Monthly Archives: January 2026

Study finds possible connection between brain injuries and suicide risk

Adults who sustain a head injury face a markedly increased risk of attempting suicide compared with those who have not experienced such injuries, according to a major new study conducted in the UK. The research provides some of the most comprehensive evidence to date that head injuries are associated not only with physical harm, but also with longer-term psychological vulnerability.

The study, published in Neurology, the medical journal of the American Academy of Neurology, was led by researchers at the University of Birmingham. It represents the first population-wide investigation to examine suicide risk across all forms of head injury in the general adult population, rather than focusing narrowly on traumatic brain injuries within military, sporting, or hospital-based groups. By taking this broader approach, the researchers aimed to capture risks that may previously have been underestimated or overlooked.

To achieve this, the team carried out an extensive population-based matched cohort study using nationally representative electronic primary healthcare records from more than 1.8 million adults. These records were linked with Hospital Episode Statistics and data from the Office for National Statistics, allowing the researchers to follow participants’ health outcomes over a period of up to 20 years. This extended follow-up and extensive data linkage provided a robust foundation for analysing patterns of suicide attempts following head injury.

The findings showed that adults with a history of head injury were 21 per cent more likely to attempt suicide than those without such injuries, even after accounting for factors such as age, sex, socioeconomic deprivation, and previous mental health conditions. In practical terms, the incidence rate of suicide attempts was 2.4 per 1,000 person-years among people with head injuries, compared with 1.6 per 1,000 person-years in the matched control group. While the absolute increase in risk was modest, the consistency of the association across a huge population highlights its clinical and public health significance.

Notably, the elevated risk was observed across all subgroups studied, including individuals with no recorded history of mental health conditions. This suggests that head injuries themselves may contribute to psychological distress or vulnerability, independent of pre-existing mental illness. The researchers also found that the risk of suicide attempts was highest during the first 12 months following a head injury, indicating a critical period during which individuals may be particularly in need of monitoring and support.

Professor Nicola Adderley, Professor of Epidemiology and Real-World Evidence at the University of Birmingham and a lead author of the study, emphasised that the consequences of head injuries extend beyond immediate physical symptoms. She noted that such injuries can have profound psychological effects. She argued that suicide risk assessments should be considered for anyone who has recently sustained a head injury, regardless of their prior mental health history, to improve patient safety and outcomes.

Although suicide attempts were more frequent among people with head injuries, the study did not identify a significant increase in deaths by suicide once other competing risks were taken into account. This finding suggests that head injuries may be associated with a higher likelihood of non-fatal attempts rather than an increase in suicide mortality. Nonetheless, given that nearly 6,000 deaths each year in the UK are attributed to suicide and that attempts are far more common, the implications remain serious.

The authors argue that their findings have clear implications for both clinical practice and health policy. They call for routine suicide risk screening in primary and secondary care for patients with head injuries, enhanced mental health support during the first year after injury, and greater public awareness to help families and caregivers recognise warning signs. Further research is also needed to develop and test targeted suicide prevention strategies for people with head injuries, particularly during this high-risk early period.

More information: Tiffany E. Gooden et al, The Risk of Suicide Attempts After Head Injury
A Matched UK Population–Based Cohort Study, Neurology. DOI: 10.1212/WNL.0000000000214474

Journal information: Neurology Provided by University of Birmingham

Nearly 1.6 Million Adults in the UK Turned to Weight Loss Drugs Last Year

Leave a Reply

An estimated 1.6 million adults in England, Wales and Scotland used prescription weight loss drugs such as Wegovy and Mounjaro between early 2024 and early 2025, according to new research led by University College London. The study, published in BMC Medicine and funded by Cancer Research UK, also found substantial unmet demand, with a further 3.3 million people saying they would consider using weight loss medication over the next year.

