Tag: ageing

Standing on One Leg is a Good Indicator of Ageing

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How long a person can stand on one leg is a more tell-tale measure of ageing than changes in strength or gait, according to new Mayo Clinic research published in the journal PLOS ONE.

Good balance, muscle strength and an efficient gait contribute to people’s independence and well-being as they age. How these factors change, and at what rate, can help clinicians develop programs to ensure healthy ageing. Individually, people can train their balance without special equipment and work on maintaining it over time.

In this study, 40 healthy, independent people over 50 underwent walking, balance, grip strength and knee strength tests. Half of the participants were under 65; the other half were 65 and older.

In the balance tests, participants stood on force plates in different situations: on both feet with eyes open, on both feet with eyes closed, on the non-dominant leg with eyes open, and on the dominant leg with eyes open. In the one-legged tests, participants could hold the leg they weren’t standing on where they wanted. The tests were 30 seconds each.

Standing on one leg, specifically the nondominant leg, showed the highest rate of decline with age.

“Balance is an important measure because, in addition to muscle strength, it requires input from vision, the vestibular system and the somatosensory systems,” says Kenton Kaufman, PhD, senior author of the study and director of the Motion Analysis Laboratory at Mayo Clinic. “Changes in balance are noteworthy. If you have poor balance, you’re at risk of falling, whether or not you’re moving. Falls are a severe health risk with serious consequences.”

Unintentional falls are the leading cause of injuries among adults who are 65 and older. Most falls among older adults result from a loss of balance.

In the other tests:

  • Researchers used a custom-made device to measure participants’ grip. For the knee strength test, participants were in a seated position and instructed to extend their knee as forcefully as possible. Both the grip and knee strength tests were on the dominant side. Grip and knee strength showed significant declines by decade but not as much as balance. Grip strength decreased at a faster rate than knee strength, making it better at predicting aging than other strength measures.
  • For the gait test, participants walked back and forth on an 8-metre, level walkway at their own pace and speed. Gait parameters didn’t change with age. This was not a surprising result since participants were walking at their normal pace, not their maximum pace, Dr Kaufman says.
  • There were no age-related declines in the strength tests that were specific to sex. This indicates that participants’ grip and knee strength declined at a similar rate. Researchers did not identify sex differences in the gait and balance tests, which suggests that male and female subjects were equally affected by age.

Dr Kaufman says that people can take steps to train their balance. For example, by standing on one leg, you can train yourself to coordinate your muscle and vestibular responses to maintain correct balance. If you can stand on one leg for 30 seconds, you are doing well, he says.

“If you don’t use it, you lose it. If you use it, you maintain it,” Dr Kaufman says. “It’s easy to do. It doesn’t require special equipment, and you can do it every day.”

Source: Mayo Clinic

Older Women more Vulnerable to Heat than Men, Researchers Find

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As global climate change causes extreme heat waves to become more common around the world, epidemiological studies have shown that heat kills more women than men. Now, a new study by researchers at Penn State has found that older women are physiologically more vulnerable to high heat and humidity than older men, and that women between the ages of 40 and 64 are as vulnerable as men 65 years of age or older. This is the first study to determine this disparity exists due to physiological differences rather than from a preponderance of women at old age due to greater longevity.

Led by Olivia Leach, doctoral candidate in kinesiology at Penn State, and her adviser, W. Larry Kenney, professor of physiology and kinesiology at Penn State, the researchers demonstrated that middle-aged and older women were affected by heat at lower temperature/humidity combinations than middle-aged and older men. The results, published in the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, were somewhat unexpected, according to Leach, because there are no differences in heat vulnerability based on biological sex in adults younger than 30.

While the researchers did not directly compare middle-aged men to middle-aged women, the physiological responses of middle-aged women were similar to the responses of older men in the study, which demonstrated that middle-aged women are more vulnerable to heat than men of the same age.

“In addition to demonstrating that middle-aged and older women are at greater risk from extreme heat, we also identified what levels of heat and humidity are safe for women as they age,” Leach said. “This information is presented as a temperature/humidity curve based on a person’s age, and it can be useful for setting policies designed to keep people safe during a heat wave.”

