Monthly Archives: July 2025

Workout-triggered protein restores strength to ageing muscles and bones

The adage “Exercise is good for your health” is widely accepted, yet few people can explain with precision the biological mechanisms that underpin this truth. A groundbreaking discovery by a joint research team sheds new light on this topic, identifying a key protein that mediates the health benefits of physical activity. The study was led by Dr Yong Ryoul Yang of the Aging Convergence Research Group at the Korea Research Institute of Bioscience and Biotechnology (KRIBB), alongside Professor Nak-Sung Kim of Chonnam National University. Together, they identified cardiotrophin-like cytokine factor 1 (CLCF1), a protein secreted by muscles during exercise, as a crucial player in enhancing both muscular and skeletal health.

The research demonstrated that CLCF1 contributes to the prevention of musculoskeletal ageing by strengthening muscles and bones. In human trials, the team observed that CLCF1 levels rose sharply after just one exercise session in young participants. However, in older adults, the same increase in CLCF1 was only seen after more than 12 weeks of sustained exercise. This finding indicates a significant age-related difference in how the body produces and responds to this protein, potentially explaining why older individuals often require more extended periods of activity to experience the same benefits as their younger counterparts.

To better understand the physiological role of CLCF1, the team conducted a series of experiments on elderly mice. Administering CLCF1 to these mice resulted in marked improvements in muscle strength and bone density. Conversely, when CLCF1 activity was blocked, the beneficial effects of exercise were entirely nullified. These results confirmed that CLCF1 is not merely a byproduct of exercise but a necessary component of its positive impact. In essence, the presence and activity of this protein determine whether the body reaps the regenerative rewards of physical training.

Further cellular analysis revealed the mechanisms behind CLCF1’s efficacy. The protein enhances mitochondrial function in muscle cells, thereby improving energy production and cellular endurance. It also inhibits the formation of osteoclasts—cells that break down bone tissue—while promoting the activity of osteoblasts, which are responsible for bone formation and repair. This dual action supports not only muscle vitality but also bone density, making CLCF1 a key agent in the fight against age-related conditions such as sarcopenia and osteoporosis.

Dr Yang emphasised the significance of the discovery, noting that this is the first scientific evidence linking diminished protein secretion with the reduced effectiveness of exercise in older individuals. “This research provides a biological basis for why exercise becomes less effective with age,” he explained. “It also lays the groundwork for developing new therapeutic strategies for healthy ageing.” The study’s insights could lead to treatments that mimic or enhance the action of CLCF1, offering hope to those unable to maintain regular exercise due to ageing or illness, and opening a new frontier in the science of longevity and musculoskeletal health.

More information: Yong Ryoul Yang et al, Exercise-induced CLCF1 attenuates age-related muscle and bone decline in mice, Nature Communications. DOI: 10.1038/s41467-025-59959-w

Journal information: Nature Communications Provided by National Research Council of Science & Technology

Regular Physical Activity Could Help Preserve Cognitive Function

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Physical activity has long been recognised as a key component of overall health and wellbeing. Still, new research from the University of Georgia (UGA) sheds light on a more specific benefit—its potential to slow cognitive decline. Conducted by the College of Public Health at the University of Georgia, the study examined long-term data from over 13,000 participants aged 50 and older. The findings reveal that individuals who maintained consistent levels of physical activity over time experienced significantly slower rates of cognitive deterioration, suggesting that the effects of exercise extend well beyond the physical body and into the preservation of mental function.

Dr Suhang Song, assistant professor in the Department of Health Policy and Management at UGA, led the study. She and her team used data from the Health and Retirement Study, a nationally representative longitudinal survey that followed participants for 16 years. Respondents regularly reported how often they engaged in physical activity and the intensity of those activities. From vigorous forms such as running and jogging to more moderate efforts like gardening or dancing, and even lighter tasks like vacuuming or home repairs, all levels of activity were assessed. The team found that greater frequency and longer duration of physical engagement correlated with slower rates of cognitive decline.

One of the most compelling aspects of the study was the discovery that even modest increases in physical activity made a measurable difference. For example, individuals who shifted from engaging in vigorous exercise a few times per month to once per week showed a noticeable slowing in the decline of their cognitive abilities. Likewise, those who increased moderate activity from once a week to several times a week benefited similarly. The research did not measure exercise in terms of duration per session. Instead, it focused on the consistency and pattern of activity over time, highlighting the importance of regular movement as a lifestyle habit.

