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Off-Label Antipsychotic Prescriptions Prevalent in Older Adult Population, Study Shows

A large registry-based investigation conducted in Finland by researchers from the University of Oulu and the University of Eastern Finland has found that a substantial number of older adults are prescribed antipsychotic medications for conditions that fall outside their officially approved medical indications. This practice, commonly known as off-label prescribing, occurs when physicians use a medication to treat symptoms or disorders not specified in the drug’s regulatory approval. While off-label prescribing is legal and sometimes clinically justified, the study highlights how frequently it occurs among older adults and raises questions about the circumstances that lead to such prescribing patterns.

The research team examined comprehensive national registry data covering 209,346 community-dwelling older adults in Finland who did not have Alzheimer’s disease. By analysing this large population dataset, the investigators were able to explore patterns of antipsychotic medication use among older people living at home rather than in institutional care settings. Participants were divided into three comparison groups: individuals who received antipsychotics for conditions that were not officially approved indications, patients who were prescribed these medications for approved indications, and individuals who were not using antipsychotic drugs at all.

The analysis revealed a striking pattern. Approximately 70 per cent of all antipsychotic use in the study population occurred in situations classified as off-label. In addition to being common, off-label prescribing also increased during the study period, suggesting a growing reliance on these medications outside their formally approved uses. Among the drugs involved, risperidone and quetiapine were the most frequently prescribed antipsychotics for off-label purposes.

Doctors sometimes prescribe antipsychotic medications to older patients in an attempt to manage persistent behavioural symptoms, agitation, or sleep disturbances. However, these conditions are generally not included among the medications’ approved indications. Earlier research has raised concerns about this pattern of prescribing, particularly when non-pharmacological approaches are not attempted first. Some experts have argued that relying on these medications without exploring alternative strategies may even constitute a form of elder mistreatment. Structural challenges in elderly care—including limited staffing, insufficient resources, and restricted access to non-drug interventions—may contribute to the increasing use of antipsychotics in these circumstances.

The Finnish registry study also identified important differences in the health profiles of patients receiving antipsychotics off-label. Compared with individuals in the other study groups, off-label users were more likely to have cardiovascular diseases and cerebrovascular disorders. They were also more frequently prescribed opioid medications, which may indicate more complex health conditions or symptom management challenges.

According to Tuomas Majuri, a postdoctoral researcher at the University of Oulu involved in the study, this finding was particularly unexpected. Off-label users, he explained, actually showed higher rates of cardiovascular and cerebrovascular conditions than patients who were prescribed antipsychotics for approved indications such as psychotic disorders. Majuri suggested that this pattern may reflect inadequate monitoring of the metabolic and cardiovascular side effects associated with antipsychotic medications when they are used outside their intended indications.

The researchers emphasise that their findings highlight an urgent need to develop better treatment options for symptoms that are currently managed through off-label antipsychotic prescribing. They argue that clearer clinical guidelines are necessary to ensure appropriate monitoring of potential metabolic side effects and to encourage safer prescribing practices. Expanding access to non-pharmacological treatments and strengthening support within elderly care systems may also help reduce reliance on these medications in situations where safer alternatives could be used.

More information: Tuomas Majuri et al, Characteristics and predictors of antipsychotic medication off-label use among community-dwelling older people, Nordic Journal of Psychiatry. DOI: 10.1080/08039488.2026.2631597

Journal information: Nordic Journal of Psychiatry Provided by University of Oulu, Finland

Continuous Cognitive Activity Throughout Life Tied to Reduced Alzheimer’s Risk

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A new study published on February 11, 2026, in Neurology®, the medical journal of the American Academy of Neurology, reports that taking part in a wide range of intellectually stimulating activities throughout life may be associated with a lower risk of Alzheimer’s disease and a slower rate of cognitive decline. Activities such as reading, writing and learning a new language were among those examined in the research. The authors emphasised that the findings demonstrate a relationship rather than proof of cause and effect, meaning the study shows an association between lifelong learning and Alzheimer’s risk rather than confirming that such activities directly prevent the disease.

According to the findings, individuals who reported the highest levels of lifelong learning and cognitive engagement tended to develop Alzheimer’s disease later than those who reported the lowest levels. On average, Alzheimer’s disease appeared about five years later among participants with the most extensive exposure to intellectually stimulating experiences. Mild cognitive impairment, which is often considered an early stage of dementia, also appeared later, with an average delay of roughly seven years among those with the highest levels of lifelong learning.

“Our study examined cognitive enrichment from childhood through later adulthood, focusing on activities and resources that stimulate the mind,” said study author Andrea Zammit, PhD, of Rush University Medical Center in Chicago. Zammit explained that the results suggest cognitive health in older age may be strongly influenced by the extent to which people are exposed to intellectually stimulating environments across their lives.

The study followed 1,939 participants who had an average age of 80 and did not have dementia at the beginning of the research. They were monitored for an average of eight years. During this period, researchers collected information about the participants’ learning experiences and mentally stimulating activities across three different stages of life: childhood, midlife and later adulthood.

