Monthly Archives: November 2025

Protecting Brain Health: Why Tackling Midlife Obesity Matters

Obesity remains one of the most pressing global health concerns, and weight loss is routinely encouraged as a way to reduce the risks linked to excess body fat. Yet emerging research indicates that losing weight during midlife may not have the same effects as losing weight earlier in adulthood. While metabolic improvements are still achievable, the body — and particularly the brain — may respond in more complex ways than expected. This growing body of evidence suggests that the timing of weight reduction could influence both physical and neurological outcomes.

A new study from Ben-Gurion University of the Negev (BGU) sheds light on these age-related differences by comparing how young adult and middle-aged mice reacted to diet-induced obesity followed by weight loss. In both groups, restoring healthy blood glucose levels during weight reduction was a promising sign, reinforcing the idea that weight loss remains beneficial for improving metabolic health at any age. However, the researchers uncovered a significant divergence in how the two age groups responded at the brain level. While the younger mice appeared unaffected, the middle-aged mice developed an unexpected surge of hypothalamic inflammation. This brain region regulates appetite, energy expenditure, and several essential physiological functions.

This neuroinflammatory response was identified through molecular analyses and advanced microscopic imaging of microglia, the brain’s immune cells. Notably, the inflammation persisted for several weeks before gradually subsiding. Although this effect was temporary, its appearance raises essential questions. Prolonged or dysregulated inflammation in the brain has long been associated with cognitive decline and neurodegenerative diseases, making any disturbance within this region a potential cause for concern. The study, therefore, highlights a previously underappreciated aspect of midlife weight loss. Despite improvements in metabolic markers, the brain may experience short-term stress that younger individuals do not.

Alon Zemer, the study’s first author and an M.D.-Ph.D. candidate, noted that weight loss in midlife is not simply a replication of what works in younger adults. While the metabolic gains are clear, the neurological response appears more complicated, underscoring the need to understand the whole picture before assuming uniform benefits across age groups. He emphasised the importance of considering brain health alongside more familiar measures, such as blood sugar regulation, when evaluating weight-loss interventions for older adults.

Dr Alexandra Tsitrina highlighted the study’s two-pronged approach, combining molecular data with high-resolution imaging to capture subtle structural changes. This comprehensive approach enabled the team to identify early shifts in the brain’s inflammatory landscape that might otherwise go unnoticed. Such techniques are vital for understanding how weight loss interacts with ageing biological systems and for detecting potential risks before they manifest in more severe ways.

Although the findings raise caution, they also point to opportunities for future research. The scientists stress the need to explore further why the midlife brain responds differently, how long these effects last, and whether they represent an adaptive mechanism rather than a harmful one. A deeper understanding could lead to weight-loss strategies that preserve their metabolic advantages while minimising unintended effects on the brain. In the long term, this line of inquiry may help refine recommendations for healthy ageing, ensuring that efforts to lose weight in midlife support both physical and cognitive wellbeing.

More information: Alon Zemer et al, Weight loss aggravates obesity-induced hypothalamic inflammation in mid-aged mice, GeroScience. DOI: 10.1007/s11357-025-01933-x

Journal information: GeroScience Provided by Ben-Gurion University of the Negev

Older adults who dine alone may face lower nutritional intake

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New research from Flinders University has shown that older adults who routinely eat their meals alone tend to have poorer nutrition and less favourable health outcomes than those who share food with others. The study, a systematic review published in Appetite, drew together evidence from 20 international investigations examining how solitary eating affects measurable health indicators among people aged 65 and over living independently in the community. Across these studies, the researchers consistently observed links between eating alone and reduced diet quality, including lower consumption of essential food groups such as fruit, vegetables and meat, as well as a heightened risk of unintended weight loss and frailty.

The lead author, Caitlin Wyman—an Accredited Practising Dietitian and PhD candidate at the Caring Futures Institute—emphasises that the findings underline the social significance of shared meals for older adults. She notes that food offers far more than nutrition alone, describing mealtimes as critical social occasions that influence appetite, dietary variety and overall wellbeing. Although earlier research had already connected loneliness and social isolation with diminished food intake, this review is the first to clearly examine the broader nutritional and physical consequences of eating alone compared with eating in company.

Drawing on data from more than 80,000 older adults across 12 countries, the team found wide-ranging implications of mealtime social settings. While a handful of studies reported little difference in outcomes, the majority demonstrated that solitary eaters tended to make poorer food choices and consume less protein, a macronutrient crucial for maintaining muscle mass and functional ability in later life. In some cases, eating alone was also linked with a greater likelihood of weight loss and an increased risk of frailty, both of which can severely impact independence and long-term health.

