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Brain shunts deliver major benefits for older adults with hydrocephalus, UCalgary researchers report

When Jill Knaus arrived at the Adult Hydrocephalus Program at the University of Calgary, she was desperate for answers. Once active and independent, she suddenly needed a cane or walker to move about safely. Her gait had become unsteady, her balance unreliable, and her quality of life had deteriorated. “I wasn’t walking anymore, not properly. I wore through five pairs of shoes because my feet were dragging when I tried to step,” she recalls. “I couldn’t go for daily walks with my dog, Lucy.”

Worried about falling, Knaus reluctantly made the difficult decision to move into an assisted living facility. At 79, she felt the move had come far too soon, but she wanted the reassurance that someone would be nearby if she needed help. Her experience mirrors that of many older adults who unknowingly live with idiopathic Normal Pressure Hydrocephalus (iNPH), a brain condition often mistaken for normal ageing.

Dr Mark Hamilton, Director of the Calgary Adult Hydrocephalus Program at the Cumming School of Medicine, explains that iNPH occurs when cerebrospinal fluid builds up in the brain’s ventricles. The condition causes problems with walking and balance, cognitive decline, and bladder difficulties. Unlike other forms of hydrocephalus, which may be caused by trauma or bleeding, iNPH has no known cause. It affects about 1.5 per cent of people in their late sixties and nearly 8 per cent of those in their mid-eighties. Left untreated, it can strip away independence, increase the risk of falls, and lead to severe disability or premature death.

For years, uncertainty surrounded treatment. Many neurologists and neurosurgeons questioned whether shunt surgery—a procedure in which a small tube diverts excess fluid from the brain—was truly effective. A groundbreaking international trial has now put an end to that debate. Published in the New England Journal of Medicine, the double-blind, randomised, placebo-controlled study found that patients who received an active shunt experienced remarkable improvements in walking speed and balance after just three months. The results were so compelling that the trial was halted early.

“Completing this randomised clinical trial was necessary because many specialists were unsure whether shunts could effectively treat iNPH, which meant patients were often denied diagnosis and care,” says Hamilton, who is also a neurosurgeon at the Foothills Medical Centre and one of the study’s principal investigators. “Now, there is no doubt. Shunt surgery for iNPH improves mobility, reduces falls, and restores independence. It is both safe and effective.” Conducted at 17 centres in Canada, the United States, and Sweden, the trial showed that 80 per cent of the 49 participants with open shunts had significant clinical improvements. At the same time, those in the placebo group saw little or no change.

Although she was not part of the study, Knaus underwent shunt surgery in 2024 and has felt the benefits first-hand. “I’m walking my dog again up to four times a day without the use of a cane or walker. I’ve lost 20 pounds,” she says. “I feel much younger and happier. I’ve got my life back.”

More information: Mark Hamilton et al, A Randomized Trial of Shunting for Idiopathic Normal-Pressure Hydrocephalus, New England Journal of Medicine. DOI: 10.1056/NEJMoa2503109

Journal information: New England Journal of Medicine Provided by University of Calgary

Bone health at risk from microplastics

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The global reliance on plastic has reached staggering proportions, with more than 400 million tonnes produced annually. This immense volume has left an indelible mark on the planet’s ecosystems, contaminating not only beaches and rivers but also the remotest regions of the ocean, where traces of plastic have been detected as deep as 11,000 metres. Beyond the visible scars on landscapes and waterways, plastic production is also a significant contributor to climate change. Current estimates suggest that the manufacturing of plastic alone releases around 1.8 billion tonnes of greenhouse gases into the atmosphere each year, compounding environmental crises. At the same time, a growing body of scientific evidence indicates the pervasive impact of plastics on human health, suggesting that exposure is far more intimate and insidious than previously imagined.

Every day life exposes people to countless invisible particles that detach from common household items, such as curtains, furniture, textiles, and packaging. These microplastic fragments do not simply vanish; instead, they circulate in the air, dissolve into drinking water, adhere to food surfaces, and settle into dust, making them easily inhaled, ingested, or absorbed through the skin. Researchers have detected microplastics in some of the most sensitive areas of the human body, including blood, the brain, the placenta, breast milk, and, more recently, within bone tissue. These discoveries underscore the fact that plastic is not only an environmental pollutant but also a potential internal contaminant, capable of infiltrating human physiology in ways that are still being uncovered.

A recent review published in Osteoporosis International, linked to a project funded by FAPESP, examined 62 scientific studies to assess the relationship between microplastics and bone health. The review highlighted mounting evidence that plastic particles compromise skeletal integrity through multiple mechanisms. One of the most striking findings concerns their effect on bone marrow stem cells. Microplastics appear to stimulate the overproduction of osteoclasts—large, multinucleated cells that degrade bone tissue in a process called resorption. This disruption in cellular balance has significant implications for maintaining healthy bone density and strength.

