Monthly Archives: December 2025

Research Isolates Population Ageing as the Dominant Influence on Musculoskeletal Health Trends

New research shows that, in around one-third of countries and territories worldwide, population ageing was the single most significant contributor to the rising burden of musculoskeletal disorders between 1990 and 2021. Published in Annals of the Rheumatic Diseases by Elsevier, the study offers substantial evidence to support more targeted public health planning and healthcare resource allocation, with the potential to reduce both the health and economic consequences of these widespread conditions.

Musculoskeletal disorders, such as arthritis, osteoporosis, and chronic back pain, are among the leading causes of disability globally. As populations age at an accelerating pace, the number of people affected by pain, reduced mobility, and long-term disability continues to increase. Although this trend has raised growing concern, it remains unclear how much of the expanding burden is explicitly driven by population ageing rather than by overall population growth or changes in disease rates within age groups.

To clarify this issue, the researchers quantified the independent effect of population ageing on the global burden and healthcare costs of musculoskeletal disorders. Using data from the Global Burden of Disease 2021 study, they separated the impact of ageing from that of population growth and age-specific epidemiological changes. Their analyses accounted for geographic variation, sociodemographic factors, sex differences, and major categories of musculoskeletal disease, while also estimating healthcare expenditure attributable to ageing populations.

The results show that, in approximately one-third of countries and territories, population ageing was the dominant driver of increasing musculoskeletal disease burden. Middle-income countries experienced the most significant proportional increases linked to ageing, despite generally having younger populations than high-income countries. This reflects the speed of demographic change in these regions, combined with healthcare systems that are often less prepared to meet the needs of older adults. Globally, men were more affected by ageing-related increases in musculoskeletal burden in higher-income settings, while women experienced greater impact in low- and middle-income countries. Osteoarthritis emerged as the most affected condition worldwide, followed by gout and rheumatoid arthritis.

The study also highlights the substantial economic implications of population ageing. In 2021, healthcare costs associated with ageing-related musculoskeletal disorders were estimated at US$96 billion, equivalent to around 0.10 per cent of global gross domestic product. This figure exceeds the expenses attributed to several common modifiable risk factors, underscoring the scale of the financial challenge posed by these conditions.

Overall, the findings underline that population ageing is an unavoidable global trend, but its impact on musculoskeletal health is unevenly distributed. The authors stress that their results can help policymakers prioritise interventions suited to local demographic and socioeconomic contexts, address sex-specific differences, and focus on the most affected conditions. Strengthening prevention, improving long-term management, and ensuring sustainable healthcare financing will be essential to reducing disability, improving the quality of life for older adults, and enhancing the resilience of healthcare systems worldwide.

More information: Shi-Yang Guan et al, The impact of population ageing on musculoskeletal disorders in 204 countries and territories, 1990-2021: global burden and healthcare costs, Annals of the Rheumatic Diseases. DOI: 10.1016/j.ard.2025.08.002

Journal information: Annals of the Rheumatic Diseases Provided by Elsevier

Europe’s evolving demographics may heighten the burden of antimicrobial resistance

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Rates of bloodstream infections caused by antibiotic-resistant bacteria are expected to rise substantially across Europe over the next five years, mainly driven by ageing populations, according to new research published on 4 November in the open-access journal PLOS Medicine. Led by Gwenan Knight of the London School of Hygiene and Tropical Medicine, the study highlights how demographic change is likely to intensify the future burden of antimicrobial resistance across the region.

Antimicrobial resistance, commonly known as AMR, is widely recognised as a significant global public health threat. Resistant infections make routine treatments less effective, increase the risk of severe illness and death, and place growing pressure on healthcare systems. To guide prevention strategies and monitor progress towards international targets, it is essential to understand not only current levels of resistance but also how the burden of AMR is likely to change over time as populations evolve.

To address this, the researchers analysed data from more than 12 million routine blood culture susceptibility tests collected in 29 European countries between 2010 and 2019. These data were used to estimate the incidence rates of bloodstream infections caused by different bacteria and to assess patterns of antibiotic resistance. The team then modelled how rates of drug-resistant bloodstream infections might change through to 2050, incorporating projected shifts in population size, age structure, and sex.

The results suggest that bloodstream infection rates will increase overall, although the scale of the rise varies considerably between countries and between different bacteria–antibiotic combinations. A clear demographic pattern emerged. Rates were projected to increase more in men than in women for most of the bacteria studied, and to rise most sharply in older age groups. In particular, adults aged 74 and over are expected to experience the most significant increases, while rates in younger populations are predicted to stabilise or even decline.