Early-life enrichment, referring to experiences before the age of 18, included factors such as how often participants were read to, how frequently they read books themselves, and whether resources like newspapers and atlases were available in the home. It also considered whether individuals studied a foreign language for more than five years. Midlife enrichment involved measures such as income level at age 40, the presence of household resources like magazine subscriptions, dictionaries and library cards, and how frequently participants visited places such as museums or libraries. Later-life enrichment, beginning around the average age of 80, focused on the frequency of activities like reading, writing and playing games, as well as financial resources including Social Security, retirement income and other sources.

Using this information, researchers calculated enrichment scores for each participant. Over the course of the study, 551 participants developed Alzheimer’s disease and 719 developed mild cognitive impairment. When researchers compared the participants with the highest enrichment scores, representing the top 10 per cent, with those in the lowest 10 per cent, clear differences emerged. Among those with the highest enrichment levels, 21 per cent developed Alzheimer’s disease, compared with 34 per cent among those with the lowest enrichment levels.

After adjusting for factors such as age, sex and education, the researchers found that higher lifetime enrichment scores were associated with a 38 per cent lower risk of Alzheimer’s disease and a 36 per cent lower risk of mild cognitive impairment. Participants with the highest levels of enrichment developed Alzheimer’s at an average age of 94, compared with age 88 for those with the lowest levels. Mild cognitive impairment appeared at an average age of 85 among those with the highest enrichment, compared with age 78 among those with the lowest.

Researchers also analysed a smaller group of participants who died during the study and had brain autopsies performed. The results showed that those with higher lifetime enrichment maintained stronger memory and thinking abilities and experienced slower cognitive decline before death, even when early biological signs associated with Alzheimer’s disease, such as the accumulation of amyloid and tau proteins, were present. Zammit said the findings suggest that consistently engaging in a variety of mentally stimulating activities across the lifespan may help support cognitive function. However, the researchers noted a limitation of the study: participants reported details about their early and midlife experiences later in life, meaning some memories may not have been completely accurate.

More information: Andrea Zammit et al, Associations of Lifetime Cognitive Enrichment With Incident Alzheimer Disease Dementia, Cognitive Aging, and Cognitive Resilience, Neurology. DOI: 10.1212/WNL.0000000000214677

Journal information: Neurology Provided by American Academy of Neurology

Scientists Discover Energy Metabolism Changes in Parkinson’s Disease

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Weight loss is a common but still poorly understood feature of Parkinson’s disease. Many people living with the condition gradually lose weight as the illness progresses, often at the same time that movement problems and daily functioning worsen. Until recently, scientists were unsure why this happens. Some believed it might be caused by muscle loss, reduced appetite, or poor nutrition. However, new research suggests a different explanation. The study shows that most of the weight loss in Parkinson’s disease comes from a reduction in body fat rather than muscle. At the same time, the body appears to shift the way it produces energy, indicating bigger metabolic changes.

Although Parkinson’s disease is mainly known as a disorder of the brain, researchers increasingly believe it also affects the body’s metabolism. Many patients experience fatigue and declining nutritional status, but medical advice has usually focused on encouraging people to eat more calories. The new findings challenge this approach. They suggest that weight loss may not simply result from eating less food. Instead, the body’s normal systems for producing energy may not be working efficiently. When these systems struggle, the body may change how it fuels itself, leading to gradual fat loss even if calorie intake does not fall dramatically.

The research was led by Professor Hirohisa Watanabe from Fujita Health University in Japan, along with colleagues Dr Atsuhiro Higashi and Dr Yasuaki Mizutani. Their goal was to understand exactly what happens in the body when people with Parkinson’s disease lose weight. To investigate this, the team studied 91 people with Parkinson’s disease and compared them with 47 healthy volunteers. They analysed body composition using a technique called bioelectrical impedance analysis, which can measure fat mass, muscle mass, and other components separately. At the same time, they examined blood samples using advanced metabolic testing to track how the body processes energy.

The results revealed a clear pattern. Compared with healthy participants, people with Parkinson’s disease tended to have lower body weight and a lower body mass index. A loss of body fat mainly explained this difference. Muscle mass, however, was largely preserved, especially in the earlier stages of the disease. The prevalence of muscle loss was similar to what is normally seen in ageing adults. According to Professor Watanabe, this finding changes how doctors should think about weight loss in Parkinson’s disease. Instead of muscle wasting, the condition appears to involve a selective reduction in fat stores.

Further analysis showed that this fat loss may occur because the body’s normal energy systems are not functioning properly. The researchers found lower levels of certain metabolic compounds that are involved in processes such as glycolysis and the Krebs cycle, which normally help cells convert glucose into energy. When these pathways become less efficient, the body cannot rely on its usual carbohydrate-based energy production. As a result, it begins to activate alternative pathways. The study found higher levels of molecules linked to ketone bodies and amino acid breakdown, suggesting the body turns to fat and protein as emergency energy sources.