Dr Song emphasised that although the improvements might appear incremental, they accumulate significantly over the years. “The improvement of the decline rate may seem modest, but it builds up over time,” she explained. “If this slower decline continues, it could potentially delay the onset of dementia by many years.” Such a delay could have a profound impact on individuals and their families, allowing them to enjoy more years of independent living and preserve their quality of life. The cumulative nature of the benefit means that starting or maintaining physical activity—even at a low level—could yield significant long-term advantages.

What sets this study apart from previous research is its focus on the duration and regularity of activity rather than isolated snapshots of physical engagement. While previous studies have established the link between exercise and brain health, UGA’s contribution lies in its emphasis on the role of sustained, long-term commitment to physical activity. The researchers advocate that promoting regular exercise should be an integral part of dementia prevention strategies, both in clinical practice and in public health policy. Supporting older adults in establishing and maintaining routines could be key to protecting cognitive function into advanced age.

Ultimately, Dr Song’s message is a clear and encouraging one: keep moving, and do so consistently. Whether through high-intensity workouts or gentle, everyday tasks, the act of staying active offers meaningful protection for the brain. The research highlights the importance of incorporating physical activity into daily life as a preventive health measure. As policymakers, healthcare providers, and individuals look for ways to mitigate the growing burden of cognitive decline and dementia, encouraging consistent physical activity may be one of the most effective, accessible, and sustainable approaches available.

More information: Suhang Song et al, Long-term cumulative physical activity associated with less cognitive decline: Evidence from a 16-year cohort study, The Journal of Prevention of Alzheimer’s Disease. DOI: 10.1016/j.tjpad.2025.100194

Journal information: The Journal of Prevention of Alzheimer’s Disease Provided by University of Georgia

Emerging Study Reveals Hidden Contributions of Nieces and Nephews in Dementia Care

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A recent Virginia Tech study has drawn attention to the important yet often unrecognised role that nieces and nephews play in caring for ageing relatives living with dementia. Published in The Gerontologist, the study is the first to offer a focused examination of dementia caregiving by extended family members beyond the usual scope of spouses and adult children. Led by Dr Tina Savla and Dr Karen Roberto, the research forms part of the broader CareEx project funded by the National Institutes of Health. The findings reveal that many of these caregivers never expected to assume such a role, but instead stepped into it out of necessity and familial affection, often with little preparation or support.

Dr Savla, a professor of human development and family science, noted that this sudden shift into caregiving reflects both deep empathy and considerable strain. “That spontaneity shows extraordinary love and empathy while masking a lot of real stress,” she explained. “They carry all of the responsibilities associated with primary caregiving while also managing their households, children, and work.” The study highlights the complexity of modern caregiving dynamics, in which nieces and nephews must balance competing demands on their time, finances, and emotional well-being—while providing consistent, often intensive support to relatives with cognitive decline.

The participants, comprising 20 nieces and five nephews aged between 38 and 67, were located across several states, including Virginia, Maryland, and North Carolina. All either lived with their relatives or maintained close contact, typically visiting at least three times a week. Interviews conducted between 2021 and 2025 explored how these individuals became caregivers, the nature of the care they provide, and the impact of this experience on their quality of life. Many of them had lifelong relationships with their aunts and uncles, formed through strong generational bonds. This emotional foundation was a powerful motivator in their willingness to take on such a demanding role, often rooted in a sense of gratitude and moral responsibility.

“Many participants told us, ‘I’m just paying back the love my aunt showed me when I was a kid,’” said Savla, who also serves as core faculty at Virginia Tech’s Centre for Gerontology. This sense of reciprocity, the study suggests, provides a resilience that can sometimes surpass the more transactional nature of obligatory care. Yet even with such heartfelt motivation, the practical challenges remain significant. Like traditional caregivers, these extended family members must handle a range of responsibilities—organising transport to medical appointments, managing medications and finances, assisting with daily tasks, and navigating complex healthcare systems—often with limited access to formal resources or recognition.