The authors note that models which fail to account for age and sex differences are likely to miss a substantial share of the future burden of antimicrobial resistance, especially among older adults and men. Even under scenarios assuming strong public health interventions, the study found that achieving a 10 per cent reduction in resistant infections by 2030—aligned with United Nations targets—would be possible for only around two-thirds of the bacteria–antibiotic combinations examined.

Gwenan Knight emphasised that the future impact of drug-resistant infections will not be evenly distributed. Significant differences are expected across countries, age groups, and sexes. The steepest increases are projected among older adults, particularly those over 65, meaning that simply preventing further rises in resistant bloodstream infections in these groups would already represent a significant public health achievement. Co-author Catrin Moore added that understanding how age and sex shape future AMR trends is a crucial step towards designing targeted interventions that focus on the populations most at risk, helping to reduce illness and deaths associated with drug-resistant infections across Europe.

More information: Naomi R. Waterlow et al, Combining demographic shifts with age-based resistance prevalence to estimate future antimicrobial resistance burden in Europe and implications for targets: A modelling study, PLOS Medicine. DOI: 10.1371/journal.pmed.1004579

Journal information: PLOS Medicine Provided by PLOS

Digital innovations for improving dementia care among people ageing at home and their caregivers

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Digital technology is now woven into everyday life, shaping how people communicate, organise support, and maintain relationships. From messaging platforms to video calls, these tools are often promoted as effective alternatives to in-person interaction. Yet for a long time, it remained unclear whether such benefits extended to people living with dementia and to those who care for them, given the cognitive, emotional, and practical challenges associated with the condition.

Recent research helps clarify this uncertainty. Findings led by Li-Mei Chen, Assistant Professor of Social Work at George Mason University and a gerontologist specialising in dementia care and digital health, indicate that technology-enabled interventions can meaningfully support both people living with dementia and their caregivers. Rather than serving merely as substitutes for face-to-face contact, these digital approaches have been shown to improve self-efficacy, emotional wellbeing, social connectedness, and coordination of care. Together, these outcomes suggest that digital tools can contribute to both quality of life and more effective caregiving when thoughtfully designed and implemented.

For caregivers, the benefits are particularly evident in areas such as mental health, confidence, and access to information. Digital education programmes, online peer support, and care coordination platforms can reduce feelings of isolation and enhance caregivers’ sense of competence. People living with dementia may also benefit through improved emotional wellbeing and sustained social engagement, challenging assumptions that digital tools are inherently unsuitable for individuals with cognitive impairment. Instead, the findings highlight that usefulness depends less on diagnosis and more on how technology aligns with users’ abilities and needs.

Crucially, no single type of technology emerges as universally superior. The success of digital dementia care interventions appears to rest on personalisation, ease of use, and the integration of multiple care approaches. Tools that combine communication, education, monitoring, and psychosocial support are more effective than those relying on a single function. This reinforces the importance of viewing digital solutions as part of a broader, person-centred care system rather than isolated technological fixes.

Digital tools are generally feasible and acceptable, particularly when they are intuitive and culturally responsive. However, the research also reveals significant equity gaps. Most interventions have focused on English-speaking, higher-income, and urban populations, leaving non-English speakers, lower-income individuals, and those in rural areas underrepresented. These limitations restrict who can benefit from current digital dementia care and risk reinforcing existing inequalities in access to support.

The study underpinning these conclusions takes a novel, integrative approach. It reviews 27 studies on technology-based interventions designed to support ageing in place, meaning enabling people with dementia to remain in their own homes as they age. Unlike earlier reviews that examined single technologies in isolation, this work maps how different types of digital interventions function together to support everyday living. Using the World Health Organization Digital Health Intervention framework, the research systematically categorises intervention types and examines social determinants of digital access. It also highlights a persistent lack of inclusive, culturally adapted design processes that meaningfully involve people living with dementia themselves. Addressing these gaps will be essential if digital dementia care is to become more equitable, effective, and responsive to diverse lived experiences.