This metabolic shift was not the same for everyone. Patients who were thinner and those with more advanced disease tended to show higher levels of ketone-related compounds, indicating a stronger reliance on fat breakdown for energy. According to the researchers, this may mean that weight loss is a visible sign of a deeper energy problem occurring inside the body. The findings also suggest that simply increasing calorie intake may not fully solve the issue if the body cannot efficiently use glucose for energy. Understanding these hidden metabolic changes may help doctors develop better nutritional strategies and new treatments aimed at supporting the body’s energy systems in people with Parkinson’s disease.

More information: Atsuhiro Higashi et al, Metabolic profiles associated with fat loss in Parkinson’s disease, Journal of Neurology Neurosurgery & Psychiatry. DOI: 10.1136/jnnp-2025-336929

Journal information: Journal of Neurology Neurosurgery & Psychiatry Provided by Fujita Health University

University of Michigan Study Connects Chronic Lead Exposure With Increased Dementia Risk

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As rates of dementia continue to climb across the United States, new research from the University of Michigan School of Public Health suggests that long-term exposure to lead may play a significant role in the development of cognitive decline. The study indicates that older adults who have accumulated higher levels of lead in their bodies over the course of their lives face a substantially greater likelihood of developing Alzheimer’s disease and other forms of dementia. While lead exposure has long been recognised as harmful to the brain, the findings highlight how its effects may continue to influence neurological health decades after initial exposure.

According to the researchers, the scale of the potential impact is considerable. Kelly Bakulski, an associate professor of epidemiology at the University of Michigan School of Public Health and one of the study’s senior authors, explained that the analysis provides the first empirical evidence suggesting that roughly 18 per cent of new dementia cases in the United States each year may be connected to cumulative lead exposure. With around half a million Americans diagnosed with dementia annually, this estimate suggests that close to 90,000 cases could potentially be linked to the long-term effects of lead stored in the body.

The study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, found striking differences in risk between individuals with varying levels of lifetime exposure. Participants whose bone lead concentrations ranked in the highest quarter faced nearly three times the risk of developing Alzheimer’s disease compared with those in the lowest quarter. They were also more than twice as likely to develop dementia from any cause. These results point to cumulative lead exposure as a major environmental factor that may contribute to neurodegenerative disease, yet one that has historically received less attention in dementia research.

To explore this relationship, the research team analysed data from participants in the National Health and Nutrition Examination Survey (NHANES), linking these records with Medicare claims and mortality data spanning up to three decades of follow-up. The investigators used machine learning techniques to estimate the amount of lead stored in bone tissue, which acts as a biological archive of lifetime exposure. Unlike measurements that capture only recent contact with lead, bone lead levels reflect the accumulation of the metal over many years.

One of the most important findings of the study was that bone lead levels showed a strong association with dementia risk, while current blood lead levels did not. Sung Kyun Park, a professor of epidemiology and environmental health sciences and a senior author of the research, noted that this distinction is crucial for understanding the long-term consequences of exposure. Lead circulating in the blood typically reflects exposure from the past few weeks, whereas lead embedded in bones can remain for decades. As a result, bone lead provides a much clearer picture of the lifetime burden that may contribute to chronic diseases such as dementia.

Many of the adults included in the study were born before 1980, when environmental lead exposure was significantly higher due to the widespread use of leaded petrol and lead-based paint. Researchers explain that once lead enters the body, it can become stored in bone tissue and remain there for many years. As people age, some of this stored lead may gradually be released back into the bloodstream and potentially reach organs such as the brain. The researchers emphasise that reducing remaining sources of lead exposure—including ageing paint, old plumbing systems, contaminated soil, and industrial pollution—remains essential for protecting both current and future generations from accumulating levels that may increase the risk of dementia later in life.

More information: Xin Wang et al, Exposure to lead and incidence of Alzheimer’s disease and all-cause dementia in the United States, Alzheimer’s & Dementia. DOI: 10.1002/alz.71075

Journal information: Alzheimer’s & Dementia Provided by University of Michigan School of Public Health

New Evidence Links Binge Drinking in Later Life to Elevated Death Risk

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Binge drinking among older adults is linked to a markedly higher risk of death, according to new research published in Alcohol. While heavy episodic drinking is often portrayed as a problem largely confined to younger people, the study suggests that the behaviour remains both common and potentially dangerous well into later life. By examining long-term health outcomes among older Canadians, the researchers found that frequent binge drinking was associated with significantly greater mortality risk compared with those who avoided the behaviour altogether. The findings highlight a growing public health concern as populations age and alcohol use patterns among older adults receive increasing scrutiny from researchers and healthcare professionals.

The research team analysed information from a large national dataset covering more than 129,000 Canadian adults aged 50 and above. The data were drawn from the Canadian Community Health Survey conducted between 2005 and 2014 and were linked with records from the Canadian Vital Statistics Death Database. Participants were followed for as long as 12 years, allowing the researchers to examine how drinking habits related to mortality over time. Their analysis revealed a clear graded relationship between how often people engaged in binge drinking and their likelihood of dying during the study period, even when accounting for a wide range of personal and socioeconomic characteristics.