The researchers tested the heat thresholds of 72 participants between 40 and 92 years of age in a specialized environmental chamber in Kenney’s laboratory. Before the experiment, participants swallowed a tiny device encased in a capsule that measured their core temperature throughout the experiment.

During the study, participants entered the specialised environmental chamber where they performed light physical activity to simulate the effort of minimal day-to-day tasks – the types of things people would need to do even during a heat wave. The researchers then gradually increased the temperature and/or humidity in the chamber until the participant’s body could no longer adequately cool itself, and their core temperature began to rise.

The study is part of the PSU HEAT, or Human Environmental Age Thresholds, project, led by Kenney. For five years, researchers in the PSU HEAT project have examined the levels of combined heat and humidity that humans can tolerate before their core temperatures begin to rise. When core temperatures rise, people become vulnerable to heat-related illnesses including heat exhaustion, heat stroke and even death.

“We’re not saying that people who experience a certain temperature will necessarily become sick or die,” Kenney said. “We are identifying the limits of livability – the thresholds where people can no longer continue their daily life unimpeded. Once people reach these temperatures, they need to take actions like seeking air conditioning to cool their bodies.”

Previous research by Kenney and others demonstrated that people become increasingly vulnerable to heat as they age, because their ability to efficiently sweat and pump blood to the skin – two primary cooling mechanisms – decreases. Sweat evaporation carries heat away from the body, while extra blood pumped to the skin dissipates heat to the environment and supports sweating.

To date, the PSU HEAT project has conducted more than 600 experiments on nearly 200 participants between ages 18 and 92, but the results of this experiment still yielded surprises, according to Leach.

“Among young adults, there is no difference in heat vulnerability between men and women,” Leach said. “Young people tend to be healthier, so any measurable health metric – from blood pressure to cholesterol – is more homogeneous among young people than it is among older people.”

As with other health measures, older adults have a wide range in their vulnerability to heat, Leach explained.

“We have examined many factors that might explain who faces the most risk in a heat wave,” Leach said. “We found that age and biological sex are the two most important factors that can predict whether a healthy adult would be at risk from high heat and humidity.”

While cardiovascular health and certain medications can affect a person’s sensitivity to heat, biological sex and age appear to be the two primary drivers of heat vulnerability among healthy people, the researchers said.

“Other factors – for example someone’s cardiovascular fitness or their body mass – have little impact on how vulnerable a person is to heat at rest or during light activity,” Leach continued. “Older women really are at greater risk from heat than other people. As governments and other social leaders prepare for extreme heat to become more common, the vulnerability of older women needs to factor into their planning.”

Source: Penn State

The Ageing Process Makes Big Jumps in Our 40s and 60s

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If it’s ever felt like everything in your body is breaking down at once, that might not be your imagination. A new Stanford Medicine study shows that many of our molecules and microorganisms dramatically rise or fall in number during our 40s and 60s.

Researchers assessed many thousands of different molecules in people from age 25 to 75, as well as their microbiomes – the bacteria, viruses and fungi that live inside us and on our skin – and found that the abundance of most molecules and microbes do not shift in a gradual, chronological fashion. Rather, we undergo two periods of rapid change during our life span, averaging around age 44 and age 60. A paper describing these findings was published in the journal Nature Aging.

“We’re not just changing gradually over time; there are some really dramatic changes,” said Michael Snyder, PhD, professor of genetics and the study’s senior author. “It turns out the mid-40s is a time of dramatic change, as is the early 60s. And that’s true no matter what class of molecules you look at.”

Xiaotao Shen, PhD, a former Stanford Medicine postdoctoral scholar, was the first author of the study. Shen is now an assistant professor at Nanyang Technological University Singapore.

These big changes likely impact our health – the number of molecules related to cardiovascular disease showed significant changes at both time points, and those related to immune function changed in people in their early 60s.