Rodrigo Bueno de Oliveira, coordinator of the Laboratory for Mineral and Bone Studies in Nephrology (LEMON) at the Faculty of Medical Sciences of the State University of Campinas (FCM-UNICAMP), explains that the risks cannot be dismissed. “In vitro studies with bone tissue cells have shown that microplastics impair cell viability, accelerate ageing, and interfere with differentiation, in addition to triggering inflammatory responses,” he notes. These findings underscore the notion that microplastics, although tiny, have the capacity to disrupt essential cellular processes and promote tissue decline prematurely.

Animal research adds another dimension to this concern. Oliveira points to studies in which accelerated osteoclast senescence—driven by the presence of microplastics—has undermined bone microarchitecture, leading to dysplasia. Such changes are not merely structural curiosities; they manifest in weaker bones, greater susceptibility to deformities, and in severe cases, pathological fractures. In one particularly troubling outcome, exposure to microplastics appeared to halt skeletal growth altogether in laboratory animals. Although the exact ways in which these particles compromise bone mechanics remain under investigation, there is an increasing consensus that their presence in the bloodstream and marrow can profoundly disturb bone metabolism.

These findings have spurred Oliveira’s team to embark on a new research project designed to test in practice what current theory strongly suggests: a link between microplastic exposure and the exacerbation of metabolic bone diseases. Using animal models, the group aims to investigate the impact of microplastics on the strength of femurs in rodents, to establish a clear relationship between exposure and compromised skeletal integrity. Such investigations take on particular urgency given the rising global burden of osteoporosis. According to the International Osteoporosis Foundation, fractures related to the disease are projected to increase by 32% by 2050, mainly driven by the world’s ageing population.

As Oliveira stresses, improving bone health is a fundamental priority in healthcare. Strategies such as exercise, balanced nutrition, and pharmacological treatments already play a well-documented role in preventing fractures and maintaining mobility. Yet, while osteometabolic diseases have long been the focus of medical research, the environmental dimension—specifically the influence of microplastics—remains a glaring gap in scientific understanding. “Our goal,” Oliveira explains, “is to generate evidence that highlights microplastics as a potentially controllable environmental factor in the growing burden of bone fractures. If we can demonstrate a direct link, it could transform how we think about prevention and public health policy.”

More information: Rodrigo Bueno de Oliveira et al, Effects of microplastics on the bones: a comprehensive review, Osteoporosis International. DOI: 10.1007/s00198-025-07580-4

Journal information: Osteoporosis International Provided by Fundação de Amparo à Pesquisa do Estado de São Paulo

Groundbreaking research shows seniors can bounce back to wellness

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A new Canadian study is delivering a hopeful message to older adults and those who care for them: it is never too late to recover. Researchers at the University of Toronto have found that almost one in four adults aged 60 or older, who began a national study reporting poor well-being due to health problems, pain, low mood, or social isolation, were able to achieve optimal well-being within just three years. This remarkable rebound challenges conventional assumptions about ageing and offers fresh insight into resilience later in life.

Lead author Mabel Ho, a recent doctoral graduate from the University of Toronto’s Factor-Inwentash Faculty of Social Work (FIFSW) and the Institute for Life Course and Aging, emphasised the practical importance of the findings. “This isn’t just a story of resilience—it’s a roadmap for how we can help more older adults recover and thrive,” she said. “Our results highlight the powerful role that lifestyle choices and psychosocial supports can play in shaping healthy ageing trajectories.”

For the study, “optimal well-being” was defined as more than the absence of illness. Participants had to be free from severe physical, cognitive, mental, or emotional problems that interfered with daily life, while also reporting strong physical health, happiness, mental wellness, and life satisfaction. Notably, the study focused only on those who began in suboptimal health, allowing the researchers to examine the extent of improvement over time.

The findings revealed that certain factors significantly increased the likelihood of recovery. Participants who reported strong psychological and emotional wellness at the outset were more than five times as likely to achieve optimal well-being as those struggling with poor psychological health. Other characteristics associated with recovery included maintaining a healthy body weight, exercising regularly, avoiding insomnia, refraining from smoking, and participating in social activities. Together, these findings show the importance of both physical and social health in promoting recovery.

“It’s incredibly encouraging to see that with the right supports and lifestyle, many older adults can reclaim full health, happiness, and independence—even after serious challenges,” said Ho. Senior author Esme Fuller-Thomson, Director of the Institute for Life Course and Aging and Professor at the FIFSW, added: “Too often, the focus in ageing research and geriatric practice is on decline and disability. Our findings disrupt that narrative. Older adults can and do bounce back—and we need to build systems that support recovery.”