More information: Li-Mei Chen et al, Technology that Supports Extending Dementia-Friendly Community-Based Care: A Scoping Review, Current Geriatrics Reports. DOI: 10.1007/s13670-025-00446-x

Journal information: Current Geriatrics Reports Provided by George Mason University

Ageing may be slowed by a key chemical found in dark chocolate

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A chemical naturally present in dark chocolate may help slow the pace of biological ageing, according to new research that sheds light on how everyday foods could influence long-term health. Scientists suggest that the compound, known as theobromine, may be linked to biological markers that indicate a younger physiological age than a person’s actual years.

Researchers at King’s College London examined theobromine, a plant-derived compound found in cocoa, after identifying a potential association between its presence in the bloodstream and indicators of slower ageing. Their findings, published in the journal Aging, focused on biological age rather than chronological age, offering a more nuanced view of how the body ages at a cellular and molecular level.

Biological age reflects how well the body is functioning and is often assessed by measuring chemical changes in DNA called methylation. These small molecular “tags” change predictably over time and can reveal whether someone is ageing faster or more slowly than expected. By analysing these patterns in blood samples, scientists can estimate the biological wear and tear of the body, rather than simply counting the number of years a person has lived.

The study analysed data from two large European population cohorts, including 509 participants from the UK-based TwinsUK study and 1,160 individuals from the German KORA cohort. Across both groups, people with higher levels of theobromine circulating in their blood tended to have a biological age that appeared younger than their chronological age. This pattern suggested a consistent association between the compound and healthier ageing across different populations.

To strengthen their findings, the researchers also assessed telomere length, another widely used marker of ageing. Telomeres are protective caps at the ends of chromosomes that shorten as cells divide, with shorter telomeres linked to ageing and age-related disease. Participants with higher theobromine levels showed signs of more favourable telomere profiles, reinforcing the idea that the compound may be connected to slower biological ageing. Other cocoa- and coffee-related metabolites were tested, but none showed the same relationship, indicating that the effect was specific to theobromine.

Despite the promising results, the researchers stress caution in interpreting the findings. While theobromine has previously been linked to benefits such as reduced cardiovascular risk in humans, dark chocolate also contains sugar, fat, and other compounds that may be harmful if consumed in excess. The team emphasises that their work does not suggest eating more dark chocolate, but rather highlights how studying naturally occurring dietary compounds can deepen understanding of ageing processes and potentially guide future research into healthier, longer lives.

More information: Jordana Bell et al, Theobromine is Associated with Slower Epigenetic Ageing, bioRxiv. DOI: 10.1101/2025.04.15.648884

Journal information: bioRxiv Provided by King’s College London

Longevity gene found in supercentenarians could help combat rapid-ageing disease in children

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Researchers have identified a promising new approach to treating a rare and devastating genetic condition that causes children to age at an unusually rapid rate, drawing on the biology of people who live exceptionally long lives. The study shows that “longevity genes, commonly found in centenarians and supercentenarians, may help protect the heart and blood vessels from the severe damage caused by this life-limiting disease. By harnessing mechanisms linked to healthy ageing, the findings offer a fresh and hopeful direction for future therapies.

The research is the first to demonstrate that a gene associated with extreme longevity can slow heart ageing in a model of Hutchinson–Gilford Progeria Syndrome (HGPS). Progeria is a rare and fatal condition in which children develop symptoms of old age within the first years of life, despite appearing healthy at birth. The disease is driven by a mutation in the LMNA gene, which results in the production of a toxic protein called progerin. Over time, progerin accumulates in cells and causes widespread damage, particularly to the cardiovascular system. As a result, most children with progeria die in their teens from heart attacks or strokes, although a small number, such as Sammy Basso, have lived into early adulthood.

Progerin disrupts the structure of the cell nucleus, often described as the cell’s control centre, leading to premature cellular ageing. The heart and blood vessels are especially vulnerable, developing stiffness, scarring, and reduced function. Currently, treatment options are minimal. The only drug approved by the United States Food and Drug Administration is lonafarnib, which reduces the build-up of progerin and modestly extends life expectancy, but does not halt disease progression. Newer clinical trials are exploring drug combinations to improve outcomes.

Rather than attempting to eliminate progerin, the research team explored whether the protein’s damaging effects could be mitigated by strengthening the body’s natural defences. They focused on a longevity-associated gene, LAV-BPIFB4, previously shown to support cardiovascular health during normal ageing. Using genetically engineered mouse models of progeria, the researchers observed early heart problems similar to those seen in affected children. A single administration of the longevity gene significantly improved heart function, particularly the heart’s ability to relax and fill with blood. It also reduced fibrosis, lowered the number of senescent cells, and stimulated the growth of new small blood vessels.