According to the authors, these patterns suggest that mealtime behaviour may be a modifiable risk factor for poor nutrition in older age, particularly within Australia’s rapidly ageing population. Wyman explains that although age-related changes, such as reduced hunger cues and altered taste perceptions, are well known, the social aspects of eating are equally influential. She argues that shared meals support not only nourishment but also connection and enjoyment, and that encouraging opportunities for communal dining—whether with relatives, friends or through community initiatives—could meaningfully improve food intake and quality of life for older adults living at home.

Co-author Dr Alison Yaxley, also an Accredited Practising Dietitian at Flinders University, adds that the findings highlight the value of integrating simple social and nutritional screening into routine primary and aged care. Asking straightforward questions about mealtime habits could help clinicians identify individuals at greater nutritional risk, allowing them to be referred to community meal programmes or social dining opportunities that could substantially improve their well-being.

The researchers note that community-based initiatives such as neighbourhood dining groups, intergenerational meal schemes and partnerships with local cafés might help reduce the prevalence of solitary eating among older Australians. Wyman points out that recent aged-care reforms provide a timely opening to embed food and nutrition more centrally within home-based care services, helping to optimise both nutritional status and overall health in an expanding older population. Nevertheless, she stresses that further research is needed to determine which strategies are most effective at encouraging regular shared meals and how they can be best implemented in real-world community settings.

More information: Caitlin Wyman et al, Associations between nutritional and physical outcomes of community-dwelling older adults eating alone, versus with others: A systematic review, Appetite. DOI: 10.1016/j.appet.2025.108327

Journal information: Appetite Provided by Flinders University

Global disease-spanning atlas decodes molecular fingerprints of human health and ageing

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A significant international research effort has revealed that dozens of common diseases leave distinct molecular traces in the proteins circulating through human blood, offering a path towards far more precise diagnostic testing. By analysing how thousands of proteins change with age and illness, the team has created a reference tool that may help clinicians distinguish between harmless biological fluctuations and genuine markers of disease. Rather than focusing on a single condition at a time, the study compares fifty-nine diseases side by side, enabling researchers to separate signals that are shared broadly—such as inflammation—from those that point to specific pathologies.

Published today in Science, the work maps how blood proteins behave across a wide range of severe conditions, including cancer, cardiovascular disorders and autoimmune diseases. The researchers have compiled these data into the Human Disease Blood Atlas, which documents the changing landscape of blood proteins not only during illness but also throughout the normal course of human life. The atlas shows that every person has a distinctive blood protein profile, a kind of molecular fingerprint that shifts through childhood before stabilising in adulthood. In clinical settings, such stable individual baselines might someday be used to flag early changes that precede symptoms, transforming diagnostics from reactive to preventive.

The project’s senior author, Mathias Uhlén, and lead author, María Bueno Álvez, explain that the study employed machine-learning approaches designed to identify molecular signatures that remain reliable outside controlled laboratory testing. By training algorithms on multiple diseases simultaneously, the team demonstrated that many proteins rise and fall across unrelated conditions, particularly those tied to inflammation. These overlapping responses frequently mislead researchers in traditional biomarker studies, which typically compare a disease to a healthy control group without considering how proteins behave across different illnesses.

Uhlén, a professor at KTH Royal Institute of Technology and director of the Human Protein Atlas project, argues that this broader comparative approach is essential. “When diseases are analysed side by side, we can separate universal inflammatory alarm bells from signals that are truly specific to individual disorders,” he says. He emphasises that distinguishing these patterns is critical to developing blood tests that do not misclassify patients or yield misleading results in real clinical settings. Some disease signatures cluster by organ system, such as those related to the liver, whereas others reveal shared pathways that span conditions like cancer, autoimmune illness, and infection.

The study also highlights a significant challenge in modern biomedical research: reproducibility. According to Bueno Álvez, around seventy biomarker papers are published each day, yet many are not reproducible because they test only one condition against controls. Proteins that change in several diseases are frequently misrepresented as unique markers. By exposing these shared features and identifying reliable, disease-specific patterns, the Human Disease Blood Atlas offers a corrective framework and demonstrates how future biomarker discovery can avoid this pitfall.

Among the atlas’s most intriguing findings are early protein changes detected in individuals approaching cancer diagnosis, suggesting that some molecular shifts precede clinical signs by a significant span. This glimpse into pre-symptomatic disease suggests the long-term potential of proteomics for early detection. As the atlas continues to expand, it sets the stage for diagnostic tests that can interpret the complexities of blood proteins with unprecedented accuracy, reducing false alarms while capturing disease at its earliest stages.

