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Breakthrough study finds strong genetic risk factor for rare dementia

Researchers at the VIB and University of Antwerp have identified a major genetic risk factor for a rare form of frontotemporal dementia, marking an important advance in understanding this complex condition. The discovery, reported in Nature Genetics, provides a crucial biological entry point into a disease subtype that has long been difficult to investigate. This insight has the potential to improve diagnostic precision and patient stratification while opening new directions for the development of targeted treatments tailored to specific disease mechanisms.

Frontotemporal dementia is less common and less widely recognised than Alzheimer’s disease, yet it is one of the leading causes of dementia in younger adults. The condition primarily affects brain regions responsible for behaviour, personality, decision-making, and language, meaning that early symptoms often manifest as changes in social conduct, reduced empathy, impulsivity, or language difficulties. These symptoms can appear long before memory problems become evident, often complicating early diagnosis and contributing to delays that may affect careers, relationships, and overall quality of life.

One specific subtype, known as aFTLD-U, is characterised by atypical frontotemporal lobar degeneration and the presence of ubiquitin-positive inclusions, which distinguish it from other forms of frontotemporal dementia. Individuals with this subtype may begin to exhibit behavioural symptoms as early as their thirties or forties, yet a definitive diagnosis has historically been possible only through post-mortem examination. Its rarity has made large-scale study challenging, even as the need to distinguish between different subtypes has become increasingly important, given that they may respond differently to emerging therapies.

The research team undertook a global effort to assemble a sufficiently large dataset of confirmed aFTLD-U cases. Using a genome-wide association approach across dozens of cases and thousands of controls, combined with advances in long-read sequencing technology, they identified a repeat expansion located within an intron of the GOLGA8A gene. This repeat varies in both length and sequence composition, with longer expansions showing a particularly strong association with the disease. Notably, this represents the first instance of a disease-linked repeat involving only two nucleotides, highlighting a previously underappreciated form of genetic variation.

The strength of the genetic signal observed in this study is striking, especially when compared with findings from larger studies of more common conditions. Long-read sequencing proved essential for detecting and characterising this complex repeat region, as traditional short-read methods are often unable to resolve such intricate genomic structures, particularly in areas like GOLGA8A that exist in multiple copies across the genome. This technological advantage enabled researchers to uncover a level of detail that would otherwise have remained hidden.

Although the functional impact of this repeat expansion is not yet fully understood, its presence in a substantial proportion of cases suggests a fundamental role in disease biology. Ongoing work is focused on determining how this genetic feature influences gene regulation and cellular processes in vulnerable brain regions. The findings also reinforce a broader perspective that even conditions considered sporadic may have significant genetic contributions. Identifying such factors offers a pathway towards earlier diagnosis and more precise classification, and ultimately supports the development of therapies that target the underlying biological mechanisms of disease.

More information: Wouter De Coster et al, A repeat expansion in GOLGA8A is a major risk factor for atypical frontotemporal lobar degeneration with ubiquitin-positive inclusions, Nature Genetics. DOI: 10.1038/s41588-026-02537-7

Journal information: Nature Genetics Provided by Vlaams Instituut voor Biotechnologie

From Pollution to Prescription: Plastic Bottles Become Parkinson’s Drug

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A pioneering study has demonstrated that a drug used to treat Parkinson’s disease can be produced from waste plastic bottles using an innovative biological method. The research introduces a novel approach that transforms post-consumer plastic into L-DOPA, a key frontline medication for managing the condition. By leveraging engineered bacteria, scientists have created a process that not only addresses plastic waste but also contributes to sustainable pharmaceutical production.

At the centre of this breakthrough is the use of bacteria to convert polyethylene terephthalate (PET), a common plastic found in food and drink packaging, into valuable chemical compounds. Researchers at the University of Edinburgh modified E. coli bacteria to carry out a sequence of biological reactions. These reactions ultimately convert PET-derived molecules into L-DOPA, marking the first time a natural biological system has been engineered to transform plastic waste into a therapeutic drug for a neurological condition.