The team then tested the gene in human cells taken from progeria patients and found comparable benefits. Markers of cellular ageing and tissue damage were reduced, even though progerin levels remained unchanged. This suggests the gene helps cells tolerate the toxic effects of progerin rather than removing it directly. The researchers believe this strategy, based on the biology of healthy ageing, could lead to a new class of therapies for progeria and potentially for more common age-related heart diseases. In the longer term, the findings point to the possibility of gene-, protein-, or RNA-based treatments that could improve both survival and quality of life for patients, while also offering insights into how we all age more healthily.

More information: Yan Qiu et al, A longevity-associated variant of the human BPIFB4 gene prevents diastolic dysfunction in progeria mice, Signal Transduction and Targeted Therapy. DOI: 10.1038/s41392-025-02416-3

Journal information: Signal Transduction and Targeted Therapy Provided by University of Bristol

FAU-led research provides further evidence linking alcohol consumption to cancer

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As the holiday season approaches and social gatherings become more frequent, new research serves as a timely reminder to consider the long-term health implications of alcohol consumption. Although alcohol is widely known to increase the risk of several cancers, even at levels many regard as moderate, drinking remains common across the United States. This disconnect has left important questions unresolved about how both the frequency and quantity of alcohol intake shape cancer risk, and why public awareness and policy often fail to highlight cancer as a key consequence of drinking.

Health risks linked to alcohol are not evenly shared across the population. Biological differences, social conditions, and patterns of exposure mean that some groups experience far greater harm than others. Despite this, alcohol policies and public health messaging have tended to focus on immediate harms such as liver disease or injury, rather than cancer prevention. To address these gaps, researchers from Florida Atlantic University’s Charles E. Schmidt College of Medicine conducted a comprehensive systematic review examining how different levels of alcohol consumption affect cancer risk among U.S. adults.

The review analysed data from 62 studies, with participant numbers ranging from just 80 individuals to nearly 100 million. This broad evidence base allowed the researchers to assess cancer risk across diverse populations and drinking patterns, including excessive, moderate, and mild alcohol use. The analysis also accounted for comorbid conditions such as obesity and chronic liver disease, which are known to increase vulnerability. It examined how social and demographic factors influence exposure and outcomes.

Published in the journal Cancer Epidemiology, the findings confirmed that both how often people drink and how much they consume significantly affect cancer risk. Strong associations were identified for breast, colorectal, liver, oral, laryngeal, oesophageal, and gastric cancers. Alcohol was also linked to poorer outcomes once cancer develops; for example, individuals with alcoholic liver disease were more likely to present with advanced liver cancer and experienced lower survival rates. Higher alcohol intake was associated with particularly elevated risk among African Americans, people with genetic predispositions, and individuals with obesity or diabetes. Factors such as race, age, income, and education further shaped vulnerability, leaving lower socioeconomic and some racial or ethnic groups disproportionately affected despite similar or lower levels of consumption.

The review also highlighted that healthier lifestyle choices can reduce risk. Following guidance from organisations such as the American Cancer Society—combining limited alcohol intake with broader healthy behaviours—was associated with lower cancer incidence and mortality. The researchers noted additional complexities, including differences by beverage type and sex, with some evidence that frequent drinking posed a greater risk for men. In contrast, episodic heavy drinking was more harmful for women. Smoking amplified alcohol-related cancer risk, and factors such as infections, low physical activity, and poor diet further compounded harm. Overall, the authors emphasise that alcohol-related cancer risk arises from a complex interaction of biological, behavioural, and social factors, underscoring the need for clearer public messaging, stronger policies, and targeted interventions to reduce preventable cancer burden.

More information: Isabella Abraham et al, A systematic review on the risk of developing cancer and frequency of alcohol consumption behaviors in US adults, Cancer Epidemiology. DOI: 10.1016/j.canep.2025.102956

Journal information: Cancer Epidemiology Provided by Florida Atlantic University

Tea consumption associated with improved bone strength in older women, as coffee raises potential concerns

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A new study from Flinders University provides fresh insight into how two of the world’s most popular beverages, tea and coffee, may influence bone health in older women.

Published in the journal Nutrients, the research followed nearly 10,000 women aged 65 and over for about ten years. The study set out to examine whether regular tea or coffee consumption was associated with changes in bone mineral density (BMD), a key indicator of osteoporosis risk and fracture likelihood later in life.