The prevalence of binge drinking among older adults was notable. Among participants who reported drinking alcohol at least once a month, around 40 per cent said they had engaged in binge drinking at least once during the previous year. A smaller but still significant group, roughly 8 per cent, reported binge drinking every week or more frequently. In the study, binge drinking referred to consuming a large quantity of alcohol on a single occasion, a pattern that can place considerable stress on the body. These findings suggest that heavy episodic drinking remains a widespread behaviour among older drinkers, despite the perception that such habits tend to decline with age.

When researchers adjusted their statistical models to account for demographic factors such as age, sex, education and income, striking differences in mortality risk emerged. Individuals who reported never engaging in binge drinking experienced a 34 per cent lower risk of death compared with those who reported binge drinking weekly or more. Even after incorporating additional variables such as self-reported health, the presence of chronic illness, smoking habits, levels of physical activity and mental health conditions, the association persisted. Under these more stringent adjustments, participants who never binge drank still had a 19 per cent lower risk of mortality than frequent binge drinkers.

The researchers also emphasised that alcohol studies can sometimes produce misleading patterns if underlying health differences between groups are not carefully considered. In initial analyses, non-binge drinkers appeared to have higher mortality rates than some drinkers. This counterintuitive pattern is commonly attributed to what researchers call the “sick quitter” effect. Individuals who experience health problems may reduce or stop drinking entirely, meaning that groups of non-drinkers or moderate drinkers can contain people with pre-existing health issues. Once the research team adjusted for these health and socioeconomic factors, the elevated mortality risk associated with frequent binge drinking became much clearer.

Overall, the findings reinforce the need to broaden public health discussions about alcohol beyond youth-focused messaging. Campaigns addressing alcohol-related harm often emphasise risks such as accidents, injuries or impaired driving among younger people. However, the study suggests that heavy episodic drinking later in life may carry substantial long-term health consequences as well. As Canada’s population continues to age, researchers argue that prevention strategies, clinical screening and health education should increasingly address alcohol use among older adults. Further studies that track drinking patterns over time may provide even deeper insight. Still, the current evidence already indicates that frequent binge drinking poses a meaningful threat to longevity in later life.

More information: Andie MacNeil et al, Binge drinking and mortality among older adults: Findings from the Canadian Community Health Survey linked to the Canadian Vital Statistics Death Database, Alcohol. DOI: 10.1016/j.alcohol.2026.02.002

Journal information: Alcohol Provided by University of Toronto

Protecting Brain Health: The Impact of Virgin Olive Oil on the Gut Microbiota

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Virgin olive oil is widely regarded as a central component of the Mediterranean diet and is well known for supporting cardiovascular and metabolic health. It contains a range of beneficial compounds, including antioxidants and polyphenols, which have been linked to reduced inflammation and improved heart function. Despite these recognised benefits, researchers have only recently begun to investigate how olive oil might influence the brain through the digestive system. A new study conducted by researchers from the Human Nutrition Unit at the Universitat Rovira i Virgili, the Pere Virgili Health Research Institute, and CIBERobn suggests that extra virgin olive oil may help protect cognitive function by influencing the gut microbiota.

The research team carried out what they describe as the first long-term human study specifically examining the relationship between olive oil consumption, gut microbiota, and cognitive function. The study analysed data from 656 participants between the ages of 55 and 75 who were overweight or obese and had metabolic syndrome, a group of conditions that increases the risk of cardiovascular disease. These individuals were part of the PREDIMED-Plus project, a large study focused on diet and health. Over two years, researchers monitored the participants’ diets, particularly their intake of different types of olive oil, while also examining the composition of their gut microbiota and assessing changes in their cognitive performance.

The findings showed clear differences between those who regularly consumed virgin olive oil and those who mainly used refined olive oil. Participants who consumed virgin olive oil demonstrated better cognitive performance over time. They also showed greater diversity in their gut microbiota, which is often considered an indicator of good intestinal and metabolic health. A diverse microbial community in the gut is associated with improved digestion, stronger immune function, and better regulation of inflammation. In contrast, participants who primarily consumed refined olive oil tended to show less diversity in their gut microbiota as the study progressed.

Researchers also identified a particular bacterial genus called Adlercreutzia that appeared to play a role in the relationship between olive oil consumption and cognitive health. Higher levels of this bacterium were linked to both increased intake of virgin olive oil and better preservation of cognitive function. This suggests that certain gut bacteria may help explain how dietary fats influence brain health. The study, therefore, highlights the possibility that the benefits of virgin olive oil extend beyond its direct nutritional properties and may involve complex interactions between diet, gut microorganisms, and brain function.