The process begins with breaking down PET, of which approximately 50 million tonnes are produced annually, into its core chemical component, terephthalic acid. This intermediate compound is then processed by the engineered bacteria through a series of enzymatic steps, resulting in the production of L-DOPA. The approach effectively captures carbon embedded in plastic waste and repurposes it into a high-value medical product, demonstrating a creative and practical application of engineering biology.

Compared with conventional pharmaceutical manufacturing, which typically depends on finite fossil fuels, this method offers a more sustainable alternative. Plastic waste, often derived from oil and gas, is repurposed rather than discarded, reducing reliance on non-renewable resources. Existing recycling methods for PET remain imperfect and continue to contribute to global pollution, making this new technique particularly significant as a complementary solution that adds value while reducing environmental harm.

Beyond its immediate application in producing Parkinson’s medication, the innovation signals broader possibilities for a bio-upcycling industry. The same principles could potentially be applied to create a wide range of products, including flavourings, fragrances, cosmetics, and industrial chemicals. By demonstrating the feasibility of converting waste into useful and valuable outputs, the study highlights how biological systems can be harnessed to reshape manufacturing and resource use in more sustainable ways.

The findings, published in Nature Sustainability, were supported by organisations including UK Research and Innovation. Researchers are now working to scale up the process, improve efficiency, and evaluate its environmental and economic viability for industrial use. As the technology advances, it may help redefine how society views waste—not as a problem to discard, but as a resource with untapped potential to support both environmental sustainability and human health.

More information: Benjamin Royer et al, Microbial upcycling of plastic waste to levodopa, Nature Sustainability. DOI: 10.1038/s41893-026-01785-z

Journal information: Nature Sustainability Provided by University of Edinburgh

New evidence connects brain immune cells to Alzheimer’s plaque growth

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A new study led by researchers from VIB and KU Leuven reveals that immune cells in the brain known as microglia may actively promote the formation of plaques in Alzheimer’s disease. This challenges the long-standing assumption that these cells function solely as defenders that clear harmful buildup. The findings, recently published in Proceedings of the National Academy of Sciences, suggest that microglia may play a more complex and previously underappreciated role in disease development.

For decades, prevailing research has characterised microglia as protective cells tasked with removing amyloid plaques from the brain. However, this new work indicates that their role may be more paradoxical. According to co-senior author Joost Schymkowitz, microglia do not merely respond to plaque accumulation but may also contribute to it. Rather than plaques forming independently through spontaneous aggregation, the study suggests that microglial activity—while attempting to mitigate damage—may inadvertently amplify the very processes that drive plaque formation.

Alzheimer’s disease affects nearly 55 million people worldwide and is defined by the accumulation of toxic protein aggregates, commonly referred to as amyloid plaques, in the brain. These plaques are closely associated with neuronal damage, cognitive decline, and progressive dementia. Microglia have long been considered a key line of defence against this pathology and have therefore become a central focus of therapeutic strategies. Yet the new findings indicate that, particularly in earlier stages of the disease, microglia may also act as active contributors to plaque formation, prompting a reconsideration of current therapeutic approaches.

The research team demonstrated that microglia can transform soluble amyloid-beta proteins into structured fibrils with strong seeding activity. This seeding process is especially significant, as it allows a single aggregate to give rise to many more, accelerating disease progression. Notably, the fibrils generated by microglia resemble those found in the brains of patients, suggesting that cellular processes may play a more direct role in shaping disease pathology than previously understood.

Co-senior author Frederic Rousseau highlighted that these findings point to an additional, previously unrecognised function of microglia. Using seeding assays, the team showed that amyloid produced by cells more closely mimics patient-derived material and elicits biologically relevant responses. This represents an important advance, as it provides a model that better reflects the conditions occurring in human disease and may improve the relevance of experimental studies.

The study also underscores the limitations of traditional laboratory models, where amyloid plaques are typically formed under simplified conditions that differ significantly from those in patients. By developing approaches that generate plaques more representative of those observed in the human brain, researchers may gain deeper insight into the mechanisms of aggregation and identify more effective therapeutic targets. Importantly, while several experimental treatments aim to stimulate microglia to clear plaques, these new findings suggest that their effects may vary depending on the stage of the disease. This nuanced understanding could prove critical in refining future strategies for treating Alzheimer’s disease.