More information: María Bueno Álvez et al, A human pan-disease blood atlas of the circulating proteome, Science. DOI: 10.1126/science.adx2678

Journal information: Science Provided by KTH, Royal Institute of Technology

Research shows flu vaccine effectiveness differs across age groups

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Recent research comparing four influenza vaccines has shown that not all flu jabs stimulate the immune system in the same way, and that their performance varies according to age. Although the vaccines produced similar levels of antibodies—the standard measure of vaccine response—scientists found significant differences in how each one activated cellular immunity, a deeper layer of defence that helps build long-lasting protection. These findings could reshape how annual flu vaccines are recommended, especially for older adults.

The study followed one of the most severe recent flu seasons, during which roughly 47 million people in the United States became ill, and an estimated 27,000 died. In light of these high numbers, researchers publishing in The Journal of Immunology set out to expand the way flu vaccine effectiveness is evaluated. While antibodies are essential for reducing illness severity, they do not guarantee complete immunity. Many people still experience breakthrough infections, even when vaccinated. This limitation has encouraged scientists to explore how vaccines interact with the immune system beyond antibody production, particularly through cells that coordinate memory and long-term defence.

To gain a fuller picture, the team measured how four different vaccines—Fluzone High-Dose, Fluzone Standard-Dose, Flucelvax, and Fluad—activated B cells and T cells, the key immune cells that help build durable protection. Blood samples were collected before vaccination, and then at 7, 28, and 90 days afterwards. This allowed researchers to observe how quickly responses formed and how well they were maintained.

Among adults aged 65 to 85, the Fluzone High-Dose vaccine generated the strongest cellular response. It quickly activated circulating T follicular helper cells and antibody-secreting cells, both of which help the body form immune memory. Because immune responses weaken with age, this heightened activation indicates why older adults often benefit from high-dose vaccines: they provide the additional stimulus required for robust protection.

The results differed for younger adults aged 28 to 60. Flucelvax, a mammalian cell-based vaccine, outperformed the standard egg-based Fluzone dose in this group. Flucelvax elicited a stronger response from multifunctional cytokine-secreting CD4⁺ T cells and a more durable memory B cell response. This suggests that younger adults may derive greater benefit from cell-based vaccines, which appear to stimulate a broader, more coordinated immune response.

According to Dr Ted M. Ross, senior author and Global Director of Vaccine Development at the Cleveland Clinic, these age-specific findings illustrate why vaccine evaluation must move beyond antibody measurements alone. Understanding cellular immunity, he argues, can guide more tailored recommendations and accelerate the development of next-generation or universal flu vaccines. Such future vaccines aim to provide broader and longer-lasting protection without the need for yearly reformulation.

The research team now plans to expand the study to a larger population and hopes to identify biomarkers that predict strong, lasting immunity. If successful, these insights could reshape how influenza vaccines are designed and recommended, ensuring more consistent protection across age groups and ultimately reducing seasonal illness and deaths.

More information: Vanessa Silva-Moraes et al, Comparative analysis of cellular immune responses to four seasonal inactivated influenza vaccines in younger and older adults, The Journal of Immunology. DOI: 10.1093/jimmun/vkaf286

Journal information: The Journal of Immunology Provided by American Association of Immunologists Inc

Study reveals shared genetic basis for obesity in diverse ancestral groups

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Obesity is recognised as a worldwide health crisis that affects millions of people and contributes to a wide range of serious medical and social problems. It increases the risk of Type 2 diabetes, heart disease, osteoarthritis and various forms of stigma that impact quality of life. Although lifestyle choices play a clear part in the development of obesity, genetic research has long shown that some individuals carry inherited factors that greatly heighten their risk. More than twenty genes are already known to have substantial effects on the likelihood of becoming obese. Yet, most of this knowledge comes from studies of people with predominantly European ancestry.

A new study published on 30 October in Nature Communications by researchers at Penn State reveals how much more remains to be learned when research includes diverse populations. Using genetic data from around 850,000 adults across six continental ancestries, the team identified thirteen genes associated with obesity that show consistent links across populations. Eight of these had been previously discovered, but five—YLPM1, RIF1, GIGYF1, SLC5A3, and GRM7—had never been linked to obesity. These newly identified genes are essential because their effects are as strong as those of some of the best-known obesity genes, tripling the risk of severe obesity.