Osteoporosis is a primary global health concern, particularly for women, with around one in three affected after the age of 50. It contributes to millions of fractures each year and can have serious consequences for mobility, independence, and quality of life. Given how widely tea and coffee are consumed worldwide, even minor effects on bone health could have significant implications at a population level. Previous studies have produced mixed results, and few have examined these relationships over such a long period.

To address this, the researchers analysed data from the Study of Osteoporotic Fractures, using repeated measurements of both beverage intake and bone density. Bone mineral density was assessed at the total hip and femoral neck, areas closely linked to fracture risk, while participants regularly reported their tea and coffee consumption throughout the follow-up period.

The results suggested that tea consumption was associated with slightly higher total hip bone mineral density compared with not drinking tea. Although the difference was modest, it was statistically significant, meaning it was unlikely to be due to chance alone. According to Adjunct Associate Professor Enwu Liu, even minor improvements in bone density can matter when considered across large populations, potentially translating into fewer fractures overall.

Coffee showed a more complex pattern. Moderate intake, around two to three cups per day, did not hurt bone health. However, drinking more than five cups daily was associated with lower bone mineral density, indicating that very high consumption may be detrimental. The effects of heavy coffee intake were more pronounced in women with higher lifetime alcohol consumption, while tea appeared to be particularly beneficial for women with obesity.

These differences may be explained by the compounds found in each beverage. Tea contains catechins, which have been shown in experimental studies to support bone formation and slow bone breakdown. Coffee’s caffeine content, by contrast, can slightly interfere with calcium absorption and bone metabolism, although these effects are generally minor and may be reduced by adding milk.

The authors emphasise that the findings should not prompt dramatic lifestyle changes. The observed differences in bone density are relatively small, and moderate coffee consumption appears to be safe for most older women. However, the results do suggest that very high coffee intake may not be ideal, particularly for women who also consume alcohol.

Overall, while calcium and vitamin D remain central to maintaining healthy bones, the study indicates that everyday choices may also play a role. For older women, enjoying a daily cup of tea can be a simple, accessible way to support bone health as part of a balanced lifestyle.

More information: Ryan Yan Liu et al, Longitudinal Association of Coffee and Tea Consumption with Bone Mineral Density in Older Women: A 10-Year Repeated-Measures Analysis in the Study of Osteoporotic Fractures, Nutrients. DOI: 10.3390/nu17233660

Journal information: Nutrients Provided by Flinders University

Breaking Down the Complex: A Key Step in the Inhibition of Alzheimer’s Disease

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Alzheimer’s disease (AD) is one of the most common and complex neurodegenerative disorders worldwide. It mainly affects older adults and leads to permanent changes in the brain that gradually impair memory, thinking, behaviour, and everyday functioning. Despite more than a hundred years of scientific research, there is still no treatment that can stop or reverse the disease. For this reason, researchers continue to explore new approaches that target the underlying biological mechanisms of Alzheimer’s rather than its symptoms alone. Recent work by an international team of scientists from Poland and Spain highlights how combining different analytical techniques can help identify and better understand potential drug candidates.

One of the key features of Alzheimer’s disease is the accumulation of β-amyloid peptides in the brain, along with increased oxidative stress. Oxidative stress occurs when harmful reactive oxygen species are produced in excess, damaging neurons and other brain cells. A trace metal that plays a vital role in this process is copper. Under normal conditions, copper is essential for life, supporting enzymes involved in energy production, brain signalling, and protection against oxidative damage. However, when copper levels are not adequately regulated, the metal can become toxic. In Alzheimer’s disease, copper can bind to amyloid peptides, forming complexes that promote the production of free radicals and intensify oxidative stress, contributing to neuronal damage and disease progression.

To reduce this harmful activity, scientists are investigating molecules that can bind copper safely and control its reactivity in the brain. One promising compound is TDMQ20, a molecule designed to bind copper ions selectively. By acting as a chelator, TDMQ20 can potentially neutralise copper’s toxic effects while preserving its essential biological roles. The recent study focused on understanding how copper behaves when bound to TDMQ20, particularly during oxidation and reduction processes closely linked to oxidative stress. This is an important step in determining whether such a molecule could be safe and effective as a future drug.