More information: Katerina Konstantoulea et al, Phagocytes as plaque catalysts: Human macrophages generate seeding-competent Aβ42 fibrils with cross-seeding activity, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2516774123

Journal information: Proceedings of the National Academy of Sciences Provided by Vlaams Instituut voor Biotechnologie

Daily Multivitamin Use Associated with Reduced Biological Ageing in COSMOS Study

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An analysis led by investigators at Mass General Brigham has found that daily multivitamin use may slow biological ageing in older adults. Drawing on data from a large, randomised clinical trial, the researchers observed that two years of supplementation was associated with measurable reductions in biological ageing, with the greatest benefits seen among individuals who entered the study with signs of accelerated ageing.

Biological age refers to how quickly the body is ageing at a cellular level, which may differ from a person’s chronological age. In this study, researchers examined multiple indicators of biological ageing over two years and found that participants taking a daily multivitamin experienced a modest but meaningful slowing of this process. The effect was equivalent to approximately four months less biological ageing compared with those who did not receive the supplement.

The findings, published in Nature Medicine, contribute to a growing body of research focused not only on extending lifespan but also on improving healthspan—the number of years lived in good health. According to senior author Howard Sesso, the results are particularly notable given the accessibility and safety profile of multivitamins. The study highlights the potential for relatively simple interventions to support healthier ageing trajectories.

To assess biological ageing, the research team used epigenetic clocks, which estimate ageing based on patterns of DNA methylation—small chemical modifications that regulate gene activity and change over time. These markers are increasingly recognised as reliable indicators of ageing and are associated with risks of disease and mortality. The analysis included blood samples from 958 healthy participants with an average age of 70, all drawn from the larger COSMOS trial.

Participants in the trial were randomly assigned to one of four groups: multivitamin and cocoa extract, multivitamin and placebo, cocoa extract and placebo, or double placebo. Over the course of two years, researchers measured changes across five established epigenetic clocks. Compared with the placebo group, those taking a multivitamin showed consistent slowing across all five measures, with statistically significant improvements observed in the clocks most strongly linked to mortality risk.

Importantly, the benefits were most pronounced among individuals whose biological age exceeded their chronological age at baseline, suggesting that those already experiencing accelerated ageing may derive greater value from supplementation. While these findings are promising, further research is needed to determine whether these effects persist over time and how they translate into real-world health outcomes, such as improved cognition or reduced risk of chronic conditions.

More information: Sidong Li et al, Effects of daily multivitamin–multimineral and cocoa extract supplementation on epigenetic aging clocks in the COSMOS randomized clinical trial, Nature Medicine. DOI: 10.1038/s41591-026-04239-3

Journal information: Nature Medicine Provided by Mass General Brigham

Experts fine-tune genetic maps to trace DNA influences on human traits and disease susceptibility

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Scientists have uncovered how specific genetic changes function inside cells to influence disease risk and a wide range of human health traits. By closely examining regions of DNA already linked to disease, the team produced high-resolution maps showing how individual DNA variants behave. This approach helps identify the exact changes that shape complex traits such as blood pressure, cholesterol levels, and blood sugar. Rather than broadly associating regions of the genome with disease, the study focuses on pinpointing the precise genetic differences that have real biological effects.

The research, published in Nature and led by teams from The Jackson Laboratory, the Broad Institute, and Yale University, addresses a long-standing challenge in human genetics. For many years, scientists have known that certain stretches of DNA are connected to disease, but these regions often contain many possible variants. This made it difficult to determine which specific changes were actually responsible. Testing each variant individually was slow and labour-intensive, limiting progress in understanding how genetic risk truly works.

To overcome this, the researchers used a large-scale experimental approach capable of analysing thousands of DNA variants at once. In total, they examined more than 220,000 previously identified genetic changes across five different cell types. This allowed them to clarify about 20 per cent of the targeted regions in the genome. By doing so, they revealed new insights into how these variants influence gene activity, offering a clearer picture of how genetic differences contribute to health outcomes and disease risk.