To better understand the intricacies of this caregiving role, Savla and Roberto identified four major themes across the interviews: relationship foundations, pathways to caregiving, care systems, and the trials and tribulations associated with caregiving. These categories shed light on how past personal histories shape caregiving responsibilities, how caregivers adapt (or struggle to adapt) to their new roles, and the types of support systems—or lack thereof—that impact both their experience and effectiveness. The study makes a significant contribution to the field by demonstrating that caregiving is not limited to nuclear family structures and that extended relatives are a vital yet underexplored aspect of the care landscape.

With America’s ageing population growing and dementia diagnoses on the rise, the researchers argue that understanding extended caregiving dynamics is more urgent than ever. Current policies and research often overlook the diversity of caregiving arrangements, focusing instead on more traditional family roles. Moving forward, Savla and Roberto plan to broaden their scope by including adult grandchildren and siblings in future phases of the study. “Understanding the contributions of extended family caregivers provides a more complete picture of the family caregiving ecosystem,” Roberto explained. “Learning about their experiences will help identify unmet care needs and guide interventions to sustain caregiver wellbeing—ultimately improving outcomes for both carers and the individuals they support.”

More information: Tina Savla et al, Niece and Nephew Dementia Caregivers: Family Relationships and Care Dynamics, The Gerontologist. DOI: 10.1093/geront/gnaf154

Journal information: The Gerontologist Provided by Virginia Tech

Neighbourhood Environment Linked to Inflammation and Early Signs of Dementia

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A recent study, published on June 25, 2025, in Neurology®, the medical journal of the American Academy of Neurology, has drawn attention to the possible connection between neighbourhood disadvantage and early biological indicators linked to inflammation and Alzheimer’s disease. The researchers found that individuals residing in more socioeconomically challenged areas were more likely to exhibit elevated levels of biomarkers associated with both brain inflammation and neurodegeneration. Importantly, the study does not claim that living in such neighbourhoods causes these changes. Instead, it demonstrates a significant association, which adds nuance to the growing understanding of how environmental and socioeconomic factors might influence long-term brain health.

The study was led by Dr Angela L. Jefferson, a neuroscientist at Vanderbilt University Medical Centre and a member of the American Academy of Neurology. She noted that while previous research had already indicated a higher risk of Alzheimer’s disease among those living in disadvantaged neighbourhoods, little was known about the physiological mechanisms that might explain this risk. According to Jefferson, the findings suggest that chronic stressors associated with deprived environments may contribute to increased levels of inflammation within the body and brain. This inflammation, in turn, may lay the groundwork for the development of neurodegenerative diseases like Alzheimer’s, as well as directly raising levels of disease-specific biomarkers such as tau protein.

The longitudinal study followed 334 participants, with an average age of 73, over a period of nine years. Throughout this period, participants underwent regular cognitive tests, blood analyses, and brain imaging at intervals of 18 months, 3, 5, 7, and 9 years. Additionally, a subgroup of 180 individuals provided samples of cerebrospinal fluid, which allowed researchers to examine markers present in the central nervous system. This multifaceted approach enabled the researchers to track both the initial biomarker levels and how these levels changed over time, offering a more dynamic picture of disease development about neighbourhood conditions.

Neighbourhood disadvantage was calculated using an index that incorporated several key factors, including income, employment status, education levels, and rates of disability. Individuals residing in areas characterised by greater disadvantage were found to have higher concentrations of tau in their cerebrospinal fluid at the study’s outset. Tau is a protein that, when abnormally accumulated, is closely linked to the progression of Alzheimer’s disease. The researchers interpreted this as a possible indication that environmental stressors may contribute to early neurodegenerative changes in the brain, well before the onset of visible cognitive symptoms.

In addition to elevated tau, participants from more disadvantaged neighbourhoods also had higher levels of YKL-40, a protein associated with brain inflammation. These results remained consistent even after researchers accounted for a range of other factors that could influence biomarker levels, such as age, sex, and educational attainment. Furthermore, over time, researchers observed that levels of high-sensitivity C-reactive protein (CRP)—a well-known marker of systemic inflammation—rose more rapidly among individuals in disadvantaged areas. For every ten percentile increase in neighbourhood disadvantage, there was an associated yearly increase of 0.05 milligrams per litre in CRP levels. This pattern suggests a cumulative effect of chronic exposure to stressful or unhealthy environments, resulting in sustained inflammation throughout the body.