The researchers used a combination of electrochemical techniques and spectroscopy to study the copper–TDMQ20 complex. These methods allowed them to observe how the complex responds to changes in electrical potential and how its structure and optical properties change during redox reactions. Their results showed that when copper is bound to TDMQ20, it becomes much less likely to participate in harmful redox reactions under normal physiological conditions. In particular, the reduction of the copper ion occurs only at very low potentials, which are not present in the human body. This suggests that the copper–TDMQ20 complex does not contribute to oxidative stress, making it a safer way to control copper activity.

The study also showed that the behaviour of the copper–TDMQ20 complex depends on pH, which is important because different parts of a cell have different acidity levels. Even when the complex is oxidised, copper remains bound to TDMQ20 rather than being released in a harmful form. These findings indicate that TDMQ20 forms a stable, predictable complex with copper under conditions similar to those in biological systems. Overall, this research suggests that TDMQ20 is a promising candidate for reducing copper-related oxidative stress in Alzheimer’s disease. Just as importantly, it demonstrates how combining electrochemistry, spectroscopy, and modelling can provide more precise and more reliable insight into how potential drug molecules behave in the body.

More information: Martin Perez-Estebanez et al, Spectroelectrochemical studies of TDMQ20: A potential drug against Alzheimer’s disease – part 2 – Cu-complexes, Bioelectrochemistry. DOI: 10.1016/j.bioelechem.2025.109115

Journal information: Bioelectrochemistry Provided by Institute of Physical Chemistry of the Polish Academy of Sciences

Exercise as a potential intervention for age-related mobility decline

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A surge of brain chemicals triggered by running may improve coordination and speed in both younger and older individuals, according to new research in middle-aged mice. The study suggests that aerobic exercise can help restore smooth, agile movement—abilities that often decline with age—by boosting dopamine release in the brain. The findings add to growing evidence that physical activity supports mobility not only in youth but also later in life.

Led by researchers at NYU Langone Health, the investigation examined how aerobic exercise influences dopamine, a neurotransmitter central to movement, motivation, reward, and memory. The team built on earlier work showing that young male mice experienced lasting increases in dopamine release after a month of voluntary wheel running. The new study asked whether a similar response occurs in older animals, whose brains are typically assumed to be less adaptable.

To explore this, the researchers studied twelve-month-old male mice, roughly equivalent to humans in their fifties. After 30 days of access to a running wheel, these middle-aged mice showed dopamine increases that matched or even exceeded those seen in younger animals. This finding challenges the idea that ageing brains lose their ability to respond to the neurochemical benefits of exercise, instead suggesting that key movement-related pathways remain responsive well into midlife.

The changes in brain chemistry translated into clear functional improvements. Compared with age-matched mice that did not exercise, the runners were faster and more agile when descending a pole or navigating an open arena—tasks that assess balance, coordination, and motor control. Significantly, grip strength did not change after the exercise period. This indicates that the gains were driven by improved neural coordination rather than increased muscle strength, highlighting a direct link between brain chemistry and movement quality.

Senior author Margaret Rice, PhD, a professor at NYU Grossman School of Medicine, emphasised that the benefits of exercise are not limited to the young. She noted that sufficient physical activity can still stimulate dopamine release later in life, helping people move more easily and efficiently. This perspective reframes exercise as a meaningful intervention for age-related mobility decline, rather than simply a lifestyle choice.

Aerobic exercise—such as running, swimming, cycling, or dancing—has long been known to support brain health and stimulate dopamine release. However, the biological mechanisms underlying these effects in ageing brains have been poorly understood, particularly given that dopamine-producing neurons gradually decline with age. The new findings, published on 9 December in npj Parkinson’s Disease, help clarify this relationship by directly linking exercise-driven dopamine release to improved motor performance in ageing mice of both sexes.

The results may also have implications for Parkinson’s disease, a condition marked by the loss of dopamine-producing neurons and characterised by tremors, slowed movement, and balance problems. Physical activity has long been observed to ease symptoms, but this study provides neurochemical evidence explaining why exercise can improve movement, mood, and memory. While Rice cautions that human studies are still needed, the work strengthens the case for exercise as a powerful, accessible way to support brain health and mobility across the lifespan.