The study identified over 13,000 single-letter DNA changes that affect how strongly genes are expressed. While many of these variants act independently, the researchers found that about 11 per cent behave differently when combined with nearby variants. This suggests that some genetic effects are not simply additive but depend on specific combinations of changes working together. In some cases, these combinations were linked to lower levels of LDL cholesterol, while others appeared to influence genes related to blood pressure or developmental processes.

Another important finding highlights the value of studying genetic variation across diverse populations. The researchers identified a DNA variant linked to long-term blood sugar control that had been discovered mainly in people of European ancestry. Based on its biological behaviour, they predicted that similar variants in people of African ancestry would show comparable effects. Follow-up analysis confirmed this, demonstrating how understanding genetic mechanisms can improve equity in research and ensure that findings are relevant across different populations.

Although the study provides detailed insights into how many DNA variants regulate gene activity, it is only one step towards fully understanding disease. The human body contains many different tissues and cell types, and gene regulation can vary widely between them. Many genetic variants also remain untested. Even so, the findings offer valuable data that can strengthen future research, improve genetic risk prediction, and support the development of targeted therapies. By moving from broad associations to precise biological understanding, this work helps bridge a critical gap in human genetics.

More information: Layla Siraj et al, Functional dissection of complex trait variants at single-nucleotide resolution, Nature. DOI: 10.1038/s41586-026-10121-6

Journal information: Nature Provided by Jackson Laboratory

Fall Prevention Clinics: A Smart Investment in Older Adult Health

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Falls remain one of the leading causes of injury and hospitalisation among older adults, creating considerable pressure on individuals, families, and the health-care system. Beyond the immediate physical harm, falls often trigger a cascade of complications, including loss of independence, increased reliance on caregivers, and transitions into long-term care. As populations age, the cumulative impact of falls is becoming an increasingly urgent public health and economic concern.

New research led by Jennifer Davis at the University of British Columbia, Okanagan, highlights a compelling solution. The findings demonstrate that investing in targeted fall prevention for older adults at high risk not only reduces injuries but also delivers substantial financial returns. In essence, relatively modest upfront investments can prevent far more costly downstream health-care use.

Dr Davis, a Tier 2 Canada Research Chair in Applied Health Economics and an associate professor in the Faculty of Management, specialises in evaluating the economic impact of clinical interventions. Her work integrates economic analysis into randomised controlled trials, examining both cost-effectiveness and cost-utility across areas such as falls prevention, cognitive health, and chronic disease management.

Her most recent study, published in Maturitas, presents a 12-month cost analysis of the Falls Prevention Clinic at Vancouver General Hospital. The results show that each dollar invested in the clinic generates meaningful financial and health returns. By intervening early—before additional falls, fractures, or complications occur—the clinic significantly reduces the need for emergency visits, hospital admissions, and long-term care placement.

The clinic is a referral-based, research-informed service designed for adults aged 65 and older who are at high risk of falling. Many patients arrive with a history of repeated falls—on average, three within the previous year. Through comprehensive risk assessments and tailored interventions, the clinic addresses underlying risk factors while supporting independence and mobility. A core component is a personalised exercise programme delivered by a physiotherapist, focusing on progressive strength and balance training proven to reduce falls.

The outcomes are striking. The programme reduced falls by 36 per cent and produced a return on investment estimated between 500 and 2,700 per cent. In a single year, the clinic generated nearly one million dollars in health-care savings while operating with relatively modest costs, including approximately $103,000 for physiotherapy staffing. These findings illustrate how targeted, evidence-based enhancements to existing care models can yield substantial clinical and economic benefits while reinforcing the importance of prevention in sustaining health systems.

More information: Jennifer C. Davis et al, Twelve-month cost analysis of a geriatrician-led falls prevention clinic in Canada, Maturitas. DOI: 10.1016/j.maturitas.2026.108862

Journal information: Maturitas Provided by University of British Columbia Okanagan campus

USC research shows early Alzheimer’s brain markers vary across diverse populations

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A team of researchers from the USC Mark and Mary Stevens Neuroimaging and Informatics Institute at the Keck School of Medicine of USC has identified meaningful differences in how early brain changes linked to Alzheimer’s disease appear across racial and ethnic groups. The findings highlight the importance of using more inclusive approaches when studying and diagnosing Alzheimer’s, particularly as current knowledge has largely been based on more limited populations. The study has been published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.