These findings carry important implications for public health strategies and medical practice. Dr Jefferson emphasised that healthcare providers should consider the broader social and environmental context when working with older adults or individuals at risk for cognitive decline. Lifestyle interventions aimed at reducing inflammation—such as regular physical exercise, a balanced diet, and stress-reduction techniques—could be particularly beneficial for individuals in high-risk communities. The study also highlights the importance of including individuals from disadvantaged backgrounds in clinical trials and preventive health studies, as these groups are often underrepresented in research but may benefit the most from targeted interventions.

However, the study’s authors acknowledged several limitations. Most notably, the participant pool was not fully representative of the broader U.S. population, as the majority were white, well-educated, and living in relatively less disadvantaged areas. As such, while the findings are valuable, they may not fully capture the experience of more severely disadvantaged or ethnically diverse populations. Further research will be necessary to confirm these trends across a broader demographic range and to gain a better understanding of how the lived experience of environmental hardship becomes biologically embedded in ways that affect brain ageing. Nevertheless, the study contributes essential insight into how place and circumstance intersect with biology to influence the risk of diseases like Alzheimer’s.

More information: Angela L. Jefferson et al, Cross-Sectional and Longitudinal Associations of Neighborhood Disadvantage With Fluid Biomarkers of Neuroinflammation and Neurodegeneration, Neurology. DOI: 10.1212/WNL.0000000000213770

Journal information: Neurology Provided by American Academy of Neurology

Cannabis Consumption Associated with Twice the Risk of Fatal Cardiovascular Disease

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Cannabis use has been found to significantly increase the risk of dying from cardiovascular disease, according to a newly published meta-analysis in the journal Heart. The study reports that individuals who use cannabis face a doubling in the risk of fatal cardiovascular events. Additionally, cannabis use is associated with a 29% greater risk of acute coronary syndrome—defined as sudden, reduced blood flow to the heart—and a 20% higher risk of experiencing a stroke. These findings come from an extensive analysis of real-world data and provide fresh insights into the potential dangers of cannabis use, particularly in the context of shifting public attitudes and increased legalisation.

The editorial accompanying the study argues that cannabis should be treated in regulatory frameworks much like tobacco: not criminalised, but actively discouraged. In a linked editorial, Emeritus Professor Stanton Glantz and Dr Lynn Silver call for robust public health interventions to limit secondhand exposure and improve awareness of the drug’s cardiovascular effects. As cannabis use has become more widespread—driven in part by legalisation and the expansion of medical cannabis programmes—many people now perceive it as harmless or even health-promoting. This shift in perception, the editorial warns, is not grounded in scientific evidence and could be placing millions at unnecessary risk.

In response to these trends, researchers conducted a systematic review of studies published between January 2016 and December 2023, focusing on cannabis use and serious cardiovascular outcomes, including death from cardiovascular disease, heart attack, and stroke. From a pool of over 3,000 articles, 24 studies met the inclusion criteria for the pooled data analysis. These encompassed a range of designs, including cross-sectional, cohort, and case-control studies, and represented a combined population of roughly 200 million individuals. Most participants were aged 19 to 59, with cannabis users skewing younger and more likely to be male compared to non-users.

The results confirmed a substantial association between cannabis use and cardiovascular harm. Specifically, the data showed a 29% higher risk of acute coronary events, such as heart attacks, and a 20% increase in the likelihood of stroke among cannabis users. Perhaps most concerning was the twofold increase in the risk of cardiovascular death. While the precise causal mechanisms remain unclear, the findings challenge the notion that cannabis is a benign recreational or medicinal substance. They suggest instead that the drug carries serious health consequences that may parallel those of tobacco, particularly when used regularly or in high-potency forms.

However, the researchers acknowledge that the included studies had limitations. Many exhibited moderate to high risk of bias due to missing data, inconsistent definitions of cannabis exposure, and reliance on self-reporting. Furthermore, because most of the studies were observational, they cannot definitively establish a cause-and-effect relationship. Some of the research also reused datasets, which may limit the breadth of applicability. Nonetheless, the authors argue that their meta-analysis is the most thorough examination to date of the connection between cannabis and cardiovascular risk, drawing on an unprecedented scale of population-level evidence.