Abrupt changes in number

Snyder, the Stanford W. Ascherman, MD, FACS Professor in Genetics, and his colleagues were inspired to look at the rate of molecular and microbial shifts by the observation that the risk of developing many age-linked diseases does not rise incrementally along with years. For example, risks for Alzheimer’s disease and cardiovascular disease rise sharply in older age, compared with a gradual increase in risk for those under 60.

The researchers used data from 108 people they’ve been following to better understand the biology of aging. Past insights from this same group of study volunteers include the discovery of four distinct “ageotypes,” showing that people’s kidneys, livers, metabolism and immune system age at different rates in different people.

The new study analysed participants who donated blood and other biological samples every few months over the span of several years; the scientists tracked many different kinds of molecules in these samples, including RNA, proteins and metabolites, as well as shifts in the participants’ microbiomes. The researchers tracked age-related changes in more than 135 000 different molecules and microbes, for a total of nearly 250 billion distinct data points.

They found that thousands of molecules and microbes undergo shifts in their abundance, either increasing or decreasing – around 81% of all the molecules they studied showed non-linear fluctuations in number, meaning that they changed more at certain ages than other times. When they looked for clusters of molecules with the largest changes in amount, they found these transformations occurred the most in two time periods: when people were in their mid-40s, and when they were in their early 60s.

Although much research has focused on how different molecules increase or decrease as we age and how biological age may differ from chronological age, very few have looked at the rate of biological aging. That so many dramatic changes happen in the early 60s is perhaps not surprising, Snyder said, as many age-related disease risks and other age-related phenomena are known to increase at that point in life.

The large cluster of changes in the mid-40s was somewhat surprising to the scientists. At first, they assumed that menopause or perimenopause was driving large changes in the women in their study, skewing the whole group. But when they broke out the study group by sex, they found the shift was happening in men in their mid-40s, too.

“This suggests that while menopause or perimenopause may contribute to the changes observed in women in their mid-40s, there are likely other, more significant factors influencing these changes in both men and women. Identifying and studying these factors should be a priority for future research,” Shen said.

Changes may influence health and disease risk

In people in their 40s, significant changes were seen in the number of molecules related to alcohol, caffeine and lipid metabolism; cardiovascular disease; and skin and muscle. In those in their 60s, changes were related to carbohydrate and caffeine metabolism, immune regulation, kidney function, cardiovascular disease, and skin and muscle.

It’s possible some of these changes could be tied to lifestyle or behavioural factors that cluster at these age groups, rather than being driven by biological factors, Snyder said. For example, dysfunction in alcohol metabolism could result from an uptick in alcohol consumption in people’s mid-40s, often a stressful period of life.

The team plans to explore the drivers of these clusters of change. But whatever their causes, the existence of these clusters points to the need for people to pay attention to their health, especially in their 40s and 60s, the researchers said. That could look like increasing exercise to protect your heart and maintain muscle mass at both ages or decreasing alcohol consumption in your 40s as your ability to metabolise alcohol slows.

“I’m a big believer that we should try to adjust our lifestyles while we’re still healthy,” Snyder said.

Source: Stanford Medicine

Study Tallies Heatwave Deaths over Recent Decades

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Between 1990 and 2019, more than 150 000 deaths around the globe were associated with heatwaves each year, according to a new study published May 14 in PLOS Medicine by Yuming Guo of Monash University, Australia, and colleagues.

Heatwaves, periods of extremely high ambient temperature that last for a few days, can impose overwhelming thermal stress on the human body.

Studies have previously quantified the effect of individual heatwaves on excess deaths in local areas, but have not compared these statistics around the globe over such a prolonged period.

In the new study, researchers used data from the Multi-Country Multi-City (MCC) Collaborative Research Network that included daily deaths and temperatures from 750 locations across 43 countries.

With the MCC data, the researchers estimated excess heatwave deaths around the world spanning 1990 to 2019 and mapped the variance in these deaths across continents.

During the warm seasons from 1990 to 2019, heatwave-related excess deaths accounted for 153 078 deaths per year, a total of 236 deaths per 10 million residents or 1% of global deaths.

While Asia had the highest number of estimated deaths, Europe had the highest population-adjusted rate, at 655 deaths per 10 million residents.