Lead author Deepro Banerjee explained that most earlier research focused overwhelmingly on Europeans, meaning genes that are rarer in those populations may never have been detected. This ancestral bias has limited scientific understanding and restricted the discovery of clinically relevant genes, especially those that may only become evident in more diverse groups. The Penn State study overcame this limitation by combining data from the UK Biobank, which includes primarily European participants, and the All of Us Research Program, a U.S. National Institutes of Health initiative designed to reflect the ancestral diversity of the United States. Together, the datasets allowed researchers to study genetic effects separately and collectively across African, American, East Asian, European, Middle Eastern and South Asian populations.

The study focused on rare loss-of-function variants—genetic changes that disrupt normal gene function and often have more potent effects on health. By analysing these variants across the protein-coding regions of the genome, the researchers confirmed that the thirteen genes they detected are associated with higher body mass index (BMI), a standard indicator of obesity. These genes are expressed primarily in the brain and adipose tissue, supporting the current understanding that both the neurological regulation of appetite and fat metabolism contribute to obesity.

Beyond identifying the genes, the team also explored how they influence related diseases. Using mediation analysis, they determined whether the increased risk of conditions such as Type 2 diabetes and heart disease arises directly from the genes or indirectly through increased BMI. Some genes, including BSN, GIGYF1 and SLTM, were found to elevate disease risk through both pathways, highlighting biological mechanisms that might require treatment beyond weight reduction alone.

The researchers also analysed blood plasma proteins in a subset of participants and identified potential biomarkers and drug targets associated with obesity-related genes. These findings help guide the development of personalised treatments and improve how doctors track patient responses to future therapies. Senior author Santhosh Girirajan emphasised that cross-ancestry studies like this are crucial for developing precision medicine strategies that benefit a global population rather than a single group.

More information: Deepro Banerjee et al, Discovery of obesity genes through cross-ancestry analysis, Nature Communications. DOI: 10.1038/s41467-025-64933-7

Journal information: Nature Communications Provided by Penn State

Women experiencing early menopause may face greater risk of dementia, study suggests

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An extensive international study led by the University of Galway has identified a significant link between the timing of menopause and women’s risk of dementia, suggesting that reproductive hormones may play an essential role in protecting brain health. The research indicates that women who enter menopause earlier in life are more likely to develop dementia. In contrast, those who receive hormone replacement therapy (HRT) after menopause appear to face a lower risk. The findings were published in the Journal for Alzheimer’s Disease, underscoring growing interest in how hormones influence long-term cognitive decline.

The study was conducted by researchers from the University of Galway, in collaboration with Boston University, and drew on data from 1,329 cognitively healthy women participating in the renowned Framingham Heart Study. This long-running project, which began in 1948, provides an unusually rich dataset for examining how health, lifestyle, and biology intersect over time. For this particular research, scientists focused on a range of reproductive factors: the age at which a woman had her first period, when she reached menopause, the number of years she spent in her reproductive phase, her oestrogen levels, and whether she had received HRT. These elements were then compared with cognitive test results, MRI scans showing changes in brain structure, and the later risk of dementia.

The results revealed several clear patterns. Women who reached menopause at an earlier age were more likely to experience dementia later on, while women who took post-menopausal HRT had a reduced risk. Additionally, more prolonged exposure to oestrogen over a woman’s lifetime appeared to offer cognitive benefits. Those with more years between the onset of menstruation and menopause performed better on tests assessing memory, reasoning, and visuospatial skills—the ability to interpret and work with spatial information. MRI scans also showed that longer reproductive lifespan and higher oestrogen exposure were linked with greater brain volume in regions that typically shrink during Alzheimer’s disease. This suggests that oestrogen may help preserve brain structure and cognitive function.

Interestingly, the study also found that having more children and higher blood oestrogen levels were associated with stronger cognitive performance. Women with more children showed larger brain volumes in areas commonly affected by Alzheimer’s disease. While the reasons for this are not yet fully understood, pregnancy involves repeated periods of high hormone exposure, which may contribute to long-term brain resilience.

Professor Emer McGrath, Associate Professor at the University of Galway and Consultant Neurologist at Galway University Hospital, emphasised that the findings point to a complex relationship between hormones and brain ageing. Although the results suggest that prolonged exposure to oestrogen may protect cognitive health, she cautioned that further research is needed to confirm the associations and determine the best use of hormonal therapies.

Women account for nearly two-thirds of people living with Alzheimer’s disease, yet scientific understanding of sex-specific risk factors remains limited. While longer life expectancy in women partly explains this imbalance, the study highlights that reproductive biology and hormonal changes may also strongly influence brain health. The research underscores the need to consider women’s hormonal history when exploring dementia risk and developing preventative strategies for cognitive ageing.