One important factor that distinguishes extra virgin olive oil from refined olive oil is the way it is produced. Extra virgin olive oil is obtained solely through mechanical pressing of olives, without chemical processing or high heat. This method helps preserve naturally occurring compounds such as antioxidants, polyphenols, and vitamins. Refined olive oil, however, undergoes industrial treatments designed to remove impurities and improve stability. While this process creates a more neutral product, it also removes many of the bioactive substances believed to contribute to olive oil’s health benefits. As a result, not all olive oils provide the same nutritional value.

The researchers emphasise that these findings highlight the importance of both the type and quality of dietary fats. While olive oil is already recognised for its role in heart health, the study suggests it contributes to maintaining cognitive function during ageing. As populations grow older and cases of cognitive decline and dementia become more common, improving diet quality may be a practical strategy for supporting long-term brain health. Choosing extra virgin olive oil instead of refined varieties represents a simple dietary change that may help promote healthier gut microbiota and protect cognitive function over time.

More information: Jiaqi Ni et al, Total and different types of olive oil consumption, gut microbiota, and cognitive function changes in older adults, Microbiome. DOI: 10.1186/s40168-025-02306-4

Journal information: Microbiome Provided by Universitat Rovira i Virgili

Researchers uncover a promising new drug target for Alzheimer’s disease

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Scientists at Indiana University School of Medicine have uncovered a promising new therapeutic target for Alzheimer’s disease, offering a potential fresh direction for treatment development. Their research shows that removing a specific enzyme from neurons in the brain can dramatically reduce amyloid plaques, one of the defining pathological features of the disease. Beyond lowering plaque levels, this approach may also strengthen the brain’s resilience to ongoing neurodegeneration, raising hope for more durable clinical benefits.

In recent years, progress in Alzheimer’s treatment has begun to accelerate. The U.S. Food and Drug Administration has approved two disease-modifying therapies, lecanemab and donanemab, which work by clearing amyloid plaques from the brain. These drugs have shown that it is possible to slow disease progression and stabilise patients at their current level of function. However, their effects are limited, and there remains an urgent need for alternative strategies that target the disease through different biological mechanisms.

The Indiana University team, led by Hande Karahan and Jungsu Kim, focused on an enzyme known as IDOL. Their findings suggest that suppressing IDOL specifically in neurons offers a new way to reduce amyloid accumulation while also improving communication between brain cells and regulating lipid metabolism. According to the researchers, this dual effect could be particularly valuable, as Alzheimer’s disrupts not only protein clearance but also fundamental cellular signalling and metabolic balance in the brain.

Kim emphasised that the appeal of IDOL lies in its suitability as a drug target. Enzymes have clearly defined active sites, which makes it possible to design highly specific molecules that block their activity. This precision increases the likelihood of developing treatments that are both effective and associated with fewer side effects. The identification of IDOL, therefore, opens the door to an entirely new class of therapeutic compounds aimed at Alzheimer’s disease.

To explore how IDOL functions in different brain cell types, the researchers created two animal models of Alzheimer’s disease. In one, the IDOL gene was deleted from neurons, while in the other, it was removed from microglia, the brain’s immune cells. The team initially expected microglia to play the dominant role in clearing amyloid, as immune cells are known to be heavily involved in plaque removal and are the primary producers of IDOL in the brain.

Unexpectedly, the most striking effects were seen when IDOL was removed from neurons. This intervention not only reduced amyloid plaques but also lowered levels of apolipoprotein E, a protein strongly linked to Alzheimer’s risk and disease progression. In addition, receptors involved in lipid metabolism and healthy neuronal communication increased in abundance, suggesting broader protective effects. Previous research has shown that activating related pathways can help preserve cognitive function even in patients with high plaque burdens.

From a clinical perspective, these findings are especially significant. Most patients are diagnosed only after substantial amyloid accumulation has already occurred. An approach that both lowers amyloid levels and enhances the brain’s resilience to existing pathology could therefore maximise therapeutic impact. Looking ahead, Kim and his colleagues plan to develop and test compounds that inhibit IDOL, carefully assessing their safety and effects in preclinical models. They will also investigate whether targeting this enzyme can preserve synaptic connections and reduce tau pathology, two critical factors in the progression of Alzheimer’s disease.

More information: Hande Karahan et al, Deletion of neuronal Idol ameliorates Alzheimer’s disease–related pathologies via APOE receptors, Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. DOI: 10.1002/alz.70949

Journal information: Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association Provided by Indiana University

Fall-prevention efforts in emergency departments could benefit older adults once they return home

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Falls are among the most frequent reasons older adults seek care in emergency departments, and many of these patients are sent home on the very same day. The point of discharge can be particularly risky, as the underlying causes of a fall are not always fully explored or managed during a brief hospital visit. Emerging evidence now indicates that emergency departments can use this critical window to introduce practical measures that help older adults remain safer once they return home.