The research drew on a large and diverse group of older adults who did not have dementia. It found that Black and Hispanic participants showed higher levels of tau, a protein associated with Alzheimer’s disease, in key areas of the brain involved in memory. Notably, these higher tau levels were observed even before the buildup of amyloid plaques, which are typically considered an early sign of Alzheimer’s. This suggests that the sequence or pattern of brain changes may differ across populations.

At the same time, the study found that the link between these brain changes and memory performance was not the same for all groups. While higher levels of tau were generally associated with poorer memory, the role of amyloid in strengthening this relationship varied. In particular, amyloid appeared to intensify the connection between tau and memory decline in non-Hispanic white and Hispanic participants, but not in Black participants. This indicates that common Alzheimer’s biomarkers may not fully explain cognitive changes in every population.

The data came from the Health and Aging Brain Study–Health Disparities (HABS-HD), one of the largest and most diverse brain imaging studies of ageing in the United States. Researchers used advanced PET scans to detect abnormal protein buildup in the brain years before symptoms appear. They analysed brain scans and memory test results from more than 1,500 participants who were either cognitively healthy or experiencing mild cognitive impairment.

The findings also suggest that factors beyond amyloid and tau may play a larger role in cognitive changes for some groups. These may include vascular health, other medical conditions, long-term exposure to stress, and broader social influences. In addition, researchers noted that some differences in tau levels might be linked to technical limitations in imaging methods, as certain scans can produce signals that are not directly related to tau. This reinforces the need to validate diagnostic tools across diverse populations.

Overall, the study points to the possibility that Alzheimer’s disease may develop through different biological pathways in different groups. This has important implications for how the disease is detected, monitored, and treated. Future research will continue to follow participants over time to better understand how biological, genetic, and social factors interact to shape cognitive ageing across communities, to improve care and prevention for all populations.

More information: Koral V. Wheeler et al, The relationships between ethnoracial identity, Aβ positivity, APOEε4, and medial temporal lobe tau PET, Alzheimer’s & Dementia. DOI: 10.1002/alz.71226

Journal information: Alzheimer’s & Dementia Provided by Keck School of Medicine of USC

Researchers find gut health supplement may help relieve arthritis pain

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A new study has found that a prebiotic fibre supplement can reduce pain, enhance grip strength, and lower pain sensitivity in people living with knee osteoarthritis (OA), while also achieving markedly better adherence than a digital physiotherapy programme. The findings come from the INSPIRE clinical trial, led by researchers at the University of Nottingham, and point to a simple, diet-based approach that may complement or, in some cases, outperform existing non-pharmacological interventions.

The trial demonstrated that a daily supplement of inulin—a naturally occurring dietary fibre found in foods such as chicory root and Jerusalem artichokes—significantly reduced pain levels among participants with OA. Published in the journal Nutrients, the results suggest that targeting gut health may offer a promising and accessible strategy for managing a condition that affects hundreds of millions of people globally, particularly older adults.

Knee osteoarthritis remains a leading cause of chronic pain and disability, with current treatment options often centred on pain medications or structured exercise programmes. However, medications can carry risks of side effects, and exercise regimens are frequently difficult for patients to maintain over time. In this context, a dietary supplement that is easy to incorporate into daily routines may provide a practical and sustainable alternative or complement to existing therapies.

According to lead author Dr Afroditi Kouraki, the findings highlight the potential of small dietary changes to deliver meaningful clinical benefits. Adding a fibre supplement to everyday meals, such as breakfast or yoghurt, could reduce pain and improve physical function without requiring substantial lifestyle disruption. This ease of integration may explain the notably low dropout rate observed among participants assigned to the inulin group.

The underlying mechanism appears to involve the gut microbiome, the complex community of microorganisms in the digestive system that plays a crucial role in overall health, including pain perception. Inulin acts as a prebiotic, nourishing beneficial gut bacteria and promoting the production of short-chain fatty acids such as butyrate. These compounds are known to influence inflammation and pain signalling pathways. Participants who took inulin also showed increased levels of glucagon-like peptide-1 (GLP-1), a hormone associated with both pain regulation and muscle function, with higher levels linked to improved grip strength.