A substantial burden of estimated deaths was seen in southern and eastern Europe as well as the area between Northern Africa, the Arabian Peninsula and Southern Asia.

At the national level, Greece, Malta, and Italy had the highest excess death ratios.

Overall, the largest estimated rates of heatwaves deaths were seen in areas with dry climates and lower-middle incomes.

Understanding the regional disparity of heatwave-related mortality is key to planning local adaptation and risk management towards climate change.

“Heatwaves are associated with substantial mortality burden that varies spatiotemporally over the globe in the past 30 years,” the authors say.

“These findings indicate the potential benefit of government actions to enhance health sector adaptation and resilience, accounting for inequalities across communities.”

The authors add, “In the context of climate change, it is crucial to address the unequal impacts of heatwaves on human health. This necessitates a comprehensive approach that not only tackles immediate health risks during heatwaves but also implements long-term strategies to minimize vulnerability and inequality. The strategies include: climate change mitigation policy, heat action plans (e.g., heat early warning system), urban planning and green structure, social support program, healthcare and public health services, education awareness, and community engagement and participation.”

Provided by PLOS

Age-related Brain Changes Affect Stroke Recovery, Study Finds

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A new study by a global team of researchers has revealed that areas of age-related damage in the brain relate to motor outcomes after a stroke – a potentially under-recognised phenomenon in stroke research. The study was published in Neurology.

A stroke often leads to motor impairment, which is traditionally linked to the extent of damage to the corticospinal tract (CST), a crucial brain pathway for motor control. Signaling along the CST is involved in a variety of movements, including walking, reaching, and fine finger movements like writing and typing. However, stroke recovery outcomes aren’t fully predicted by damage to the CST, suggesting other factors are at play.

The new observational from the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) Stroke Recovery working group. It examines how one such factor could be white matter hyperintensities (WMHs) – areas of age-related damage in the brain’s white matter, which represent vascular dysfunction and are known to impact cognitive functions. The goal of the ENIGMA Stroke Recovery working group is to understand how changes in the brain after stroke relate to functional outcomes and recovery. ENIGMA Stroke Recovery has data from over 2100 stroke patients collected across 65 research studies and 10 countries, comprising the most extensive multisite retrospective stroke data collaboration to date.

Study leader Sook-Lei Liew, PhD, said: “We are grateful for our many collaborators around the world who lead independent stroke research programs and who are willing to come together and enable large-scale investigations into these critical questions about the role of overall brain health in stroke recovery and rehabilitation.” Dr Liew is an associate professor at the Keck School of Medicine of USC.

The study analysed data from 223 stroke patients across four countries and found that larger WMH volumes were associated with more severe motor impairment after a stroke (e.g., difficulty moving or using their arm for daily tasks), independent of CST damage. WMHs are related to chronic hypertension, diabetes, high cholesterol, and smoking, among other factors and conditions, and have been strongly related to cognitive impairment, but not extensively studied in the context of motor impairment. Interestingly, the relationship between CST damage and motor impairment varied based on WMH severity. Patients with mild WMHs showed a typical relationship between CST damage and motor impairment, while patients with moderate to severe WMHs did not have this relationship. Instead, motor impairment was related to WMH volume, not CST damage.

These findings suggest that WMHs, indicative of cerebrovascular damage from a variety of sources, could provide additional context to understand an individual’s potential for recovery post-stroke. Therefore, assessing WMH volume could improve predictive models for stroke recovery.

“WMHs are related to overall cardiovascular and brain health as we age. By integrating assessments of age-related brain health, we may be better able to predict stroke recovery and tailor rehabilitation to individual needs. This personalised approach could open avenues to improve outcomes after stroke,” says lead author Jennifer K. Ferris, PhD, of Simon Fraser University.

The researchers’ next step is to pursue longitudinal studies to confirm their findings. This insight lays the groundwork for developing more accurate markers for recovery, which could transform post-stroke care and rehabilitation.