Researchers analysed survey responses from 5,260 adults who were representative of the general population and who took part in early 2025. Overall, 4.5% reported using one of the medications in the past year for any reason, while 2.9% said they used them specifically for weight loss, equating to around 1.6 million people. A smaller group—1.7%, or roughly 910,000 adults—reported using the drugs exclusively for weight loss, without another reason such as managing type 2 diabetes or reducing cardiovascular risk.

Use of weight loss medication was not evenly distributed across the population. The researchers found it was about twice as common among women as men and most prevalent among those aged 45 to 55. Higher use was also reported by people who experienced moderate or severe psychological distress in the month before the survey. While overall usage rates were similar across social grades, interest in future use was notably higher among more disadvantaged groups, where obesity rates tend to be greater, suggesting that private prescribing may not be meeting demand.

Taken together, the findings suggest that nearly 4.9 million adults in Great Britain—almost one in ten—have either recently used a weight loss drug or are interested in doing so soon. Lead author Professor Sarah Jackson noted that this level of use and interest far exceeds NHS England’s original target of prescribing these medications to 220,000 people over three years. However, the study could not assess whether use reflected genuine medical need, as respondents’ body mass index and health conditions were not recorded.

The research also highlighted safety and equity concerns. Among those using medication for weight loss, around 15% reported taking drugs not licensed in the UK for that purpose, such as Rybelsus, which is approved only for type 2 diabetes. Using medicines “off-label”, particularly without clinical supervision, may increase health risks. The authors stressed that NHS prescribing data captures only a small proportion of overall use, as many people appear to be accessing these drugs privately.

Interest in future use was reported by 6.5% of respondents who had not taken weight loss medication in the past year, with higher interest among women, people aged 45 to 55, and those experiencing psychological distress. Commenting on the findings, Cancer Research UK said that while these drugs can support weight loss, they are not a cure-all and many people regain weight after stopping treatment. The charity emphasised the need for further research, careful medical oversight, and broader action to create healthier environments that support long-term weight management.

More information: Sarah Jackson et al, Prevalence of use and interest in using glucagon-like peptide-1 receptor agonists for weight loss: a population study in Great Britain, BMC Medicine. DOI: 10.1186/s12916-025-04528-7

Journal information: BMC Medicine Provided by University College London

Targeting senescent brain cells may offer new ways to ease epilepsy symptoms

Leave a Reply

Temporal lobe epilepsy (TLE) is a common and often severe form of epilepsy characterised by recurrent seizures and problems with memory and thinking. Increasing evidence suggests that this condition is linked to the premature ageing of brain cells. A new study from researchers at Georgetown University Medical Center provides compelling evidence that targeting these ageing, or senescent, cells may reduce seizures and improve cognitive function, at least in animal models.

The NIH-funded study, published on 22 December in Annals of Neurology, examined both human brain tissue and a well-established mouse model of TLE. The researchers focused on senescent glial cells, which are support cells that help maintain and protect neurons but do not generate electrical signals themselves. Although glial cells are essential for healthy brain function, when they become senescent, they can contribute to inflammation and tissue dysfunction.

In laboratory analyses of donated human brain tissue, the team examined samples surgically removed from the temporal lobes of people with TLE and compared them with tissue obtained during autopsies from individuals without epilepsy. They found a striking five-fold increase in senescent glial cells in the TLE samples. This suggested that cellular ageing might play a direct role in the development or persistence of seizures in this condition.

Building on these findings, the researchers studied mice that had experienced a brain injury known to trigger TLE. Within just two weeks of the injury, the mice showed clear increases in markers of cellular senescence at both the genetic and protein levels. When the investigators used either genetic techniques or drug treatment to remove senescent cells, the results were notable. Levels of ageing cells were reduced by around 50%, seizure frequency decreased, and the animals’ performance on memory-based maze tests returned to normal. Importantly, about one-third of the treated mice were protected from developing epilepsy altogether.