More information: Guendalina Bastioli et al, Voluntary exercise increases striatal dopamine release and improves motor performance in aging mice, npj Parkinson’s Disease. DOI: 10.1038/s41531-025-01213-7

Journal information: npj Parkinson’s Disease Provided by NYU Langone Health / NYU Grossman School of Medicine

Age-related energy deficits in midbrain neurons may underlie Parkinson’s disease

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A new study suggests that dopamine-producing neurons in the midbrain become increasingly vulnerable with age because of an internal energy imbalance that can spiral into degeneration, offering a potential explanation for their loss in Parkinson’s disease. Led by researchers at Weill Cornell Medicine, the work indicates that these neurons face a unique risk of fuel shortages that worsen as their function declines, creating a self-reinforcing cycle of damage.

The findings, published on 5 December in the Proceedings of the National Academy of Sciences, focus on how midbrain dopamine neurons meet their unusually high energy demands. These cells have exceptionally extensive branching, allowing them to influence many target neurons but also requiring substantial energy to sustain signalling. The researchers found that, under normal conditions, dopamine neurons protect themselves by storing glucose as glycogen. This internal reserve enables them to continue functioning for an unexpectedly long time, even when the continuous supply of glucose from the blood is interrupted.

However, the study also reveals a critical weakness in how these neurons manage their fuel. Glycogen storage is not static but tightly regulated by the neurons’ own dopamine signalling. When dopamine output is strong, glycogen synthesis is maintained, preserving energy resilience. As neurons age and dopamine release begins to decline—a process observed even in normal ageing—glycogen stores are reduced. This leaves the cells increasingly exposed to glucose shortages at precisely the stage when they are least able to cope.

“This vulnerability may explain the deaths of these midbrain neurons in Parkinson’s and is consistent with the idea that energy insufficiency is a common failure mode in neurological disorders,” said senior author Timothy Ryan. His comment situates the findings within a broader shift in neuroscience, which views metabolic stress as a central driver of neurodegeneration rather than a secondary effect.

The affected neurons are located in the substantia nigra pars compacta, which plays a key role in voluntary movement, learning, and motivation. Their degeneration is responsible for the hallmark motor symptoms of Parkinson’s disease, such as rigidity and slowed movement. While it has long been known that these neurons decline in Parkinson’s and gradually decrease with age, the reasons for their selective vulnerability have remained unclear. This study provides evidence that energy handling, rather than toxic by-products alone, may be a crucial factor.

In experiments on rat neurons, the team—including first author Camila Pulido—showed for the first time that neurons can directly synthesise glycogen, challenging the long-held view that this fuel reserve is confined mainly to muscle and liver tissue. They also demonstrated that when glycogen stores were exhausted, dopamine neurons became extremely sensitive to glucose deprivation, losing function almost immediately. The researchers propose that ageing, genetic risk factors, and environmental stressors may together push these neurons into a vicious cycle of declining dopamine output, shrinking energy reserves, and eventual cell death.

If this model is correct, it suggests new therapeutic possibilities. Interventions that enhance the ability of midbrain dopamine neurons to store or access energy could potentially slow the onset or progression of Parkinson’s disease. The team now plans to examine glycogen storage in other neuron populations, aiming to understand why some neurons are more resilient to metabolic stress than others and how this resilience might be strengthened.

More information: Camila Pulido et al, Neuromodulatory control of energy reserves in dopaminergic neurons, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2523019122

Journal information: Proceedings of the National Academy of Sciences Provided by Weill Cornell Medicine

Why didn’t the senior cross in time? Longer pedestrian phases could benefit people with reduced mobility

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Road crossings in the UK may be moving too quickly for many people, particularly older adults and those with reduced mobility, according to new academic research that challenges long-standing assumptions in pedestrian infrastructure design. The study suggests that current signal timings often fail to reflect how fast people actually walk, creating barriers that affect not only safety but also independence and everyday participation in community life.

The research, carried out by academics from the University of Bath, the University of Birmingham and the University of Exeter, found that pedestrian crossings typically allow less than 2 seconds for many people with reduced mobility to cross the road comfortably. Most crossings are designed around an assumed walking speed of 1.2 metres per second, a benchmark that does not match the realities of ageing or mobility impairment.

Led by Dr Max Western from the University of Bath, the study showed that only 1.5 per cent of older adults with mobility limitations could cross the road within the time allotted by pedestrian signals while walking at a comfortable pace. For the vast majority, this means hurrying beyond their physical limits or risk being caught in the road when the lights change.