These insights come from the GAPcare II trial, titled Emergency Department Visit Outcomes of a Multicentre Randomised Trial of a Fall Prevention Intervention, published in Academic Emergency Medicine. The study examined whether a structured fall-prevention programme could realistically be delivered during emergency department visits for adults aged 65 and over who had experienced an accidental fall within the previous seven days. All participants were expected to be discharged and did not have injuries that severely limited mobility. In total, 852 patients took part in the intervention, which combined assessments by physical therapists with medication reviews conducted by pharmacists.

The research demonstrated that these assessments could be completed during the emergency visit and resulted in tailored recommendations for individual patients. Interventions included advice on mobility support, changes to medication regimens, and referrals for further care after discharge. Participants received consultations at the bedside from both pharmacists and physical therapists, allowing recommendations to be integrated directly into the emergency care process rather than deferred to a later setting.

Pharmacists frequently suggested practical medication-related changes that could reduce fall risk. These included adjusting the timing of medications for 26 per cent of patients, discontinuing medications associated with increased fall risk in 19 per cent of cases, and modifying dosages for a further 18 per cent. Physical therapists focused on functional support and follow-up needs, recommending assistive devices for two-thirds of patients, outpatient therapy services for over a third, and admission to a skilled nursing facility for a quarter of those assessed.

Commenting on the findings, Sarah D. Berry, MD, MPH, emphasised that a fall is rarely an isolated event. Instead, it often signals unresolved health issues or environmental hazards that require attention. She noted that the study illustrates how emergency departments can move beyond simply addressing the immediate injury, helping to identify modifiable risk factors and equipping patients and caregivers with a clearer plan to reduce the likelihood of future falls once they return home.

Although the trial was primarily designed to assess how feasible the programme was to implement, rather than to measure long-term outcomes such as repeat falls or hospitalisations, the results underscore the potential of emergency departments as an important point of intervention. By integrating fall-prevention strategies into routine emergency care, hospitals can play a meaningful role in supporting safer recovery and independence for older adults after discharge.

More information: Elizabeth M. Goldberg et al, Emergency Department Visit Outcomes of a Multicenter Randomized Trial of a Fall Prevention Intervention, Academic Emergency Medicine. DOI: 10.1111/acem.70228

Journal information: Academic Emergency Medicine Provided by Hebrew SeniorLife Hinda and Arthur Marcus Institute for Aging Research

Advancing Bone Healing in Older Adults Through Non-Invasive Therapy

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Bone repair is a complex but carefully organised biological process that depends on stem and progenitor cells to rebuild damaged tissue. In younger people, these cells respond quickly after a fracture, maturing into osteoblasts, the specialised cells responsible for forming new bone. This rapid response allows broken bones to knit together efficiently and regain strength. With increasing age, however, this process becomes much slower and less reliable. Doctors have long recognised that fractures in older adults take longer to heal and are more likely to lead to complications, yet the underlying biological reasons have remained poorly understood.

This slowdown in healing is becoming an increasingly serious problem as populations age worldwide. Fractures among older adults often result in extended hospital stays, reduced mobility, and lasting loss of independence. Until recently, most treatments have focused on stabilising bones surgically rather than improving the body’s own ability to regenerate tissue. As a result, scientists have been searching for the molecular signals that actively interfere with bone repair during ageing, in the hope that targeting these signals could restore the body’s natural healing capacity.

Recent research has identified a key player in this age-related decline: apolipoprotein E, or ApoE. ApoE is a protein best known for its role in lipid transport and is produced mainly by the liver. The study found that levels of ApoE in the bloodstream rise with age and that this increase has a direct negative effect on bone healing. Rather than helping repair, ApoE acts as a systemic inhibitor, interfering with the signals that normally drive stem and progenitor cells to become bone-forming osteoblasts.

To understand how this happens, researchers compared fracture healing in young and aged animal models using a combination of molecular, cellular, and tissue-level analyses. They observed that higher ApoE levels in older subjects suppressed a key signalling pathway known as β-catenin signalling within bone marrow stromal cells. This pathway is essential for pushing immature cells towards an osteoblast fate. When β-catenin signalling is blocked, these progenitor cells stall before fully maturing, leaving the repair process incomplete and fragile.

The study also revealed how ApoE exerts this effect. ApoE binds to a receptor on bone marrow stromal cells called Lrp4, which disrupts downstream β-catenin activity and effectively places a molecular “brake” on bone formation. When researchers used antibodies to block ApoE, this brake was released. β-catenin signalling resumed, osteoblast formation increased, and fracture healing improved significantly. Notably, aged animals treated in this way formed stronger, more complete bone calluses, closely resembling the quality of healing normally seen in much younger individuals.

Perhaps most striking was how reversible the process appeared to be. Even in advanced age, bone-forming cells retained their ability to regenerate once the inhibitory influence of ApoE was removed. This suggests that ageing does not permanently damage the bone’s regenerative machinery but instead suppresses it through circulating signals. The findings also highlight the unexpected role of the liver in controlling skeletal repair, showing that organs far from the injury site can strongly influence healing outcomes.