Published this week in PLOS One, the study analysed data from 8,332 respondents who were aged 60 and older at the time of follow-up. For Ho, the implications extend beyond statistics: “We want this study to reshape how society views ageing. With the right resources and supports, older adults don’t just endure after experiencing poor health or well-being—they thrive.”

More information: Mabel Ho, Esme Fuller-Thomson, Reclaiming wellness: Key factors in restoring optimal well-being in the Canadian Longitudinal Study on Aging, PLOS One. DOI: 10.1371/journal.pone.0329800

Journal information: PLOS One Provided by University of Toronto

Scientists Uncover Protein That Ages the Brain, Along with a Way to Stop It

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Ageing is notoriously unkind to the hippocampus, the region of the brain that underpins our ability to learn, store memories, and recall past experiences. Over time, this critical structure begins to weaken, leading to forgetfulness and cognitive decline, which are often associated with the ageing process. Now, researchers at UC San Francisco believe they have uncovered one of the central drivers of this process. In a study recently published in Nature Aging, the team identified a single protein that seems to accelerate the brain’s decline — and, remarkably, showed that reducing it can restore youthful function in aged mice.

The discovery emerged from a careful analysis of the genes and proteins expressed in the hippocampus across the lifespan of mice. Amidst the thousands of potential candidates, the scientists found just one that consistently differed between young and old animals: a protein known as FTL1. In older mice, levels of FTL1 were markedly higher, and this increase coincided with a noticeable reduction in the number of synaptic connections between hippocampal neurons. Behaviourally, these animals also demonstrated poorer performance in tasks designed to measure learning and memory, suggesting that the elevated FTL1 was more than a bystander — it was actively shaping how the brain functioned.

The researchers then tested this link directly by manipulating FTL1 levels. When they artificially elevated FTL1 in young mice, the consequences were swift and dramatic: the animals’ brains began to exhibit the same cellular deterioration observed in their elderly counterparts, and their behaviour shifted accordingly. In laboratory dishes, neurons engineered to overproduce FTL1 sprouted only rudimentary, single-armed neurites rather than the complex branching structures that typically allow cells to form robust networks. These findings strongly suggested that excessive FTL1 undermines the brain’s ability to build and maintain the connections that underpin memory and learning.

Perhaps the most exciting results, however, came from the opposite experiment. When FTL1 levels were reduced in the hippocampus of old mice, their brains appeared to revert to a younger state. The animals regained synaptic density, their neurons formed healthier networks, and they performed much better on memory tests. “It is truly a reversal of impairments,” said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the study. “It’s much more than merely delaying or preventing symptoms.” Further experiments revealed another damaging effect of FTL1: in older brains, it slowed cellular metabolism. But when scientists treated the hippocampal cells with a compound that stimulates metabolism, they were able to block these harmful consequences.

For Villeda and his team, the findings point toward a new frontier in the biology of ageing. Suppose therapies can be developed to limit the effects of FTL1 in the human brain. In that case, it may one day preserve memory and learning well into old age, or even restore these abilities after decline has begun. “We’re seeing more opportunities to alleviate the worst consequences of old age,” Villeda explained. “It’s a hopeful time to be working on the biology of ageing.” While the research is still in its early stages, the notion that a single protein could be targeted to reverse age-related impairments offers a powerful sense of optimism about what the future of neuroscience might hold.

More information: Laura Remesal et al, Targeting iron-associated protein Ftl1 in the brain of old mice improves age-related cognitive impairment, Nature Aging. DOI: 10.1038/s43587-025-00940-z

Journal information: Nature Aging Provided by University of California – San Francisco

Lost Bearings: How Errors in the Brain’s Compass Heighten Dementia Risk

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Researchers at the German Centre for Neurodegenerative Diseases (DZNE) have discovered that people at higher risk of developing Alzheimer’s disease may struggle with spatial orientation, even when their memory seems normal in standard tests. In a study of just over 100 older adults, participants were asked to find their position in a virtual environment. Those who reported subjective cognitive decline (SCD)—a condition where individuals feel their memory is worsening despite normal test results—performed worse in orientation tasks compared with healthy controls. These findings, published in Science Advances, point towards new methods that may detect the earliest changes linked to Alzheimer’s.

Subjective cognitive decline has become an essential focus in dementia research. Although conventional memory and thinking tests do not show impairment, people with SCD often go on to develop Alzheimer’s dementia later in life. Professor Thomas Wolbers, who led the study in Magdeburg, explained that SCD may represent a preclinical stage of Alzheimer’s. Because the entorhinal cortex—the brain region housing our “internal compass”—is one of the first areas affected by the disease, researchers believe spatial orientation tasks may provide a more sensitive way of spotting early warning signs.