The six-week randomised controlled trial included 117 adults with knee OA and compared four groups: inulin alone, physiotherapy-supported exercise alone, a combination of both, and a placebo. While both inulin and physiotherapy reduced knee pain, only inulin improved grip strength and pain sensitivity—key indicators of how the nervous system processes pain. Importantly, adherence differed substantially, with just 3.6% of participants in the inulin group dropping out compared to 21% in the physiotherapy group. These findings underscore the potential of gut-targeted interventions as a safe, well-tolerated, and scalable approach to improving quality of life for people with osteoarthritis, while also opening new avenues for research into the broader gut–muscle–pain connection.

More information: Afroditi Kouraki et al, Effect of Prebiotic Supplementation With and Without Physiotherapy on Pain and Pain Sensitivity in People with Knee Osteoarthritis, Nutrients. DOI: 10.3390/nu18050714

Journal information: Nutrients Provided by University of Nottingham

Outages Drive Rise in Emergency Hospital Visits Among Elderly Populations

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Adults aged 65 and older experience higher rates of emergency hospitalisations for cardiovascular and respiratory conditions during and following power outages, according to a new study led by Heather McBrien of the Columbia Mailman School of Public Health and colleagues. The research, published on 12 March in the open-access journal PLOS Medicine, highlights a growing but under-recognised public health concern affecting older populations.

Across the United States, power outages have become more frequent and longer in duration, largely driven by severe weather linked to climate change and the strain on ageing electrical infrastructure. Earlier research conducted in New York State suggested that outages may contribute to increased hospitalisations among older adults, particularly for heart and lung conditions. These risks are often tied to the loss of essential services such as air conditioning, heating, communication devices, and electrically powered medical equipment, including oxygen support systems. However, until recently, national-level evidence on this issue had been limited.

To address this gap, the researchers conducted a nationwide analysis using data from 2018. They identified power outages across the country and examined healthcare records from approximately 23 million Medicare beneficiaries. By analysing daily rates of emergency hospital admissions, the study was able to estimate the broader health impacts of outages on older adults at a national scale.

The findings revealed that power outages lasting more than eight hours were associated with noticeable increases in hospitalisations for both cardiovascular and respiratory diseases. Respiratory-related admissions were most likely to occur on the same day as the outage, reflecting immediate vulnerabilities such as loss of temperature control or respiratory support. In contrast, cardiovascular-related hospitalisations were more likely to peak on the day following an outage, suggesting delayed physiological stress or complications. Overall, the researchers estimated that 4,246 additional hospitalisations among adults aged 65 and over in 2018 could be attributed to power outages.

The study underscores the importance of strengthening electrical grid reliability as a critical public health intervention. Improving infrastructure resilience could help reduce preventable health risks, particularly for vulnerable populations. In addition, targeted measures—such as ensuring access to backup batteries for medical devices and mobile phones, or providing generators to maintain heating and cooling systems—may offer practical ways to mitigate harm during outages.

The authors emphasise that their findings demonstrate a clear link between power outages and increased hospitalisation risks among older adults. They note that the magnitude of risk rises with the proportion of the population affected by an outage. As climate change continues to intensify extreme weather events and place further strain on ageing energy systems, the need for preventative strategies becomes more urgent. Future research examining individual-level data may provide deeper insights into risk patterns and help inform more precise interventions to safeguard health.

More information: Heather McBrien et al, The association between power outages and cardiovascular and respiratory hospitalizations among US Medicare beneficiaries in 2018: A case-crossover study, PLOS Medicine. DOI: 10.1371/journal.pmed.1004923

Journal information: PLOS Medicine Provided by PLOS

Physical Function and Its Importance in Heart Failure Survival Prediction

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Monitoring and treating heart failure (HF) remains difficult at any age, especially among older adults. Doctors often rely on prediction models to estimate a patient’s chances of survival. Well-known tools such as the AHEAD and BIOSTAT compact models use clinical factors like irregular heart rhythm, anaemia, age, diabetes, kidney function, and ejection fraction. However, research has shown that these models, which were mainly developed using European and North American populations, tend to underestimate risk in older East Asian patients. This raises an important question about whether including additional factors could improve survival predictions.