Together, these results reshape how ageing-related bone repair is understood. By identifying a circulating protein that actively suppresses regeneration, the research opens the door to new, non-invasive therapies aimed at neutralising systemic inhibitors rather than directly manipulating bone tissue. Such approaches could significantly improve fracture healing in older adults, reduce complications, and help preserve mobility and quality of life in an ageing society.

More information: Mingjian Huang et al, Neutralizing hepatic apolipoprotein E enhances aged bone fracture healing, Bone Research. DOI: 10.1038/s41413-025-00489-y

Journal information: Bone Research Provided by Editorial Office of West China School of Stomatology, Sichuan University

South Asian adults in the U.S. show heart disease risk factors at younger ages

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South Asian adults living in the United States were more likely to have risk factors for atherosclerotic cardiovascular disease (ASCVD) by the age of 45 compared with white, Black, Chinese and Hispanic adults of the same age, according to new research published in the Journal of the American Heart Association. ASCVD risk factors, when left untreated or poorly managed, can contribute to the earlier development of heart disease, underscoring the importance of timely detection and prevention.

To explore the reasons behind this increased risk, researchers examined health data from approximately 2,700 adults aged 45 to 55 who participated in two large, national studies conducted in the United States. These long-term studies followed diverse populations from different regions of the country: the Mediators of Atherosclerosis in South Asians Living in America (MASALA) Study and the Multi-Ethnic Study of Atherosclerosis (MESA). By comparing data across these cohorts, investigators were able to assess how cardiovascular risk factors emerged and progressed across ethnic groups.

The MASALA Study, led by research teams at Northwestern University in Chicago and the University of California, San Francisco, focused specifically on South Asian adults with ancestral roots in Bangladesh, India, Nepal, Pakistan or Sri Lanka. Initial health assessments were conducted between 2010 and 2013, with follow-up examinations taking place from 2016 to 2018. These data were compared with publicly available information from MESA, which enrolled white, Black, Hispanic and Chinese adults beginning in 2000–2002 and continued follow-up visits approximately every two years through 2016–2018.

Researchers evaluated a range of medical conditions known to increase the risk of heart disease, including high blood pressure, prediabetes and type 2 diabetes, as well as abnormal cholesterol and triglyceride levels. Lifestyle factors were also analysed, such as dietary quality, physical activity, tobacco use, alcohol consumption and differences between men and women. Several of these measures align with components of the American Heart Association’s Life’s Essential 8, with diet, exercise and alcohol intake assessed through self-reported information gathered during clinic visits. Alcohol use was defined as consuming at least one alcoholic drink per week.

The findings showed that elevated rates of prediabetes, diabetes and high blood pressure largely drove higher cardiovascular risk among South Asian adults. At age 45, South Asian men had a markedly higher prevalence of prediabetes than men from other ethnic groups, as well as higher rates of high blood pressure and dyslipidaemia. South Asian women also showed nearly double the prevalence of prediabetes compared with women in other population groups. By age 55, both South Asian men and women were at least twice as likely to develop type 2 diabetes as white adults of the same age.

Despite these elevated medical risk factors, South Asian adults demonstrated several favourable lifestyle patterns. They reported the highest diet quality overall, lower levels of alcohol consumption and physical activity levels comparable to those of other groups. These findings suggest that traditional risk factors alone do not fully explain the earlier onset of cardiovascular risk in this population.

The study highlights the need for earlier and more tailored screening and prevention strategies for South Asian adults in the U.S. Identifying cardiovascular risk factors at younger ages may allow for earlier intervention, improved management and a reduced likelihood of developing heart disease later in life. However, the researchers also noted limitations, including reliance on self-reported behaviours and the possibility that results may not be fully generalisable beyond the study populations, which tended to include participants with higher educational and socioeconomic status.

More information: Havisha Pedamallu et al, Prevalence and Trends in Cardiovascular Risk Factors Among Middle‐Aged South Asian Adults Compared With Other Racial and Ethnic Groups in the United States: A Longitudinal Analysis of 2 Cohort Studies, Journal of the American Heart Association. DOI: 10.1161/JAHA.124.041221

Journal information: Journal of the American Heart Association Provided by American Heart Association

The Hidden Cost of Age Anxiety: Faster Ageing in Women

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Anxiety about getting older, especially fears centred on declining health, may extend beyond the mind and register at a biological level, potentially speeding up the ageing process in women. New research suggests that these worries can be reflected in measurable cellular changes associated with accelerated ageing. Rather than being a purely emotional or psychological response, concern about ageing may have tangible effects on the body, reinforcing the idea that how people experience ageing internally can influence how they age physically.

The researchers behind the study argue that subjective perceptions and fears can translate into objective biological outcomes. One of the study’s authors explains that anxiety related to ageing should not be dismissed as an abstract mental state, as it may leave lasting physiological traces with meaningful consequences for long-term health. This perspective challenges the traditional separation between mental and physical health by highlighting how emotional experiences may actively shape biological processes linked to ageing.