To test this theory, scientists designed a novel experiment in virtual reality. Participants aged between 55 and 89 walked in real space while wearing VR headsets that displayed a featureless digital plain. With no visual landmarks, they had to rely entirely on their brain’s navigation system, a process called “path integration.” In each trial, they followed a moving ball along a curved path, then were asked to point back to their starting position and align themselves with their original direction. Each person completed around 70 trials, producing a large dataset of orientation performance.

The results showed that, while ageing in general led to more errors, individuals with SCD performed consistently worse than those without it. Importantly, their difficulties could not be explained by walking speed or posture; instead, the errors were linked to cognitive processing. Mathematical modelling of the data revealed that people with SCD had particular problems keeping track of their previous positions in memory—a “memory leak” that disrupted their ability to stay oriented. Researchers suspect this is tied to dysfunction in the entorhinal cortex.

This brain region contains specialised “grid cells” that act like a coordinate system, storing a sequence of past positions and allowing us to keep track of where we are. If these cells are disrupted, as often happens in the early stages of Alzheimer’s, the ability to integrate paths becomes impaired. The DZNE team believe that testing for such subtle navigation errors could be a valuable new tool for early detection. Unlike conventional memory tests, orientation tasks may be sensitive to brain changes long before dementia symptoms appear.

Looking ahead, the researchers plan to refine their virtual reality test so it can be used in clinical trials and routine medical practice. For example, path integration could provide an additional measure when assessing the impact of experimental Alzheimer’s drugs, offering a more detailed picture of how treatments affect the brain. In the future, these methods may be combined with biomarkers from blood or spinal fluid to create highly accurate early diagnostic tools. Ultimately, the hope is that identifying Alzheimer’s at its earliest stage will open the door to more effective interventions and better outcomes for patients.

More information: Thomas Wolbers et al, Path integration impairments reveal early cognitive changes in subjective cognitive decline, Science Advances. DOI: 10.1126/sciadv.adw6404

Journal information: Science Advances Provided by DZNE – German Center for Neurodegenerative Diseases

Fresh insights reveal how dietary cues influence the biology of ageing

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Diet is not merely a source of fuel for the body; it also delivers molecular signals that can either slow or hasten the pace of biological ageing, according to a new perspective published in npj Aging (Nature Portfolio). The authors emphasise that biological age—a marker of functional health—often diverges significantly from chronological age. With carefully chosen nutritional and lifestyle interventions, it may be possible to redirect this trajectory towards healthier, more resilient ageing.

“Nutrition is one of the most powerful levers we have to influence the rate of biological ageing and to strengthen our defences against chronic disease,” explains Professor Carsten Carlberg of the University of Eastern Finland. “The aim is to move beyond generic dietary advice and towards personalised strategies that can demonstrably shift biological age.”

Drawing on recent research, the article argues that daily choices around diet, physical activity, sleep, and social connection can effectively “bend the ageing curve.” Individuals who age optimally sustain a biological age younger than their chronological age, while unhealthy lifestyles accelerate decline and raise the risk of disease. Food, the authors note, contains thousands of bioactive compounds that act as molecular messengers. Although many of these are already recognised, a vast “nutrition dark matter” remains—over 139,000 largely uncharacterised compounds that may hold untapped potential for modulating critical ageing pathways.

Tracking biological age has become feasible through the use of ageing clocks—computational models based on biomarkers such as epigenetic signatures, proteomic patterns, or the composition of the microbiome. The article reviews different clocks and their relevance for healthy ageing research. For instance, risk-predictive tools like GrimAge provide valuable insight into interventions that might slow biological decline, offering a pathway for monitoring dietary and lifestyle strategies.

Despite advances in molecular science, the authors stress that whole dietary patterns remain the most effective foundation for longevity. Plant-rich diets such as the Mediterranean, AHEI, and DASH models have consistently been linked with improved odds of healthy ageing, including the preservation of cognitive, physical, and psychological function well into later life. Central to these benefits is the gut microbiome, which is profoundly shaped by diet and, in turn, influences inflammation, circadian rhythms, and immune resilience. This makes the microbiome a critical target for precision nutritional strategies. “Think of this as precision geroprevention,” says Carlberg. “With robust biomarkers and supportive policies, we can help people make daily food choices that keep their biological age consistently below their chronological age.”

