bias was linked to positive health behaviours among older adults, while implicit bias was linked to negative health behaviours among older adults.

The UMass Amherst researchers analysed data on more than one million Americans who reported their explicit bias and taken an implicit bias test between 2003 and 2018

Based on that data, the team developed aggregate estimates at the county level about how much residents like older adults. Then they linked that with the county’s death rates for individuals age 65+. Counties with higher explicit age bias had lower mortality, or 87.67 fewer deaths per 100 000 residents. In contrast, implicit bias was not associated with mortality outcomes.

“The explicit age bias-mortality association was only evident in communities with younger populations but did not depend on community ethnic composition,” the paper states.

The researchers looked at ways that the more ageist communities might be doing things that helped maintain the health of older adults. They found that greater explicit age bias also was associated with lower death rates among young and middle-aged adults in those counties, suggesting that any health benefits of living in ageist communities may begin to accrue in earlier life.

In addition, “communities with higher explicit age bias also had higher rates of exercise…, better general health…, and more days of good mental health,” the paper states. These findings point to potential pathways through which ageist communities may promote health. However, the researchers also note that factors they were unable to examine, such as better medical care and more green spaces, may also explain associations of community age bias with better health.

Reid says the surprising findings point to more areas of examination which may lead to improved longevity for all communities.

“Can we figure out what is happening in these more ageist communities that seems to be potentially promoting both better mental health and better longevity,” she says. “And if we can pinpoint those things, then that’s a flag for all communities to think about.”

Source: University of Massachusetts Amherst

Categories : AgeingTags :

Macrophages Explain Vulnerability to Influenza in Old Age

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After being suppressed during the COVID pandemic, influenza is again circulating and threatening the health of over 65s. But why are older people so more susceptible to the flu? A new study from the University of Michigan, published in Nature Communications, offers clues.

The study, led by first author Judy Chen, a PhD candidate, senior author Professor Daniel Goldstein, MD, and their team investigates why cells called alveolar macrophages, the first line of defence in the lungs, appear to be compromised with age.

Macrophages attack pathogens like the flu virus and reside in alveoli. Importantly, these cells appear to be lost with ageing.

Previous research by another group showed that when macrophages from an old mouse were put into a young mouse, and cells looked young again. “This drove us to believe that something in the environment of the lungs is contributing to this,” said Chen.

Signs pointed to a lipid immune modulator known as prostaglandin E2 (PGE2) with wide ranging effects, from labour induction in pregnancy to inflammation with arthritis. The study team discovered there is more PGE2 in the lungs with age. This increase in PGE2, Chen explained, acts on the macrophages in the lung, limiting their overall health and ability to generate.

The team suspects that the buildup of PGE2 is yet another marker of a biological process called senescence, which is often seen with age. Senescence serves as insurance against the runaway division of damaged cells; cells that are senescent are no longer able to replicate.

“One of the interesting things about these cells is they secrete a lot of inflammatory factors,” said Chen.

The study showed that with age, the cells lining the air sacs in the lungs become senescent, and these cells lead to increased production of PGE2 and suppression of the immune response.

To test the link between PGE2 and increased susceptibility to influenza, they treated older mice with a drug that blocks a PGE2 receptor. “The old mice that got that drug actually ended up having more alveolar macrophages and had better survival from influenza infection than older mice that did not get the drug,” said Chen.

The team plans to next investigate the various ways PGE2 affects lung macrophages as well as its potential role in inflammation throughout the body. “As we get older, we become more susceptible not only to influenza, but to other infections, cancers, autoimmune diseases as well.”

Source: Michigan Medicine – University of Michigan

Categories : AgeingTags :

Hormone Discovery could Predict Longevity of Men

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Researchers have discovered that a certain hormone, that develops in males during puberty, could be predictive of the risk of developing age-related disease in later life.

The novel insulin-like peptide hormone, called INSL3, was found by researchers to be consistent over long periods of time and is an important early biomarker for prediction of age-linked disease. Their latest findings have been published today in Frontiers in Endocrinology.

INSL3 is produced in the testes by Leydig cells, which also make testosterone, but unlike testosterone which fluctuates over a man’s life, INSL3 remains consistent, with the level at puberty staying about the same throughout life, decreasing only slightly into old age. This makes it the first clear and reliable predictive biomarker of age-related morbidity as compared to any other measurable parameters.

Blood levels of INSL3 were associated with a range of age-related illnesses, such as bone weakness, sexual dysfunction, diabetes, and cardiovascular disease.

Since the hormone is so consistent, a young man with high INSL3 would still have high INSL3 when he is older. But low levels of INSL3 when young will stay low when older, making a man more likely to acquire typical age-related illnesses. This opens up exciting possibilities for predicting age-related illnesses and finding ways to prevent the onset of these diseases with early intervention.