The editorial further emphasises the need to investigate how different forms of cannabis impact cardiovascular health. The cannabis landscape has evolved considerably in recent years, with new high-potency concentrates, synthetic cannabinoids, and edible products becoming increasingly common. Whether the observed cardiovascular risks stem from cannabinoids themselves, inhaled particulates, or other compounds, such as terpenes, remains uncertain. Understanding these nuances is critical to crafting effective public health messages and regulatory policies that can mitigate risk across the broad spectrum of cannabis products now available.

Ultimately, the authors conclude that cardiovascular disease prevention must become a central component of cannabis regulation. They call for the implementation of mandatory warning labels, public education campaigns, and policies that limit exposure to cannabis vapour in public spaces. They argue that current regulatory efforts have focused too narrowly on establishing legal markets, often at the expense of public health and well-being. As evidence of cannabis-related harm continues to mount, regulatory frameworks must evolve to prioritise health and safety, adopting measures similar to those used successfully in tobacco control to protect both users and the general public.

More information: Wilhelm Storck et al, Cardiovascular risk associated with the use of cannabis and cannabinoids: a systematic review and meta-analysis, Heart. DOI: 10.1136/heartjnl-2024-325429

Journal information: Heart Provided by BMJ Group

Scientists Uncover Potential of Caffeine to Delay Cell Ageing

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A recent study from the Cellular Ageing and Senescence Laboratory at Queen Mary University of London has shed new light on a surprising role for caffeine beyond its well-known effects on alertness. Published in the journal Microbial Cell, the research investigates how caffeine interacts with fundamental cellular processes, revealing that it may help slow the ageing process at a cellular level. While caffeine is already known for its association with reduced risk of age-related diseases, such as Alzheimer’s and Parkinson’s, the specific biological mechanisms behind these effects have remained somewhat mysterious—until now.

The research team, led by Dr Charalampos (Babis) Rallis, used fission yeast as a model organism. Despite its simplicity, fission yeast shares many essential cellular functions with human cells, making it an ideal system for studying conserved biological pathways. Through their experiments, the scientists discovered that caffeine exerts its influence not by directly affecting the well-known TOR (Target of Rapamycin) signalling pathway, as previously thought, but by targeting another critical molecular system: AMPK (AMP-activated protein kinase). This protein functions as a cellular energy sensor, responding to shifts in energy availability by triggering adaptive changes in metabolism, growth, and stress resistance.

In earlier research, the same group had shown that caffeine can extend the lifespan of cells by acting on TOR, a central growth regulator that responds to the cell’s nutritional state. TOR essentially acts as a growth switch—when nutrients are plentiful, it promotes cell growth and proliferation; when nutrients are scarce, it slows down the process to conserve energy. This system has played a key role in cellular evolution for over 500 million years. However, the new findings suggest that caffeine doesn’t directly engage this system. Instead, it stimulates AMPK, which in turn modulates TOR activity indirectly, offering a more nuanced understanding of caffeine’s cellular effects.

Dr Rallis explains that AMPK functions like a “fuel gauge” for the cell, becoming active when energy levels drop. When AMPK is triggered, it initiates cellular programmes that prioritise energy conservation, DNA repair, and defence against stress—processes that are tightly linked to the ageing process. The team’s discovery that caffeine activates AMPK, therefore positions it as a substance that can promote cellular maintenance and longevity, rather than merely serving as a short-term stimulant. This adds weight to the idea that caffeine’s benefits may include promoting long-term health and resilience at the molecular level.

What makes this discovery particularly significant is that AMPK is also the target of metformin, a widely prescribed diabetes medication that is currently being explored for its potential to extend human lifespan. Like caffeine, metformin activates AMPK, setting off a cascade of protective cellular responses. Moreover, the effects of caffeine appear to align with other longevity-promoting interventions, such as caloric restriction and exercise, both of which naturally stimulate AMPK as part of the body’s response to energetic stress. Thus, caffeine may be acting as a dietary mimic of these age-defying practices.

The team’s findings also suggest that caffeine’s impact on AMPK extends to key cellular activities, including growth regulation, DNA damage repair, and resistance to environmental stressors. All of these are crucial for maintaining cell function as organisms age. According to Dr John-Patrick Alao, the postdoctoral researcher who led the study, these results help explain the consistent links between moderate caffeine consumption and improved health outcomes observed in epidemiological studies. They also hint at new therapeutic avenues, where the beneficial aspects of caffeine might be harnessed more precisely, either through diet, lifestyle changes, or novel pharmaceutical compounds.