The authors conclude with a call to action. As global populations age, preventive approaches are becoming ever more urgent. To translate scientific progress into public health impact, they highlight the need for three key steps: first, the validation and standardisation of ageing biomarkers; second, comprehensive mapping of food-derived bioactives and their molecular targets; and third, the creation of partnerships across sectors to embed precision nutrition into clinical care, community practice, and health policy. They also point to initiatives such as the Biomarkers of Aging Consortium and the EIT Food Healthy Ageing Think & Do Tank, which are driving forward the translation of laboratory discoveries into practical solutions for healthier, longer lives.

More information: Carsten Carlberg et al, Modulating biological aging with food-derived signals: a systems and precision nutrition perspective, npj Aging. DOI: 10.1038/s41514-025-00266-5

Journal information: npj Aging Provided by University of Eastern Finland

Outdoor workouts surpass the benefits of exercising in cities or gyms

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A growing body of evidence suggests that where we exercise matters just as much as how we exercise. A recent study from the University of Copenhagen, in collaboration with the University of Verona, has revealed that walking in natural settings produces superior health benefits compared with identical activity carried out in city streets or indoor gyms. These findings not only enhance our understanding of how the environment influences physical activity but also offer valuable insights for improving public health and urban planning.

The research team asked twenty-five young men to take part in a controlled experiment, where each was required to walk at a brisk but consistent pace across three distinct environments: a natural area, an urban route, and an indoor fitness centre. Following each walk, participants’ moods, stress levels, and physical exertion were measured. The results highlighted striking differences. Walking in green surroundings led to more relaxed states, reduced cortisol levels, greater enjoyment, and lower fatigue, while city and indoor walks were far less effective in producing these outcomes.

Associate Professor Stefano De Dominicis, from the Department of Nutrition, Exercise and Sports at the University of Copenhagen, explained that the participants consistently felt more positive and less stressed after time in nature. This effect was not only visible in their self-reported experiences but also confirmed through physiological data. The study stands out because it is among the first to combine both subjective and objective measures to compare natural, urban, and indoor exercise environments.

The mental health benefits of exercising in green spaces were particularly striking. Participants rated natural environments as the most restorative and uplifting, reporting higher levels of joy, satisfaction, and optimism. Conversely, negative emotions such as boredom, irritation, and anxiety were significantly reduced in nature. Interestingly, feelings of boredom actually increased during indoor exercise, while they decreased in natural settings. The sense of calm reported was also greatest outdoors and weakest indoors, reinforcing the idea that nature supports psychological recovery in ways that artificial environments cannot.

These findings reflect a more profound evolutionary truth. As De Dominicis points out, humans evolved in natural environments, and our brains remain finely attuned to them. It is therefore unsurprising that time in nature continues to provide such profound benefits. What makes this study particularly compelling, however, is the participants’ expressed desire to repeat the activity. They were far more motivated to walk again when the exercise took place outdoors, suggesting that nature not only boosts mood in the short term but also sustains long-term commitment to physical activity.

Physiological measures supported these observations. Heart rates dropped more rapidly following outdoor walks, and heart rate variability—a measure of how well the body engages its parasympathetic “rest and recover” system—was 20 to 30 per cent higher compared with indoor exercise. These results demonstrate that nature helps the body return to balance more efficiently, further underscoring the restorative power of green environments. Although gyms and indoor activities provide valuable benefits, particularly through social interaction and accessibility, the evidence suggests that even occasional shifts outdoors can make a meaningful difference.

From a practical perspective, the researchers recommend incorporating nature into exercise routines at least once a week. Replacing just one indoor session with thirty minutes of brisk walking in a park, forest, or along the coast could significantly reduce stress levels, improve mood, and encourage more consistent engagement in physical activity. For those struggling to establish regular exercise habits, outdoor environments may provide the extra motivation needed to begin and maintain healthier routines.

Finally, the study highlights broader implications for public health and urban design. By showing that participants’ subjective experiences are backed up by physiological evidence, the research emphasises the importance of green spaces not only for recreation but also as tools for health promotion. Municipalities and health professionals could therefore consider prioritising parks, trails, and accessible natural spaces as part of strategies to tackle issues such as obesity, stress, and mental illness. In a world increasingly defined by urbanisation, these findings remind us that nature is not a luxury but a vital component of human health and well-being.

More information: Luca Laezza et al, Evaluating the benefits of green exercise: A randomized controlled trial in natural and built environments assessed for their restorative properties, Psychology of Sport and Exercise. DOI: 10.1016/j.psychsport.2025.102883

Journal information: Psychology of Sport and Exercise Provided by University of Copenhagen

Why meal timing matters for healthy ageing and longevity

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As people grow older, both the type and quantity of food they eat often change. Yet one dimension of eating behaviour—when meals are consumed—remains less well understood. A new study led by researchers at Mass General Brigham has shed light on this question, revealing that meal timing gradually shifts with age and that these changes may carry significant implications for health and survival. The findings, published in Communications Medicine, suggest that specific patterns of eating are linked to increased risk of illness and even earlier death.