This study from University of Nottingham was led by Professors Ravinder Anand-Ivell and Richard Ivell and is the latest of three recent studies into this hormone. Prof Anand-Ivell explains: “The holy grail of ageing research is to reduce the fitness gap that appears as people age. Understanding why some people are more likely to develop disability and disease as they age is vital so that interventions can be found to ensure people not only live a long life but also a healthy life as they age. Our hormone discovery is an important step in understanding this and will pave the way for not only helping people individually but also helping to ease the care crisis we face as a society.”

The team analysed blood samples from 3000 men, with two samples taken four years apart and found that unlike testosterone, INSL3 remains at consistent.

The study also showed that there is an almost 10-fold variation in INSL3 levels in the normal male population, even among the young and healthy.

Prof Ivell adds: “Now we know the important role this hormone plays in predicting disease and how it varies amongst men we are turning our attention to finding out what factors have the most influence on the level of INSL3 in the blood. Preliminary work suggests early life nutrition may play a role, but many other factors such as genetics or exposure to some environmental endocrine disruptors may play a part.”

Source: University of Nottingham

Categories : AgeingTags :

Friendly ‘Zombie’ Cells Help Promote Tissue Repair

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While most senescent cells may be harmful “zombies” spewing toxic compounds and should be targeted to reduce the risk of age-related disease, not all of them are like this. In fact, according to new research in Science, some of them embedded in young, healthy tissues seem to help repair damage.

Scientists have now seen these cells in action in lung tissue, as well as other organs that serve as barriers in the body, such as the small intestine, colon and skin. When they used drugs called senolytics to kill these cells, injuries to lung tissues healed more slowly.

“Senescent cells can occupy niches with privileged positions as ‘sentinels’ that monitor tissue for injury and respond by stimulating nearby stem cells to grow and initiate repair,” said Tien Peng, MD, associate professor of pulmonary, critical care, allergy and sleep medicine, and senior author of the study.

Ageing cells can both damage and heal

A/Prof Peng said it was understandable that scientists at first viewed senescent cells as purely detrimental. As people age, senescent cells – often termed “zombie cells” – accumulate that have characteristics of old, worn-out cells, including the inability to make new cells. Instead of dying like normal aged cells, they to live on, spewing a cocktail of inflammatory compounds that form the senescence associated secretory phenotype (SASP). These factors are linked to Alzheimer’s disease, arthritis, and other age-related maladies including cancer.

Using senolytics that selectively kill “zombie cells,” researchers made the exciting discovery that clearing senescent cells from animals thwarted or diminished age-related disease and extended the lifespan of the animals. Thereafter, a boom of activity ensued in research labs and pharmaceutical companies focused on discovering and refining more powerful versions of these drugs.

But killing off senescent cells has dangers, A/Prof Peng said. For one thing, this current study showed that senescent cells also possess the ability to promote normal healing through activation of stem cell repair. “Our study suggests that senolytics could adversely affect normal repair, but they also have the potential to target diseases where senescent cells drive pathologic stem cell behaviour,” said A/Prof Peng.

Lighting up senescent cells

One major challenge to studying senescent cells is that biomarkers of senescence (such as the gene p16) are often quite sparse, making it difficult to detect the cells. In early experiments, researchers extracted cells called fibroblasts into culture dishes, allowing them to grow and produce enough cells to experiment with, and then stressed the cells with chemicals that induced them to become senescent. But in living organisms, cells interact with tissues around them, strongly affecting the cells’ gene activity. This means that the characteristics of cells growing isolated in a glass dish could be quite different from that of cells in their natural environment.

To create a more powerful tool for their studies, the researchers improved on a common technique of fusing a relevant gene – in this case, the p16 gene, which is overly active in senescent cells –with green fluorescent protein (GFP) as a marker that can reveal the location of the cells under ultraviolet light. By enhancing the quantity and stability of green fluorescent protein in these senescent cells, the fluorescent signal was greatly amplified, finally enabling the researchers to see senescent cells in their natural habitat of living tissues.

“Zombies” stimulate stem cells shortly after birth

Using this highly sensitive tool, the researchers found that senescent cells exist in young and healthy tissues to a greater extent than previously thought, and actually begin appearing shortly after birth. The scientists also identified specific growth factors that senescent cells secrete to stimulate stem cells to grow and repair tissues. Relevant to aging and tissue injury is the discovery that cells of the immune system such as macrophages and monocytes can activate senescent cells, suggesting that inflammation seen in aged or damaged tissue is a critical modifier of senescent cell activity and regeneration.

In their studies of lung tissue, A/Prof Peng’s team observed green glowing senescent cells lying next to stem cells on the basement membrane that serves as a barrier preventing foreign cells and harmful chemicals from entering the body and also allows oxygen to diffuse from air in the lungs into underlying tissues. Damage can occur at this dynamic interface. The team saw senescent cells in similar positions in other barrier organs such as small intestine, colon, and skin, and their experiments confirmed that if senescent cells were killed with senolytics, lung stem cells were not able to properly repair the barrier surface.

Source: EurekAlert!