More information: Emer McGrath et al, The association between reproductive factors and neurocognitive and neuroimaging markers of brain aging, Journal of Alzheimer’s Disease. DOI: 10.1177/13872877251372430

Journal information: Journal of Alzheimer’s Disease Provided by University of Galway

Research in the Chinese Medical Journal links regular exercise to healthier vascular ageing and extended vitality

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The rapid growth of the global ageing population has intensified the burden of age-related diseases on public health systems. As physiological functions decline with increasing age, blood vessels and immune defences gradually weaken, impairing tissue repair, slowing metabolism, and leaving the body more vulnerable to chronic disorders such as cardiovascular disease, diabetes, and neurodegenerative conditions. These changes do not simply accompany ageing; they actively accelerate its progression, underscoring the urgent need for strategies that address the biological mechanisms driving physical decline rather than merely treating disease after it appears.

A recent review published on 20 October 2025 in Volume 138, Issue 20 of the Chinese Medical Journal offers new insight into how exercise may serve as a natural therapeutic tool against ageing. Authored by Professor Junjie Xiao and his team from the Cardiac Regeneration and Ageing Lab at Shanghai University’s Institute of Geriatrics, the review highlights the potential of exercise-induced angiogenesis (the formation of new blood vessels) and lymphangiogenesis (the growth of lymphatic vessels) to maintain health and slow age-related deterioration. Dr Xiao emphasises that exercise is more than a lifestyle habit; it is a potent biological stimulus that can trigger regenerative processes essential to vascular health and immune protection.

Angiogenesis ensures adequate oxygen and nutrient delivery to tissues, supports wound healing, and maintains metabolic efficiency. Lymphangiogenesis, by contrast, regulates immune activity, metabolic balance, and the removal of cellular waste. With age, both systems undergo marked decline, leading to insufficient tissue perfusion, accumulation of waste products, chronic inflammation, and impaired immune defence. By stimulating the growth and repair of these networks, exercise offers a means to counteract these fundamental causes of ageing.

The review details the molecular mechanisms behind these benefits. Physical activity upregulates vascular endothelial growth factor (VEGF) and its receptors, stimulates endothelial cell proliferation, and activates transcription factors such as hypoxia-inducible factor-1α (HIF-1α), as well as microRNAs associated with vascular growth. In lymphatic tissues, exercise activates receptors such as VEGFR-3, encouraging lymphatic remodelling. Through these pathways, exercise enhances circulation, boosts metabolic capacity, and supports immune resilience.

Organ-specific effects also make exercise a compelling anti-ageing intervention. In the heart, increased vascular regeneration improves myocardial perfusion and reduces cardiovascular risk. In skeletal muscles, denser vascular networks support strength, endurance, and delay muscle atrophy. In the brain, exercise strengthens neurovascular units, fosters cognitive vitality, and offers protection against diseases like Alzheimer’s. Exercise-induced improvements in vascular and lymphatic function have also been linked to reduced metabolic complications in obesity and diabetes.

Despite its promise, the review identifies ongoing challenges. Researchers still lack clarity regarding how different organs coordinate their vascular responses to exercise, and how factors such as exercise type, intensity, and individual variability influence outcomes. Overexertion may even cause harm, especially in elderly or clinically vulnerable individuals, making personalised exercise prescriptions essential. Integrating exercise with medical therapies remains another important frontier.

The review concludes that exercise should be viewed as a regenerative medical tool capable of stimulating vascular and lymphatic health. Future research must optimise exercise protocols for different populations and evaluate long-term safety. With further development, personalised exercise interventions may offer a safe, accessible, and effective strategy to enhance healthspan, combat disease, and support healthy ageing.

More information: Junjie Xiao et al, Exercise-induced angiogenesis and lymphangiogenesis: A potential therapeutic tool to fight aging and disease, Chinese Medical Journal. DOI: 10.1097/CM9.0000000000003831

Journal information: Chinese Medical Journal and Modeling Provided by Chinese Medical Journals Publishing House Co., Ltd.

New Research Uncovers the Cause Behind Memory Loss of Family and Friends in Alzheimer’s

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One of the most painful experiences for families of people living with Alzheimer’s is the moment when a loved one no longer recognises them. A new study from the University of Virginia School of Medicine offers a compelling explanation for why this happens and hints at a way to stop it. The research reveals that social memory loss—specifically the ability to remember faces and relationships—may be caused by the deterioration of a protective structure inside the brain, rather than by general memory decline alone.