The research team, led by Hassan Dashti, PhD, RD, a nutrition scientist and circadian biologist at Massachusetts General Hospital, discovered that monitoring mealtime habits, particularly breakfast timing, may provide an accessible marker of overall health in older adults. “Our research suggests that changes in when older adults eat, especially the timing of breakfast, could serve as an easy-to-monitor marker of their overall health status,” said Dashti. “Patients and clinicians can possibly use shifts in mealtime routines as an early warning sign to look into underlying physical and mental health issues. Encouraging consistency in meal schedules could also be an important part of strategies to promote healthy ageing and longevity.”

Dashti and colleagues—including senior author Altug Didikoglu, MSc, PhD, of the Izmir Institute of Technology—set out to determine whether evolving patterns of meal timing might signal, or even shape, health outcomes later in life. Drawing on data from 2,945 community-dwelling adults in the UK, aged 42 to 94 and followed for more than two decades, the researchers tracked both eating behaviours and health status. They found that, with advancing age, people tend to eat breakfast and dinner at progressively later hours, while also reducing the overall length of their daily eating window.

The timing of breakfast, in particular, proved to be revealing. Later breakfasts were consistently associated with poorer health outcomes, including depression, fatigue, sleep disturbances and oral health problems. Difficulty preparing meals was also linked with delayed eating. Most strikingly, individuals who shifted their breakfast later into the day faced a higher risk of death during the follow-up period. Genetic predisposition also played a role: those with traits associated with being “night owls” tended to adopt later mealtime schedules.

Until now, little was known about how meal timing evolves in later life or how such shifts relate to long-term health. According to Dashti, these results fill a significant gap. “Our findings help show that later meal timing, especially delayed breakfast, is tied to both health challenges and increased mortality risk in older adults. These results add new meaning to the saying that ‘breakfast is the most important meal of the day,’ particularly for older individuals.”

The implications are especially timely, given the growing interest in time-restricted eating and intermittent fasting. While these approaches have shown promise in younger populations, the study suggests that shifting meals to later in the day may have very different consequences for older adults. In other words, dietary strategies cannot be applied uniformly across age groups: the health effects of when we eat appear to change as we age, highlighting the need for age-specific recommendations around meal timing.

More information: Hassan Dashti et al, Meal timing trajectories in older adults and their associations with morbidity, genetic profiles, and mortality, Communications Medicine. DOI: 10.1038/s43856-025-01035-x

Journal information: Communications Medicine Provided by Mass General Brigham

Simple blood test may speed up early Alzheimer’s diagnosis

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In a landmark study focusing on Hispanic and Latino adults, researchers at the University of California, San Diego School of Medicine have uncovered a connection between self-reported cognitive decline and blood-based biomarkers. Their findings suggest the possibility of developing a simple blood test that could aid in diagnosing Alzheimer’s disease and related dementias. Such an approach holds the promise of being faster, less invasive, and more affordable than current screening methods. The results of this important work were recently published in JAMA Network Open.

According to the corresponding author, Freddie Márquez, PhD, a postdoctoral scholar in the Department of Neurosciences, there is an urgent need for tools that can identify underlying neurodegenerative conditions earlier in patients presenting with cognitive symptoms. Márquez emphasised that blood-based biomarkers may provide a more accessible and scalable option for understanding cognitive decline, particularly for communities that traditional diagnostic pathways have historically underserved.

Currently, only one blood test has been approved by the United States Food and Drug Administration for the diagnosis of Alzheimer’s disease. Known as the Lumipulse G pTau217/Aβ42 plasma ratio, this test can detect proteins associated with the disease, but it remains prohibitively expensive and limited to specialised care environments. Whether blood testing can be reliably used for large-scale early detection of Alzheimer’s remains an open question—one that the present study has sought to address.

To explore this possibility, the researchers turned to the Study of Latinos–Investigation of Neurocognitive Aging, a clinical sub-study within the larger Hispanic Community Health Study/Study of Latinos. This is the most extensive long-term study of Hispanic and Latino health in the United States, making it a rich resource for examining the links between biomarkers and cognition. The research team highlighted that Hispanic and Latino adults face a disproportionately high risk of Alzheimer’s disease and related dementias, and they are projected to experience the most significant increases in prevalence over the coming decades. Despite this, they remain markedly underrepresented in dementia research.