Source: Keck School of Medicine of USC

Essential Tremor Increases Cognitive Impairment Risks over Time

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Essential tremor, a nervous system disorder that causes rhythmic shaking, is one of the most common movement disorders. A new study published in the Annals of Neurology reveals details on the increased risk of mild cognitive impairment (MCI) and dementia that individuals with essential tremor may face.

The research represents the longest available longitudinal prospective study of rates of MCI and dementia in people with essential tremor. The study enrolled 222 patients, 177 of whom participated in periodic evaluations over an average follow-up of 5 years.

Investigators observed a cumulative prevalence of 26.6% and 18.5% for MCI and dementia, respectively. They also noted a cumulative incidence of 18.2% and 11.2% for MCI and dementia, respectively. Each year, 3.9% of patients with normal cognition “converted” to having MCI, and 12.2% of those with MCI “converted” to having dementia.

“We know from related research that the presence of cognitive impairment in patients with essential tremor has meaningful clinical consequences. For example, patients with essential tremor who are diagnosed with dementia are more likely to need to use a walker or wheelchair, to employ a home health aide, and to reside in non-independent living arrangements than are patients with essential tremor without dementia,” said corresponding author Elan D. Louis, MD, MS, of the University of Texas Southwestern Medical Center. “With this in mind, the findings of the present study highlight the importance of cognitive screening and monitoring in patients with essential tremor. Early detection of impairment may provide opportunities for interventions that may slow further cognitive decline and improve the quality of life of patients and their families.”

Source: Wiley

How Calorie Restriction Slows Aging in the Brain

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Restricting calories is known to improve health and increase lifespan, but much of how it does so remains a mystery, especially in regard to how it protects the brain. Now, scientists from the Buck Institute for Research on Aging have uncovered a role for a gene called OXR1 that is necessary for the lifespan extension seen with dietary restriction and is essential for healthy brain aging.

“When people restrict the amount of food that they eat, they typically think it might affect their digestive tract or fat buildup, but not necessarily about how it affects the brain,” said Kenneth Wilson, PhD, Buck postdoc and first author of the study, published in Nature Communications. “As it turns out, this is a gene that is important in the brain.”

The team additionally demonstrated a detailed cellular mechanism of how dietary restriction can delay aging and slow the progression of neurodegenerative diseases. The work, done in fruit flies and human cells, also identifies potential therapeutic targets to slow aging and age-related neurodegenerative diseases.

“We found a neuron-specific response that mediates the neuroprotection of dietary restriction,” said Buck Professor Pankaj Kapahi , PhD, co-senior author of the study. “Strategies such as intermittent fasting or caloric restriction, which limit nutrients, may enhance levels of this gene to mediate its protective effects.”

“The gene is an important brain resilience factor protecting against aging and neurological diseases,” said Buck Professor Lisa Ellerby, PhD, co-senior author of the study.

Understanding variability in response to dietary restriction

Members of the team have previously shown mechanisms that improve lifespan and healthspan with dietary restriction, but it was not clear why there is so much variability in response to reduced calories across individuals and different tissues. This project was started to understand why different people respond to diets in different ways.

The team began by scanning about 200 strains of flies with different genetic backgrounds. The flies were raised with two different diets, either with a normal diet or with dietary restriction, which was only 10% of normal nutrition. Researchers identified five genes which had specific variants that significantly affected longevity under dietary restriction. Of those, two had counterparts in human genetics.

The team chose one gene to explore thoroughly, called “mustard” (mtd) in fruit flies and “Oxidation Resistance 1” (OXR1) in humans and mice. The gene protects cells from oxidative damage, but the mechanism for how this gene functions was unclear. The loss of OXR1 in humans results in severe neurological defects and premature death. In mice, extra OXR1 improves survival in a model of amyotrophic lateral sclerosis (ALS).

The link between brain aging, neurodegeneration and lifespan

To figure out how a gene that is active in neurons affects overall lifespan, the team did a series of in-depth tests. They found that OXR1 affects a complex called the retromer, which is a set of proteins necessary for recycling cellular proteins and lipids. “The retromer is an important mechanism in neurons because it determines the fate of all proteins that are brought into the cell,” said Wilson. Retromer dysfunction has been associated with age-related neurodegenerative diseases that are protected by dietary restriction, specifically Alzheimer’s and Parkinson’s diseases.