The study is led by Harald Sontheimer, PhD, along with graduate student Lata Chaunsali. Together, they focused on specialised protective sheaths surrounding neurons known as perineuronal nets. These delicate, mesh-like structures support communication between brain cells and help retain long-term memories. In healthy brains, the nets act as a scaffolding, protecting neural activity essential for recognising the people who matter to us. The UVA team discovered that when these nets break down, the brain becomes unable to store or retrieve social memories. Crucially, this effect is distinct from the ability to recognise objects or remember other kinds of information.

To test their theory, the researchers studied mice whose perineuronal nets were damaged. Those mice could still remember objects but failed to recognise other mice they had interacted with before. This division between object memory and social memory mirrors what clinicians often observe in Alzheimer’s patients: they may recognise belongings and familiar places, yet still forget their spouses, children, or caregivers. The study suggests that it is not all memory that fails at once, but specifically the brain’s system for protecting memories of people.

Even more promising was the team’s attempt to protect these nets. They used a class of drugs called MMP inhibitors, compounds already under study for potential use against cancer and arthritis. When mice were treated early with these inhibitors, the perineuronal nets remained intact, and the mice retained their social memories. This did not reverse damage once it had occurred, but it prevented the loss of recognition in the first place. Such a result points toward preventative treatment strategies that could one day safeguard memory before deterioration begins.

Sontheimer emphasised that identifying a structural change tied to a specific form of memory loss marks a crucial turning point. Chaunsali echoed this, noting that protecting these nets could offer a non-traditional way to prevent Alzheimer’s. What makes their findings particularly significant is that the deterioration they observed appears to be independent of amyloid plaques—the protein deposits long thought to drive the disease. If social memory loss can occur without amyloid involvement, then current theories about Alzheimer’s may need to be re-evaluated.

More research will be needed before these drug candidates can be used safely on people, but the implications are substantial. With Alzheimer’s affecting 55 million people worldwide and numbers rapidly rising, a treatment that protects identity-defining memories could change the course of the disease. Rather than simply slowing decline, future therapies may help preserve the relationships that give life meaning.

More information: Lata Chaunsali et al, Degradation of perineuronal nets in hippocampal CA2 explains the loss of social cognition memory in Alzheimer’s disease, Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. DOI: 10.1002/alz.70813

Journal information: Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association Provided by University of Virginia Health System

New research links X-chromosome gene to elevated risk of MS and Alzheimer’s in women

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Scientists at UCLA Health have identified a gene on the X chromosome that fuels inflammation in the female brain, providing a fresh explanation for why women are more frequently affected by neurological conditions such as Alzheimer’s disease and multiple sclerosis. The gene, called Kdm6a, was shown to heighten immune activity within microglia – the brain’s specialised immune cells. Because females possess two X chromosomes rather than one, they receive a more potent dose of this inflammatory signal, which becomes particularly relevant in diseases characterised by age-related neurodegeneration.

The research, published in Science Translational Medicine, demonstrated that disabling Kdm6a in a mouse model of multiple sclerosis significantly reduced both disease severity and the damage visible in brain tissue. When the gene was genetically removed, inflammatory molecules within microglia shifted from an activated state back to a more protective, resting state. The team also used the diabetes drug metformin to reduce production of the protein linked to Kdm6a, producing similar benefits. Notably, these interventions had a meaningful impact only in female mice, suggesting that the double X chromosome dosage plays a central role and that women and men may respond differently to treatments that target this pathway.

According to study lead Dr Rhonda Voskuhl, the findings help clarify why neurological disorders disproportionately affect women and why many experience cognitive “brain fog” during menopause. She explained that women’s immune systems have evolved to strike a balance: X-linked inflammatory activity provides an advantage in combating infections during childbearing years, while oestrogen acts as a natural brake that protects the brain from inflammation-induced damage. When oestrogen levels drop during menopause, the protective balance is disrupted, allowing inflammation to exert more harmful, neurodegenerative effects.

The research points toward possible treatment strategies that restore this equilibrium. Voskuhl suggests that therapies targeting brain-specific oestrogen pathways, alongside drugs that moderate Kdm6a activity, could help shield the ageing female brain from the excess inflammation driven by sex-chromosome biology. By illuminating how genetic and hormonal factors interact, the study opens the door to more personalised approaches to neurological health, recognising that understanding women’s risk means paying close attention not only to hormones but also to the chromosomes that shape immune activity throughout life.