A research team from Juntendo University in Japan has worked to address this issue by developing a more accurate model for predicting long-term survival after heart failure. Professor Tetsuya Takahashi, Assistant Professor Kanji Yamada, and Associate Professor Nobuyuki Kagiyama led the study. They used machine learning methods to identify which patient characteristics are most important for predicting outcomes. Their findings were published in February 2026 in The Lancet Regional Health – Western Pacific.

One of the key limitations of existing models is that they mainly focus on heart-related and biological measurements. According to Dr Yamada, this approach often overlooks other important factors such as physical function, frailty, and nutritional status. These factors are especially important in older adults because they strongly influence recovery and survival. Unlike age or other fixed characteristics, physical function and nutrition can potentially be improved through rehabilitation and supportive care, making them valuable targets for treatment.

To build a better model, the researchers used data from the J-Proof HF registry, which tracks elderly heart failure patients across 96 hospitals in Japan. They analysed data from 9,700 patients who were treated between December 2020 and March 2022 and later discharged from the hospital. Using this data, they trained a machine learning algorithm called XGBoost to predict the risk of death within one year after treatment. They then created a simpler version of the model using the 20 most important variables identified by the algorithm.

Interestingly, seven of these top 20 variables were related to physical function and other non-cardiac factors. Measures such as the Barthel Index (BI) and Short Physical Performance Battery (SPPB) were especially important. These are performance-based tests that assess a patient’s ability to carry out daily activities and physical tasks. Compared to more subjective assessments, these tests provide more consistent and reliable results and better reflect a patient’s true functional ability.

Both versions of the model performed well in predicting one-year mortality, but the simplified Top-20 model was particularly effective at classifying patients into different risk levels. It also outperformed traditional models like AHEAD and BIOSTAT compact. Because it was developed using data from Japanese patients, it may be better suited for assessing risk in older individuals with heart failure in Japan and similar populations.

This new model could help healthcare professionals move away from a one-size-fits-all approach to treating heart failure. Instead, doctors could use it to identify patients who need closer monitoring or more personalised care after leaving the hospital. It could also help make better use of medical resources. Importantly, the strong role of physical function in the model highlights the value of rehabilitation and maintaining physical ability both before and after hospitalisation.

The researchers emphasise that physical function at discharge is just as important as traditional heart-related risk factors in predicting survival. Their findings support the idea that routine care for older heart failure patients should include broader assessments that consider overall physical and functional health. While the team is optimistic about the model’s potential, they note that further testing in different populations is needed. They are also working on developing a practical tool that clinicians can use to estimate a patient’s risk more easily.

More information: Kanji Yamada et al, Machine learning prediction of 1-year mortality in older patients with heart failure: a nationwide, multicenter, prospective cohort study, The Lancet Regional Health – Western Pacific. DOI: 10.1016/j.lanwpc.2026.101808

Journal information: The Lancet Regional Health – Western Pacific Provided by Juntendo University Research Promotion Center

New Perspective Positions Buildings as Critical to Health Determinants

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As populations continue to age, growing attention is being directed towards the institutional environments where many older adults live, including nursing homes and long-term care facilities. These settings play a significant role in shaping residents’ health and overall quality of life. Increasing evidence shows that the built environment can influence both the physical and cognitive wellbeing of older individuals in complex ways.
Design elements within these spaces can have meaningful consequences. Factors such as layout, lighting, materials and spatial organisation may affect risks related to falls, infection transmission, preventable hospital admissions and even cognitive disorientation. In this way, architecture does not simply provide shelter, but actively shapes health outcomes for ageing populations.

Despite this growing body of research, its application in real-world building projects remains inconsistent. Much of the existing evidence is not systematically integrated into the planning or renovation of long-term care environments. In response, a multidisciplinary team from Boston University Chobanian & Avedisian School of Medicine has introduced a new framework aimed at bridging this gap.