Overall, their results told the story of how dietary restriction slows brain aging by the action of mtd/OXR1 in maintaining the retromer. “This work shows that the retromer pathway, which is involved in reusing cellular proteins, has a key role in protecting neurons when nutrients are limited,” said Kapahi. The team found that mtd/OXR1 preserves retromer function and is necessary for neuronal function, healthy brain aging, and lifespan extension seen with dietary restriction.

“Diet is influencing this gene. By eating less, you are actually enhancing this mechanism of proteins being sorted properly in your cells, because your cells are enhancing the expression of OXR1,” said Wilson.

The team also found that boosting mtd in flies caused them to live longer, leading researchers to speculate that in humans excess expression of OXR1 might help extend lifespan. “Our next step is to identify specific compounds that increase the levels of OXR1 during aging to delay brain aging,” said Ellerby.

“Hopefully from this we can get more of an idea of why our brains degenerate in the first place,” said Wilson.

“Diet impacts all the processes in your body,” he said. “I think this work supports efforts to follow a healthy diet, because what you eat is going to affect more than you know.”

Source: Buck Institute for Research on Aging

Older Adults’ Migraine Diagnosis Linked to Tripled Risk of Vehicle Crash

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A new study from researchers at the University of Colorado Anschutz Medical Campus finds that older adult drivers who are recently diagnosed with migraines are three times as likely to experience a motor vehicle crash. Older adult drivers who reported having ever had migraines in the past were no more likely to have a motor vehicle crash than those without migraines.

The study, published in the Journal of the American Geriatrics Society, also explored the relationships medications commonly prescribed for migraine management have with increased crash risk.

“Migraine headaches affect more than 7% of US adults over the age of 60,” says Carolyn DiGuiseppi, MPH, PhD, MD, professor with the Colorado School of Public Health and study lead author.

“The US population is aging, which means increasing numbers of older adult drivers could see their driving abilities affected by migraine symptoms previously not experienced. These symptoms include sleepiness, decreased concentration, dizziness, debilitating head pain and more.”

Researchers conducted a five-year longitudinal study of more than 2500 active drivers aged 65-79 in five sites across the United States.

Participants were categorised as having previously been diagnosed with migraine symptoms (12.5%), no previous diagnosis but experienced symptoms during the study timeframe (1.3%) or never migraine respondents.

Results indicate those with previous diagnosis did not have a different likelihood of having crashes after baseline, while those with new onset migraines were three times as likely to experience a crash within one year of diagnosis.

Previously diagnosed drivers nevertheless had experienced more hard braking events compared to adults who had never experienced a migraine.

Additionally, researchers examined the role medications commonly prescribed for migraines have in motor vehicle events and found that there was no impact on the relationship between migraines and either crashes or driving habits.

Few participants in the study sample were using acute migraine medications, however.

“These results have potential implications for the safety of older patients that should be addressed,” says DiGuiseppi. “Patients with a new migraine diagnosis would benefit from talking with their clinicians about driving safety, including being extra careful about other risks, such as distracted driving, alcohol, pain medication and other factors that affect driving.”

Source: University of Colorado Anschutz Medical Campus

Inflammation Discovery Could Lead to a Way to Slow Aging

Colourised electron micrograph image of a macrophage. Credit: NIH

University of Virginia School of Medicine researchers have discovered a key driver of chronic inflammation that accelerates aging. This could lead to treatments that let people live longer, healthier lives, and prevent age-related conditions such as cardiovascular disease and devastating brain disorders.

Improper calcium signalling in the mitochondria of certain immune cells seems to be the culprit behind this chronic age-related inflammation. Mitochondria rely heavily on calcium signalling, and they are the powerhouses of cells.

The UVA Health researchers, led by Bimal N. Desai, PhD, found that in macrophages, mitochondria lose their ability to take up and use calcium with age. This, the researchers show, leads to chronic inflammation responsible for many of the ailments that afflict our later years.