More information: Yuichiro Itoh et al, Deletion of the X-chromosomal gene Kdm6a in microglia of female mice ameliorates neuroinflammation and restores translatome profiles, Science Translational Medicine. DOI: 10.1126/scitranslmed.adq3401

Journal information: Science Translational Medicine Provided by University of California – Los Angeles Health Sciences

Irregular blood pressure behaviour associated with early neurological changes in ageing adults

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Even when overall blood pressure falls within a healthy range, older adults whose readings fluctuate sharply from one heartbeat to the next may still face a greater risk of brain shrinkage and nerve cell injury. New research from the USC Leonard Davis School of Gerontology suggests that blood pressure instability, rather than high averages alone, can harm the brain and may signal early signs of neurodegeneration. The findings expand the understanding of cardiovascular risk by showing that the moment-to-moment consistency of blood pressure matters as much as long-term control.

Published online on 17 October in the Journal of Alzheimer’s Disease, the study examined a form of short-term variation known as “dynamic instability,” referring to fluctuations occurring over just minutes. Researchers found that these rapid shifts are associated with reduced volume in brain regions responsible for memory and cognition, as well as with blood markers indicating nerve cell damage. According to senior author Daniel Nation, even routine blood pressure readings may mask subtle instability that can place the brain under stress. He notes that such instability appears linked to the same kinds of changes observed early in neurodegenerative conditions such as Alzheimer’s disease.

While high average blood pressure has long been recognised as a significant risk factor for dementia, the study highlights the importance of blood pressure stability. Frequent small rises and falls may strain tiny blood vessels that supply the brain, reducing their ability to maintain steady blood flow. Over time, this stress may weaken neural tissue, suggesting that maintaining stable circulation could be key to protecting cognitive function.

To measure instability, the research team used two indicators. The first, Average Real Variability (ARV), measures the extent to which systolic blood pressure shifts between heartbeats. The second, the Arterial Stiffness Index (ASI), reflects how flexible the artery walls are as they respond to changing pressure. Together, these metrics offer a picture of how blood flow fluctuates over short periods and indicate “blood pressure dynamic instability.” Nation explains that although the cardiovascular system constantly adapts to the body’s needs, this regulation may become less precise with age, resulting in exaggerated swings that burden the brain.

The study involved 105 adults aged 55-89 with no significant neurological disease. During MRI scans, each participant’s blood pressure was recorded beat-by-beat for 7 minutes. Researchers examined how these fluctuations related to brain structure and blood biomarkers associated with neurodegeneration. Individuals with both high ARV and high ASI showed smaller volumes in the hippocampus and entorhinal cortex, regions vital for memory and among the first affected in Alzheimer’s disease. Blood samples from these individuals also revealed higher levels of neurofilament light (NfL), a marker of nerve cell damage. Notably, the associations held even after accounting for age, sex, and average blood pressure, indicating that variability itself may be an independent risk factor.

Lead author Trevor Lohman suggests that focusing solely on lowering average blood pressure may not be enough. Approaches that reduce fluctuations—through exercise, tailored medication timing, or stress reduction—may offer additional protection. Although the study cannot prove causation, it points to new ways to prevent dementia by maintaining steady blood flow. As the link between cardiovascular stability and brain health becomes clearer, protecting the brain may rely not only on lowering blood pressure but on keeping it consistently stable as we age.

More information: Daniel Nation et al, Blood pressure dynamic instability and neurodegeneration in older adults, Journal of Alzheimer’s Disease. DOI: 10.1177/13872877251386443

Journal information: Journal of Alzheimer’s Disease Provided by University of Southern California

Study reveals inherited connection between early cognitive ability and longer parental lifespan

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Researchers at the University of Edinburgh have found strong genetic evidence linking children’s intelligence to how long their parents live. The study, led by Dr W. David Hill and published in Genomic Psychiatry, is the first to show, at the molecular level, that genes influencing children’s cognitive ability also relate to lifespan. This discovery provides a scientific explanation for a well-known observation in public health: children who perform better on intelligence tests tend to live longer lives.

For decades, researchers have seen that higher childhood intelligence scores are associated with a lower risk of early death. Extensive studies from the UK, Denmark, Israel, and Sweden have shown that children with higher test scores are far more likely to live longer, regardless of their family’s income, later schooling, or social background. However, the biological reason behind this link has remained unclear. Previous findings could not rule out the possibility that poor health in adulthood might lower cognitive scores and reduce lifespan, creating a false association.

To avoid this problem, Hill’s team focused specifically on cognitive data gathered in childhood, before health problems could affect test results. They analysed genetic information from more than 12,000 people who had taken intelligence tests in youth and nearly 390,000 people whose parents’ ages at death were recorded. Using advanced statistical tools, the team measured the extent to which the genetic influences on intelligence and longevity were similar.

The results were striking. The study found a genetic correlation of 0.35 between childhood intelligence and parental lifespan, meaning the two traits share a substantial portion of their genetic basis. The research also confirmed that genes strongly influence both intelligence and longevity. Notably, the analysis showed little evidence of bias from population differences, reinforcing the reliability of the findings.