The framework, known as Bioethics Peer Review for Long-Term Care Design (BPR-LTC), is designed to guide the evaluation of architectural plans for long-term care facilities. Its central goal is to ensure that evidence-based design principles are thoughtfully incorporated into the creation of spaces intended for older adults, aligning physical environments with their specific needs.

BPR-LTC brings together several distinct approaches, including evidence-based design research, clinical ethics consultation methods for addressing complex value-driven decisions, and geriatric care frameworks that prioritise the vulnerabilities and requirements of older individuals. While each of these components has contributed independently to long-term care, they have rarely been coordinated during the early stages of architectural design.

Unlike traditional design methodologies or performance metrics, BPR-LTC functions as an ethics-informed, deliberative process that structures how evidence and values are considered in decision-making. By introducing a more systematic and research-driven approach, the framework aims to improve the design of long-term care environments, ultimately enhancing the health and wellbeing of those who live and work within them.

More information: Diana Anderson et al, Bioethics Peer Review: A Structured Evaluation Framework for Long-Term Care Environments, Journal of the American Medical Directors Association. DOI: 10.1016/j.jamda.2025.106088

Journal information: Journal of the American Medical Directors Association Provided by Boston University School of Medicine

Science Reveals Why Full Doesn’t Mean Finished When It Comes to Food

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Research carried out at the University of East Anglia (UEA) offers a compelling explanation for a familiar experience: reaching for a snack even after feeling full. Many people assume that eating behaviour is governed purely by hunger, yet this study suggests something far more complex is at play. In modern environments filled with constant food advertising, tempting displays, and easy access to treats, the brain appears to remain highly responsive to food cues regardless of physical fullness. This may help explain why maintaining a healthy weight can feel so challenging for so many individuals.

The research indicates that the human brain continues to react strongly to appealing food stimuli even after the body’s energy needs have been met. In other words, while the stomach may signal satisfaction, the brain does not necessarily follow suit. This disconnect highlights how appetite is influenced not only by biological hunger but also by learned responses and environmental triggers. The findings suggest that overeating is not simply a matter of poor self-control, but rather a natural outcome of how the brain processes reward in a food-rich world.

Lead researcher Dr Thomas Sambrook, from UEA’s School of Psychology, emphasised that rising obesity rates should not be reduced to issues of willpower alone. Instead, he explained that modern surroundings, filled with enticing food cues, can override the body’s internal appetite regulation systems. The team aimed to explore how the brain behaves when a person is already full, and whether it reduces its response to food. Their findings revealed that even after eating enough to feel satisfied, the brain continues to react to appealing food in much the same way as it would when hungry.

To investigate this, researchers monitored 76 volunteers using electroencephalogram (EEG) brain scans while they took part in a reward-based learning task involving foods such as sweets, chocolate, crisps, and popcorn. During the experiment, participants were given one of these foods to eat until they felt they could not consume any more. By all behavioural and self-reported measures, participants were genuinely full. They expressed reduced desire for the food and demonstrated less interest in obtaining it during the task.

Despite this clear sense of fullness, the brain activity told a different story. Electrical signals in regions associated with reward continued to respond strongly when participants were shown images of the same foods they had just eaten. This suggests that the brain does not easily adjust its perception of how rewarding food appears, even when the body no longer needs it. The persistence of these responses indicates that visual or environmental food cues can still trigger a desire to eat, independent of actual hunger.

The study also points to the role of habit in shaping these reactions. Over time, repeated associations between certain foods and pleasure may create automatic patterns in the brain. These responses can operate outside conscious awareness, meaning a person might believe they are eating out of hunger when they are actually responding to ingrained cues. Notably, the research found no connection between an individual’s self-control and their brain’s resistance to reducing food reward signals. This suggests that even highly disciplined individuals can struggle, as their neural wiring continues to promote eating. In this light, resisting an extra treat is not merely a test of willpower, but a challenge rooted in the brain’s fundamental design.

More information: Thomas Sambrook et al, Devaluation insensitivity of event related potentials associated with food cues, Appetite. DOI: 10.1016/j.appet.2025.108390

Journal information: Appetite Provided by University of East Anglia