Stress about ageing is common, with many people worrying about physical decline, chronic illness, and the potential loss of independence. Previous research has already demonstrated that psychological distress can influence biological ageing through epigenetic mechanisms, which affect how genes are expressed without altering the underlying DNA sequence. Anxiety and depression have long been associated with poorer physical health outcomes. Yet, little attention has been paid to whether worrying about ageing itself influences the speed at which ageing occurs.

Women, in particular, may be especially vulnerable to anxiety about ageing due to social and cultural pressures that place a high value on youth and physical appearance, alongside concerns about fertility. Midlife can be a period of intensified stress, as many women balance multiple roles, including work, family responsibilities, and caregiving for older relatives. Witnessing the illness or decline of parents and other family members may prompt fears about facing similar challenges in the future, reinforcing health-related anxieties about growing older.

To explore these links more closely, the researchers examined data from over seven hundred women participating in a large, long-running study of midlife health. Participants reported how frequently they worried about becoming less attractive, experiencing worsening health, or being too old to have children. Blood samples were also collected and analysed using two established epigenetic clocks: one designed to measure the pace of biological ageing and another that estimates cumulative biological damage over time. The results showed that higher overall anxiety about ageing was associated with a faster pace of biological ageing according to one of these measures.

Notably, worries about declining health showed the strongest connection to accelerated ageing at the cellular level, while concerns about appearance and fertility were not significantly linked. The researchers suggest this is because health-related anxieties persist and intensify over time, whereas fears about beauty or reproduction may diminish as priorities shift with age. Although the study cannot prove cause and effect, it underscores the close relationship between mental and physical health and points to ageing anxiety as a potentially modifiable factor. Further research may help clarify how reducing this type of anxiety could support healthier ageing and encourage a broader societal conversation about how ageing is understood, experienced, and supported.

More information: Mariana Rodrigues et al, Aging anxiety and epigenetic aging in a national sample of adult women in the United States, Psychoneuroendocrinology. DOI: 10.1016/j.psyneuen.2025.107704

Journal information: Psychoneuroendocrinology Provided by New York University

Cognitive Processing Speed Exercises Show Lasting Protection Against Dementia

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Older adults aged 65 and above who took part in a short course of cognitive speed training were significantly less likely to develop dementia many years later. The training focused on improving speed of processing, helping participants rapidly locate visual information on a computer screen and cope with progressively more complex tasks under time pressure. Those who completed five to six weeks of training and later attended follow-up or “booster” sessions one to three years afterwards showed a reduced likelihood of being diagnosed with dementia, including Alzheimer’s disease, even up to 20 years later. These outcomes were reported in newly published findings in a leading dementia research journal.

The National Institutes of Health funded the study and represents the first randomised clinical trial to examine dementia outcomes over 20 years. It was conducted as part of a large project designed to explore the long-term effects of different types of cognitive training in older adults. Between 1998 and 1999, researchers enrolled 2,802 participants and randomly assigned them to one of three training programmes—memory, reasoning, or speed of processing—or to a control group that received no training. Participants in the training groups completed up to ten sessions lasting just over an hour, delivered across five to six weeks.

To further test long-term impact, half of those in the training groups were randomly selected to receive additional booster sessions at approximately one and three years after the initial programme. These sessions reinforced the original training and allowed researchers to assess whether ongoing engagement made a difference. Over two decades later, the results showed a clear advantage for those who had received speed-of-processing training with boosters. In this group, 40% were diagnosed with dementia, compared with 49% in the control group, representing a meaningful 25% reduction in incidence.

Researchers based their analysis on Medicare records from 2,021 participants, covering the period from 1999 to 2019. The follow-up group closely resembled the original study population: around three-quarters were women, most were white, and the average age at enrolment was 74. During the long follow-up period, roughly three-quarters of participants died, with an average age at death of 84. Despite these changes over time, the findings remained robust and consistent.

Dementia involves a decline in thinking abilities severe enough to interfere with independent daily living, and it affects a large proportion of older adults. Alzheimer’s disease accounts for the majority of cases, while vascular and other forms make up the remainder. Researchers noted that even modest delays in dementia onset could have substantial public health benefits, reducing both personal suffering and the enormous economic costs associated with long-term care.

The authors suggest that speed training may be particularly effective because it is adaptive, adjusting task difficulty to each person’s performance in real time, and because it relies on implicit learning rather than conscious memorisation strategies. Previous work from the same research programme showed benefits for everyday functioning up to ten years later, with each booster session providing added protection. While further studies are needed to understand the biological mechanisms involved, the findings support the idea that targeted, non-drug cognitive training could play a meaningful role in healthy ageing and dementia prevention.

More information: Norma B. Coe et al, Impact of cognitive training on claims-based diagnosed dementia over 20 years: evidence from the ACTIVE study, Alzheimer’s & Dementia: Translational Research and Clinical Interventions. DOI: 10.1002/trc2.70197

Journal information: Alzheimer’s & Dementia: Translational Research and Clinical Interventions Provided by Johns Hopkins Medicine