The reason these shared genes affect both brain function and longevity remains uncertain. One explanation supports the “system integrity” idea: some people may inherit biological systems—such as more efficient cells or stronger immune responses—that naturally support both better thinking skills and longer, healthier lives. Another possibility is that intelligence indirectly supports longevity. Children with higher cognitive ability may grow up to make healthier choices, achieve better education and income, and avoid harmful behaviours, all of which support longer life.

This research opens new opportunities for studying which specific genes support both cognition and health. Understanding these biological pathways could help scientists develop strategies to support healthy ageing or identify those at higher medical risk earlier in life. However, the authors stress that genes are only part of the picture. Lifestyle, access to education, nutrition, and social conditions still profoundly influence lifespan.

The findings also suggest important implications for public health. Supporting and improving children’s cognitive development may offer benefits that extend far beyond academic success. Investing in education and childhood wellbeing may contribute not only to smarter societies, but also to healthier, longer-living populations. While genes cannot be changed, improving childhood environments may work alongside biology to support a longer, healthier life for future generations.

More information: W. David Hill et al, Shared genetic etiology between childhood cognitive function and longevity, Genomic Psychiatry. DOI: 10.61373/gp025l.0098

Journal information: Genomic Psychiatry Provided by Genomic Press

Why political misinformation circulates more often among older generations

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Older adults’ tendency to share political misinformation has long been a subject of speculation, with many assuming that age-related cognitive decline must be to blame. However, recent research from the University of Colorado Boulder suggests a very different explanation. Rather than struggling to distinguish real news from fabricated stories, adults aged fifty-five and older appear to be more deeply influenced by partisanship. As people age, their political identities often become more entrenched, and this stronger allegiance alters how they judge information that appears in their social media feeds. The issue is therefore less about gullibility and more about the subtle power of ideological loyalty.

The study, conducted with approximately 2,500 participants from the United States and Brazil, sought to uncover the mechanisms underlying this trend. Led by psychology and neuroscience professor Leaf Van Boven, the researchers presented participants with a range of political headlines, some accurate and some thoroughly debunked by fact-checking organisations. These headlines were crafted to appeal to either conservative or liberal viewpoints, depending on the context, and participants were asked how likely they would be to share each one. In an additional experiment, they were also asked to judge whether the content was accurate. What emerged was a consistent pattern: older adults were far more inclined to treat ideologically favourable headlines as precise and to share them, regardless of their actual truthfulness.

This finding challenges earlier research that linked misinformation-sharing among older adults to cognitive limitations or difficulty identifying the sources of online material. While previous studies had shown that people over sixty-five shared significantly more fake news during events such as the 2016 US election, new evidence complicates the picture. A recent meta-analysis of dozens of studies found that older adults often outperform younger adults at spotting fake news, suggesting that the problem’s roots lie elsewhere. The team’s results indicate that strong political identity exerts a powerful effect on information processing, leading older individuals to apply different standards of scrutiny depending on which side benefits from the content.

Notably, the results were consistent across both countries studied, despite their very different political landscapes. Brazil’s multi-party system and the United States’ two-party structure produced nearly identical behavioural patterns, demonstrating that this tendency is not shaped by party systems but by the broader psychological bonds of partisanship. Van Boven notes that older adults did not appear to knowingly share misinformation; instead, they reacted in a highly partisan manner when information aligned with their preferred political narrative, becoming less critical and more trusting without realising it.

The implications of these findings extend beyond individual behaviour into public policy and social media design. Traditional misinformation interventions focus heavily on improving people’s ability to spot false claims or encouraging platforms to label suspicious content. While these strategies remain important, the researchers argue that reducing partisan-driven information sharing is equally essential. Van Boven encourages individuals to reflect on their motivations when posting political material, recognising how ideological commitment can cloud judgement.

Ramos, the study’s co-author, also emphasises the importance of maintaining relationships with people who hold differing political views. Avoiding opposing perspectives—by unfriending, muting, or silencing those who disagree—creates an echo chamber that intensifies partisan reactions and allows misinformation to flourish unchecked. Sustaining cross-ideological friendships and conversations, he argues, is crucial for a functioning democracy and for tempering the biases that lead to misguided sharing behaviour.

More information: Guilherme Ramos et al, The age of misinformation: Older people exhibit greater partisan bias in sharing and evaluating (mis)information accuracy, Journal of Experimental Psychology General. DOI: 10.1037/xge0001868

Journal information: Journal of Experimental Psychology General Provided by University of Colorado at Boulder