The drug treatment used in the study combined dasatinib and quercetin. Dasatinib is an FDA-approved targeted therapy used in certain forms of leukaemia. At the same time, quercetin is a naturally occurring plant compound found in foods such as fruits, vegetables, tea, and wine. Together, these compounds have been widely used in animal studies to eliminate senescent cells selectively. Because dasatinib already has a known safety profile in humans and both drugs are being tested in early-stage clinical trials for other conditions, the researchers believe this approach could move more quickly towards human studies.

Senior author Patrick A. Forcelli emphasises the clinical importance of these findings, noting that roughly one-third of people with epilepsy do not achieve seizure control with existing medications. He suggests that senotherapy, which aims to remove senescent cells, could one day reduce the need for invasive brain surgery or improve outcomes for patients who do undergo surgical treatment.

The study also highlights broader implications beyond epilepsy. Senescent glial cells have recently been linked to ageing and neurodegenerative disorders such as Alzheimer’s disease, an area the research team continues to investigate. Ongoing work is exploring additional drugs that target cellular senescence, as well as identifying the most effective time windows for intervention. The researchers hope these efforts will ultimately lead to safer, more effective treatments for people living with epilepsy.

More information: Tahiyana Khan et al, Senescent Cell Clearance Ameliorates Temporal Lobe Epilepsy and Associated Spatial Memory Deficits in Mice, Annals of Neurology. DOI: 10.1002/ana.78118

Journal information: Annals of Neurology Provided by Georgetown University Medical Center

Do circadian rhythms play a role in dementia risk?

Leave a Reply

Circadian rhythms that are weaker, more fragmented, or that peak later in the day are associated with a higher risk of dementia, according to a study published on 29 December 2025 in Neurology, the medical journal of the American Academy of Neurology. The researchers found that people whose daily activity patterns were less clearly defined, or whose activity levels peaked later rather than earlier in the afternoon, were more likely to develop dementia over time. Notably, the findings show an association rather than proof that disrupted circadian rhythms directly cause dementia.

Circadian rhythms are the body’s internal timekeeping system. They regulate the 24-hour sleep–wake cycle and influence many other processes, including hormone release, digestion, and body temperature. The brain controls these rhythms and is strongly affected by exposure to light. When circadian rhythms are strong, the body clock stays closely aligned with the natural day–night cycle, producing clear and consistent signals that help regulate daily activity and rest.

People with robust circadian rhythms tend to keep relatively stable sleep and activity schedules, even when their routine changes slightly or the seasons shift. In contrast, weaker circadian rhythms are more easily disrupted by changes in light exposure or daily schedules. Individuals with weaker rhythms are more likely to experience shifts in their sleep and activity patterns, which may place additional strain on the body over time.

“Changes in circadian rhythms occur with ageing, and growing evidence suggests that circadian disruption may be a risk factor for neurodegenerative diseases such as dementia,” said study author Wendy Wang, MPH, PhD, of the Peter O’Donnell Jr. School of Public Health at UT Southwestern Medical Center. She explained that the study directly measured rest–activity patterns and found that participants with weaker, more fragmented rhythms, as well as those whose activity peaked later in the day, had an elevated risk of developing dementia.

The study followed 2,183 adults with an average age of 79 who did not have dementia at the beginning of the research. About 24% of participants were Black, and 76% were white. Each participant wore a small heart monitor attached to the chest for around 12 days, allowing researchers to measure periods of activity and rest continuously. Participants were then followed for an average of three years, during which time 176 people were diagnosed with dementia.

Researchers analysed several measures of circadian rhythm strength, including relative amplitude, which reflects the contrast between a person’s most active and least active periods. Higher relative amplitude indicates a stronger circadian rhythm. When participants were divided into groups, those with the weakest rhythms had nearly 2.5 times the risk of dementia compared with those with the strongest rhythms, even after accounting for factors such as age, blood pressure, and heart disease.

The study also found that people whose activity peaked later in the afternoon, from around 2:15 p.m. onwards, had a 45% higher risk of dementia than those whose activity peaked earlier. A later activity peak may indicate a mismatch between the body’s internal clock and environmental cues like daylight and darkness.