The researchers analysed walking speed data from 1,110 adults aged 65 and over who participated in two major UK research trials. The average walking speed recorded was 0.77 metres per second, well below the level assumed in most crossing designs. At this pace, an individual would need around 6.5 seconds to cross a five-metre-wide road, compared with the just over four seconds typically allowed by pedestrian signals. More than half of the participants would need to increase their comfortable walking speed by at least 50 per cent to cross safely within the current time limits.

Dr Western warned that unrealistic crossing times have consequences that extend beyond the immediate risk of accidents. He noted that when something as routine as crossing the road becomes stressful or unsafe, it can discourage older people from leaving their homes, limiting physical activity and social interaction. Over time, this can contribute to declining health, increased isolation, and a loss of independence.

Professor Afroditi Stathi from the University of Birmingham emphasised the importance of inclusive outdoor design in supporting healthy ageing. She argued that allowing sufficient time to cross the road can boost confidence, help older adults remain active, and enable them to stay connected with their communities, all of which are closely linked to quality of life.

The research team is calling for relatively simple changes, such as extending green signal times and designing crossings around a more realistic walking speed of about 0.7 metres per second. While technologies such as smart crossings and countdown timers are becoming more common, the researchers stress that meaningful improvements depend on inclusive design standards and public health strategies that recognise the needs of an ageing population and people with reduced mobility.

More information: Max Western et al, Why didn’t the senior citizen cross the road? Gait speed in community-dwelling older adults with mobility limitations relative to pedestrian crossing times, Age and Ageing. DOI: 10.1093/ageing/afaf345

Journal information: Age and Ageing Provided by University of Bath

Research highlights limits of lecture-based learning for older adults

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Learning later in life is not only possible but also plays an important role in maintaining a good quality of life. Continued education has been linked to better memory, improved emotional wellbeing, and a stronger sense of purpose. Recent research reinforces this view, showing that older adults learn most effectively under the same conditions that benefit younger learners. Active participation, meaningful discussion, and material that feels relevant to everyday life all support a more profound understanding. In contrast, traditional lecture-based learning often falls short for older adults because it relies heavily on memorisation and frequently feels disconnected from their lived experiences.

This new study builds on earlier research conducted by the same team, which focused on women in the “third age”. Through interviews with nineteen older women, the researchers uncovered findings that challenge common assumptions about ageing and learning. Many participants reported that they felt they were learning better later in life than at any previous stage. They described deeper comprehension and greater satisfaction, mainly because they could connect new ideas to a lifetime of prior knowledge and experience. Rather than being a barrier, age became an advantage when learning environments allowed for reflection, relevance, and integration of past experiences.

As societies around the world grow older, the demand for effective lifelong learning continues to rise. Education increasingly spans the whole life course rather than ending in early adulthood. In a recent paper published in Educational Gerontology, Prof. Anat Zohar of the Hebrew University of Jerusalem and Dr Yochai Z. Shavit of the Stanford Centre on Longevity argue for a rethinking of how education for older adults is designed. Later-life learning should be grounded in the same evidence-based principles that underpin effective education at any age.

Their analysis shows that active learning, connecting new information to what learners already know, engaging in meaningful tasks, and learning with others are just as crucial for older adults as they are for children and young adults. In fact, these principles may be even more important in later life, when motivation is closely tied to relevance, social connection, and personal meaning. However, many programmes for older adults continue to rely on passive lecture formats, despite growing evidence that this approach is poorly suited to their needs.

Prof. Zohar points out that lectures are built on assumptions that do not hold for older learners. They depend heavily on memorisation, even though memory is one of the abilities most likely to change with age. They also fail to draw on older adults’ rich knowledge and life experience, and rarely create the meaningful engagement that sustains motivation in later life. While older adults may enjoy attending lectures, enjoyment does not necessarily lead to lasting learning. High-quality, active education can better support cognitive health, emotional fulfilment, and social connection.

Ultimately, the researchers present a hopeful message about ageing and education. Older adulthood is a meaningful stage of life with unique strengths, and education can help people remain mentally sharp, engaged, and fulfilled. Older adults are not a separate group requiring fundamentally different learning rules. They are part of a continuous story of human learning, and they deserve educational approaches that recognise and support that continuity.

More information: Anat Zohar et al, Bridging geragogy and pedagogy: Towards a learning-sciences-based approach to older adults’ education, Educational Gerontology. DOI: 10.1080/03601277.2025.2569386

Journal information: Educational Gerontology Provided by The Hebrew University of Jerusalem