So, the next time you reach for your morning coffee or afternoon tea, you might be doing more than just sharpening your mind or shaking off fatigue. This daily ritual can help your cells remain youthful, robust, and resilient in the face of life’s stresses. While further research is needed to translate these yeast-based findings into human biology, the study offers an exciting glimpse into how something as familiar as caffeine might become a tool in the science of healthy ageing.

More information: Charalampos Rallis et al, Dissecting the cell cycle regulation, DNA damage sensitivity and lifespan effects of caffeine in fission yeast, Microbial Cell. DOI: 10.15698/mic2025.06.852

Journal information: Microbial Cell Provided by Queen Mary University of London

Scientists uncover muscle ‘command hub’ – potential breakthrough for improved healing in older adults

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When a hurricane tears through a house, the first step in recovery is to remove the wreckage before any rebuilding can begin. A similar process occurs within our muscles after they’ve been damaged—debris must be cleared to allow healing to take place. Now, researchers from Aarhus University and the Steno Diabetes Centre Aarhus have identified the key players responsible for managing this complex repair process. In a recent study published in Nature Communications, the team reveals a previously unrecognised form of cellular communication that orchestrates muscle healing and could have profound implications for treating muscle degeneration, particularly in elderly individuals.

The central discovery revolves around specialised cells known as fibro-adipogenic progenitors, or FAPs. These cells reside within muscle tissue and have long been recognised for their supporting role in muscle regeneration. However, the new research reveals that they do far more than assist—they act as coordinators, directing the immune system’s response to injury. Associate Professor Jean Farup, who led the study, likens their function to that of a foreman guiding a team of builders. By communicating with immune cells, particularly macrophages, FAPs facilitate the clearance of damaged tissue and ensure the necessary cellular machinery is in place for effective repair.

Macrophages serve as the body’s “clean-up crew,” removing cellular debris and stimulating regeneration. But what surprised the research team was the extent of the interaction between FAPs and these immune cells. Farup explains that FAPs actively influence the macrophages, enhancing their performance through targeted signalling. One of the most unexpected findings was that FAPs themselves produce a critical molecule known as complement C3. Until now, scientists believed C3 was produced exclusively in the liver and circulated through the bloodstream. This study, however, shows that C3 is also synthesised locally within muscle tissue, and that this local production is vital for regulating the inflammatory response required for healing.

This insight challenges long-standing assumptions about the source and role of inflammatory signalling during muscle repair. The presence of locally produced C3 suggests a far more refined and spatially controlled healing process than previously understood. In practical terms, this could lead to the development of treatments that enhance or mimic the role of FAPs, especially in individuals whose muscle regeneration is impaired due to age or chronic illness. The ability to modulate local inflammation more precisely could be the key to preventing long-term muscle wasting and preserving strength and mobility in later life.

For the elderly and patients with chronic diseases like type 2 diabetes, cardiovascular disease, or cancer, this discovery offers a new therapeutic avenue. Muscle loss in these populations is often driven by chronic, unresolved inflammation that impairs the repair process and accelerates decline. By targeting the newly identified communication pathway between FAPs and immune cells, scientists may be able to dampen harmful inflammation while preserving the beneficial aspects needed for recovery. “We believe that our new understanding of the interaction between FAPs and the immune system can be important in managing these conditions,” says Farup.

Moving forward, the Aarhus research team plans to investigate how this cellular coordination behaves in disease states marked by persistent inflammation. Their goal is to determine whether therapies that modulate FAP function or mimic their communication with macrophages could halt or even reverse muscle loss in affected patients. As our understanding of muscle regeneration deepens, so too does the possibility of restoring health and resilience to those whose bodies have long struggled to recover. This discovery may mark the beginning of a new era in the treatment of muscle-wasting conditions.

More information: Jean Farup et al, Complementing muscle regeneration—fibro-adipogenic progenitor and macrophage-mediated repair of elderly human skeletal muscle, Nature Communications. DOI: 10.1038/s41467-025-60627-2

Journal information: Nature Communications Provided by Aarhus University