The researchers believe that increasing calcium uptake by the mitochondrial macrophages could prevent the harmful inflammation and its terrible effects. Because macrophages reside in all organs of our bodies, including the brain, targeting such “tissue-resident macrophages” with appropriate drugs may allow us to slow age-associated neurodegenerative diseases.

“I think we have made a key conceptual breakthrough in understanding the molecular underpinnings of age-associated inflammation,” said Desai, of UVA’s Department of Pharmacology and UVA’s Carter Immunology Center. “This discovery illuminates new therapeutic strategies to interdict the inflammatory cascades that lie at the heart of many cardiometabolic and neurodegenerative diseases.”

The inflammation of aging – ‘Inflammaging’

Macrophages swallow up dead or dying cells, removing cellular debris, and patrol for pathogens and other foreign invaders. In this latter role, they act as important sentries for our immune systems, calling for help from other immune cells as needed.

Scientists have known that macrophages become less effective with age, but it has been unclear why. Desai’s new discovery suggests answers.

Desai and his team say their research has identified a “keystone” mechanism responsible for age-related changes in the macrophages. These changes, the scientists believe, make the macrophages prone to chronic, low-grade inflammation at the best of times. And when the immune cells are confronted by an invader or tissue damage, they can become hyperactive. This drives what is known as “inflammaging” – chronic inflammation that drives aging.

Further, the UVA Health scientists suspect that the mechanism they have discovered will hold true not just for macrophages but for many other related immune cells generated in the bone marrow. That means we may be able to stimulate the proper functioning of those cells as well, potentially giving our immune systems a big boost in old age, when we become more susceptible to disease.

Next steps

Fixing “inflammaging” won’t be as simple as taking a calcium supplement. The problem isn’t a shortage of calcium so much as the macrophages’ inability to use it properly. But Desai’s new discovery has pinpointed the precise molecular machinery involved in this process, so we should be able to discover ways to stimulate this machinery in aging cells.

“This highly interdisciplinary research effort, at the interface of computational biology, immunology, cell biology and biophysics, wouldn’t have been possible without the determination of Phil Seegren, the graduate student who spearheaded this ambitious project,” Desai said. “Now, moving forward, we need an equally ambitious effort to figure out the wiring that controls this mitochondrial process in different types of macrophages and then manipulate that wiring in creative ways for biomedical impact.”

Source: University of Virginia Health System

Scientists Discover That a Key Protein Boosts Cell Repair and Healthy Ageing

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Researchers have found an anti-ageing function in a protein deep within human cells. They discovered that a protein called ATSF-1 controls a fine balance between the creation of new mitochondria and the repair of damaged mitochondria. Their findings were published in Nature Cell Biology.

Mitochondria create toxic by-products during their energy production process, which contributes to the rate at which the cell ages.

Associate Professor Steven Zuryn and Dr Michael Dai at the Queensland Brain Institute made the discovery of a key repair protein. “In conditions of stress, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritises repair which promotes cellular health and longevity,” Dr Zuryn said.

As an analogy, Dr Zuryn likened the relationship to a race car needing a pitstop.

“ATSF-1 makes the call that a pitstop is needed for the cell when mitochondria need repairs,” he said.

“We studied ATFS-1 in C. elegans, or round worms and saw that enhancing its function promoted cellular health, meaning the worms became more agile for longer. They didn’t live longer, but they were healthier as they aged.”

“Mitochondrial dysfunction lies at the core of many human diseases, including common age-related diseases such as dementias and Parkinson’s. Our finding could have exciting implications for healthy ageing and for people with inherited mitochondrial diseases.”

Understanding how cells promote repair is an important step towards identifying possible interventions to prevent mitochondrial damage.

“Our goal is to prolong the tissue and organ functions that typically decline during ageing by understanding how deteriorating mitochondria contribute to this process,” Dr Dai said. “We may ultimately design interventions that keep mitochondrial DNA healthier for longer, improving our quality of life.”

Source: University of Queensland