The team analysed blood samples from 5,712 Hispanic and Latino adults aged 50 to 86, looking for proteins such as amyloid beta and tau, both of which are typically present in the brains of individuals with Alzheimer’s disease. Alongside these biomarker assessments, participants were asked about their own perceptions of cognitive decline, a measure referred to as subjective cognitive decline. This approach provided insight not only into biological changes but also into how individuals experience shifts in memory, planning, and overall cognitive ability.

The findings were striking. Elevated blood levels of neurofilament light (NfL), a marker of nerve cell injury, and glial fibrillary acidic protein (GFAP), an indicator of brain inflammation, were associated with greater self-reported difficulties in thinking and planning. Increased levels of NfL and tau protein (ptau-181) correlated with declines in memory performance. Interestingly, amyloid-beta protein levels showed no relationship with subjective cognitive decline. Notably, associations between NfL and reported cognitive changes were observed even in individuals who were otherwise cognitively healthy, suggesting that NfL could signal early changes in brain function before clinical symptoms are evident.

While these findings provide compelling evidence for the potential of blood-based biomarkers in the early detection of Alzheimer’s disease, the researchers stress the need for caution. Márquez and colleagues argue that such tests should not replace existing diagnostic approaches, but rather complement them as part of a clinician’s broader toolkit. The inclusion of participants from underrepresented backgrounds is also a key strength of the study, as it allows for better consideration of social determinants of health and comorbidities that may affect cognitive outcomes. Still, the researchers underscore that further work is required before blood-based testing can be integrated into routine clinical practice, even as the results mark a promising step forward in the search for more equitable and accessible diagnostic strategies.

More information: Freddie Márquez et al, Alzheimer Disease Biomarkers and Subjective Cognitive Decline Among Hispanic and/or Latino Adults, JAMA Network Open. DOI: 10.1001/jamanetworkopen.2025.31038

Journal information: JAMA Network Open Provided by University of California – San Diego

Scientists develop ‘metabolic clock’ to spot early indicators of disease and accelerated ageing

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A groundbreaking study published in npj Metabolic Health and Disease (Nature Portfolio) has introduced a new “metabolic clock” that can predict biological age, uncover disease-specific metabolic signatures, and support early detection of health risks. Unlike chronological age, which measures only the passage of years, this tool focuses on biological processes, offering a more accurate reflection of an individual’s actual health status.

The clock was developed from data provided by more than 13,500 participants in the AKRIBEA cohort, a large-scale health study conducted in the Basque Country in collaboration with the Mondragón Corporation. In total, the final dataset included around 20,000 people spanning a wide age range, making it one of the most comprehensive efforts to date. By building on this robust foundation, the research team has created a model with the power to transform how ageing and disease are understood.

At the heart of the innovation is nuclear magnetic resonance (NMR) metabolomics, a technology that examines small molecules circulating in the blood. Using machine-learning algorithms, the researchers developed a system capable of predicting biological age with striking accuracy. “Our goal was to obtain an independent measure of age, beyond the information on a passport,” explains Dr Óscar Millet, who led the work at CIC bioGUNE, part of the Basque Research and Technology Alliance (BRTA). “The significance of this lies in the ability to detect discrepancies between chronological and metabolic age, which may act as early indicators of disease.”

The researchers tested the clock by analysing samples from individuals with a variety of conditions. In men with prostate cancer, the average metabolic age was nearly five years older than their actual age, while in patients with fatty liver disease (MASLD), the difference rose to more than 14 years. These results suggest that “metabolic distortion” could serve as a valuable marker for identifying diseases at an early stage, potentially long before they are apparent through conventional diagnostic methods.

Beyond its predictive power, the platform is capable of estimating more than 25 standard clinical parameters from a single blood sample, including measures of inflammation and kidney function. This ability to provide a broader, more integrated picture of a person’s health could support clinicians in tailoring treatment strategies and monitoring patients more effectively. As Dr Millet notes, “It is remarkable how much information is already encoded within a serum NMR spectrum, waiting to be unlocked.”

By offering a reliable and non-invasive means of measuring biological age and disease risk, the metabolic clock paves the way for more personalised and preventative healthcare. It holds the promise not only of spotting illnesses earlier but also of helping individuals and doctors to monitor the pace of ageing, opening up new opportunities to maintain health and quality of life across the lifespan.

More information: José M. Mato et al, Metabolomic-based aging clocks, npj Metabolic Health and Disease. DOI: 10.1007/s00394-023-03123-x

Journal information: npj Metabolic Health and Disease Provided by CIC bioGUNE

New research reveals why influenza hits older adults harder

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Scientists have revealed why influenza infections are often more dangerous in older adults, and their discovery opens the door to new treatments that could reduce this heightened risk. The research, published in PNAS, identifies a key biological factor that makes elderly patients more vulnerable to severe outcomes when infected with the flu virus.