The researchers noted that circadian disruption may affect inflammation, sleep quality, and the brain’s ability to clear amyloid, a protein linked to dementia. However, a limitation of the study was the lack of data on sleep disorders, such as sleep apnoea, which could also influence dementia risk.

More information: Wendy Wang et al, Association Between Circadian Rest-Activity Rhythms and Incident Dementia in Older Adults The Atherosclerosis Risk in Communities Study, Neurology. DOI: 10.1212/WNL.0000000000214513

Journal information: Neurology Provided by American Academy of Neurology

Keep moving, live longer: Light activity associated with improved survival in diabetes, heart and kidney disease

Leave a Reply

Light-intensity activities such as walking, gardening or household chores were associated with a lower risk of death among people with cardiovascular-kidney-metabolic (CKM) syndrome, according to new research published in the Journal of the American Heart Association. The findings suggest that even modest levels of movement may offer meaningful health benefits, particularly for people living with more advanced stages of this complex condition.

CKM syndrome is common, affecting nearly nine in ten adults in the United States, and includes a combination of risk factors such as high blood pressure, unhealthy cholesterol and lipid levels, elevated blood glucose, excess body weight and impaired kidney function. While each of these factors is harmful on its own, their combination substantially increases the likelihood of serious outcomes such as heart attack, stroke and heart failure. CKM syndrome is classified into stages from 0 to 4, with higher stages indicating more severe disease and greater cardiovascular risk.

The study highlights that light physical activity is the most common form of movement among adults and may be more achievable than moderate- or vigorous-intensity exercise for people with chronic illness. While standard physical activity guidelines often emphasise higher-intensity exercise, this level of exertion may not be realistic or safe for individuals with advanced CKM syndrome. As a result, identifying benefits from lighter activities is especially important for this population.

Researchers analysed data from around 7,200 adults who participated in the National Health and Nutrition Examination Survey between 2003 and 2006. Participants’ health status was assessed using physical examinations and blood tests, while activity levels were measured objectively using accelerometers worn for up to seven days. These devices allowed researchers to distinguish between light, moderate and vigorous activity. Light physical activity was defined as movement that does not significantly increase breathing rate, such as casual walking, stretching, yoga or everyday household tasks.

When participants were grouped by CKM stage, the researchers found a clear pattern. Greater time spent in light physical activity was linked to a significantly lower risk of death among individuals in CKM stages 2, 3 and 4. On average, each additional hour of light activity per day was associated with a 14% to 20% reduction in the risk of death over a follow-up period of roughly 14 years. Notably, the benefits appeared to increase with disease severity. For example, increasing daily light activity from 90 minutes to two hours was linked to a larger reduction in risk for people in stage 4 than for those in stage 2.

Light physical activity is an under-recognised but potentially powerful tool for improving heart health in people with CKM syndrome. For individuals who are unable to meet conventional exercise recommendations, small increases in everyday movement may translate into substantial long-term benefits.

Independent experts welcomed the findings, noting that light-intensity activity remains an under-studied area despite being the most accessible form of movement for many people. Such activities support circulation, energy use and general mobility, all of which contribute to better health.

The researchers caution that the study was observational, meaning it can identify associations but cannot prove cause and effect. It is possible that people with more severe illness were both less active and at higher risk of death. Even so, the results strengthen the case for encouraging gentle, achievable movement as part of a broader approach to managing CKM syndrome.

More information: Joseph Sartini et al, Light Physical Activity and All‐Cause Mortality in US Adults Across Cardiovascular‐Kidney‐Metabolic Syndrome Stages, Journal of the American Heart Association. DOI: 10.1161/JAHA.125.046271

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

New research challenges established models of Parkinson’s disease

Leave a Reply

A new study led by researchers at McGill University is challenging a long-standing theory about how dopamine supports movement, offering insights that could reshape scientific thinking about treatments for Parkinson’s disease. By re-examining dopamine’s fundamental role in motor control, the findings suggest a more straightforward and potentially more effective way of understanding why current therapies work, and how future treatments might be designed.