The study found that older people produce much higher levels of apolipoprotein D (ApoD), a glycosylated protein involved in lipid metabolism and inflammation. While ApoD is a natural part of cellular processes, in excess, it appears to weaken the body’s defences against viral infection. This overproduction reduces the ability of older patients to mount an effective immune response, making influenza both more severe and more damaging.

Researchers showed that increased ApoD in the lungs leads to extensive tissue injury during infection. This damage undermines the body’s antiviral type I interferon response, which usually helps to contain viruses. Without this protective response, influenza infection spreads more easily and becomes more destructive, particularly in the ageing lung.

An international team of scientists from the China Agricultural University, the University of Nottingham, the Institute of Microbiology at the Chinese Academy of Sciences, the National Institute for Viral Disease Control and Prevention at the Chinese Centre for Disease Control and Prevention, and the University of Edinburgh conducted the investigation. According to Professor Kin-Chow Chang, from the School of Veterinary Medicine and Science at the University of Nottingham, “Ageing is a leading risk factor in influenza-related deaths. With global populations ageing at an unprecedented pace, understanding why older patients experience worse outcomes is crucial for healthcare and the wider economy.”

Using an ageing mouse model alongside carefully selected human tissue samples, the team investigated the mechanisms driving this age-related vulnerability. They discovered that ApoD impairs the activation of the immune system by accelerating the breakdown of mitochondria, a process known as mitophagy. Since mitochondria are essential both for producing cellular energy and for triggering protective interferons, their loss allows the virus to replicate more freely, resulting in higher viral loads and greater lung damage.

These findings identify ApoD as a critical therapeutic target. By inhibiting its harmful effects, researchers hope to develop treatments that strengthen the immune response in older patients and prevent severe influenza outcomes. As Professor Chang explained, “There is now an exciting opportunity to improve outcomes for the elderly by targeting ApoD, potentially reducing morbidity and mortality linked to influenza worldwide.”

More information: Kin-Chow Chang et al, ApoD mediates age-associated increase in vulnerability to influenza virus infection, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2423973122

Journal information: Proceedings of the National Academy of Sciences Provided by University of Nottingham

Hitting 100 grows less likely as longevity improvements lose steam

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A new study co-authored by a University of Wisconsin–Madison professor has found that the extraordinary life expectancy gains made by high-income countries in the first half of the 20th century have slowed dramatically. The researchers conclude that no generation born after 1939 will achieve an average lifespan of 100 years, marking a significant shift in expectations about longevity.

The study, published in the Proceedings of the National Academy of Sciences, was carried out by Héctor Pifarré i Arolas of the La Follette School of Public Affairs, José Manuel Aburto Andrade of the Max Planck Institute for Demographic Research, and Carlo Giovanni Camarda of the Institut national d’études démographiques. Using data from the Human Mortality Database, the team examined life expectancy trends in 23 high-income, low-mortality countries, applying six different statistical models to forecast how future lifespans might unfold.

According to Pifarré i Arolas, the steep rise in life expectancy achieved in the early 20th century was “unprecedented” and unlikely to be repeated. Even if survival among adults were to improve at twice the currently expected rate, the overall gains would not match the rapid increases of that earlier era. The analysis highlights the unique impact of that historical moment, when medical breakthroughs, better public health, and improved living conditions drastically reduced the risk of dying young.

Between 1900 and 1938, life expectancy in high-income countries rose by roughly five and a half months with each new generation. A child born in 1900 could expect to live to 62, while someone born in 1938 had a projected lifespan of 80. After 1939, however, the pace of improvement slowed to just two and a half to three and a half months per generation, depending on the forecasting method used. This decline reflects the diminishing influence of infant and child survival on overall longevity.

As Andrade explained, the dramatic gains of the past were fuelled mainly by falling child mortality, whereas future progress now depends almost entirely on extending survival at older ages. With infant and child mortality already at very low levels in high-income countries, advances in longevity are harder to achieve. The researchers forecast that those born in 1980, for example, will not reach 100 years of age on average, nor will any subsequent cohort included in their analysis.

While no projection can fully account for the possibility of unexpected developments such as pandemics, medical innovations, or societal upheavals, the study provides important insights for policymakers. Slower growth in life expectancy has profound implications for healthcare systems, pension schemes, and social planning, while also shaping individual choices about savings, retirement, and long-term care. In short, both governments and citizens need to recalibrate their expectations of human longevity in the 21st century.

More information: Héctor Pifarré i Arolas et al, Cohort mortality forecasts indicate signs of deceleration in life expectancy gains, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2519179122

Journal information: Proceedings of the National Academy of Sciences Provided by University of Wisconsin-Madison