Published in Nature Neuroscience, the research shows that dopamine does not directly determine the speed or force of individual movements, as has been widely assumed. Instead, it provides a crucial background condition that allows movement to occur at all. Rather than acting as a moment-by-moment controller of motion, dopamine functions more like a stabilising system that keeps the brain’s motor circuits ready and able to operate.

Senior author Nicolas Tritsch, an Assistant Professor in McGill’s Department of Psychiatry and a researcher at the Douglas Research Centre, explains that these results call for a fundamental rethink. According to Tritsch, restoring dopamine to a healthy baseline level may be sufficient to improve movement in people with Parkinson’s disease, without needing to recreate complex dopamine signals precisely. This reframing could simplify how researchers and clinicians approach treatment strategies.

Dopamine has long been associated with what scientists call motor vigour — the capacity to move with adequate speed, strength and fluidity. In Parkinson’s disease, dopamine-producing neurons gradually degenerate, leading to hallmark symptoms such as slowness of movement, tremors, stiffness and impaired balance. For decades, researchers have sought to understand precisely how dopamine loss translates into these motor difficulties.

The most common treatment, levodopa, is highly effective at improving movement, yet its precise mechanism has remained unclear. In recent years, sophisticated measurement techniques revealed brief, rapid bursts of dopamine release during movement. These discoveries led many scientists to conclude that such fast dopamine spikes directly control how vigorous each movement is. This interpretation has strongly influenced current theories of motor control.

The new study, however, points in a different direction. Tritsch likens dopamine’s role not to a throttle that sets movement speed, but to engine oil in a car. Without it, the system cannot function properly, but it does not dictate how fast the engine runs at any given moment. This analogy captures the idea that dopamine is essential for enabling movement, rather than fine-tuning each action as it unfolds.

To test this hypothesis, the researchers measured brain activity in mice as the animals pressed a weighted lever. Using a light-based technique, they were able to switch dopamine-producing neurons on or off with precise timing. If brief dopamine bursts were truly responsible for controlling movement vigour, altering dopamine levels at the moment of action should have changed how forcefully or quickly the mice moved. Instead, the researchers observed no such effect.

Further experiments with levodopa revealed that the drug improved movement by increasing the brain’s overall, or baseline, dopamine level rather than by restoring fast dopamine bursts. This finding provides a more straightforward explanation for why levodopa works so well, despite not precisely replicating natural dopamine signalling patterns.

The implications are significant. More than 110,000 Canadians currently live with Parkinson’s disease, and this number is expected to more than double by 2050 as the population ages. A better understanding of dopamine’s proper role opens the door to therapies focused on maintaining stable baseline dopamine levels. It also encourages a reassessment of older treatments, such as dopamine receptor agonists, which showed promise but caused side effects because they acted too broadly across the brain. With this new framework, scientists may be able to design more targeted and safer therapies in the future.

More information: Haixin Liu et al, Subsecond dopamine fluctuations do not specify the vigor of ongoing actions, Nature Genetics. DOI: 10.1038/s41593-025-02102-1

Journal information: Nature Genetics Provided by McGill University

In what ways does stroke impair speech understanding?

Leave a Reply

After a stroke, some individuals develop a language disorder that disrupts how their brains handle the sounds of speech. While their hearing itself may remain intact, the neurological processes that allow speech sounds to be interpreted as meaningful language can be compromised. To better understand how stroke alters these processes, a team of researchers examined changes in brain activity associated with speech comprehension, focusing on how the injured brain differs from a healthy one during everyday listening.

The study was led by Laura Gwilliams, a faculty scholar at the Wu Tsai Neuroscience Institute and Stanford Data Science, and an assistant professor at the Stanford School of Humanities and Sciences, together with Maaike Vandermosten, an associate professor in the Department of Neurosciences at KU Leuven. Their work compared the brain activity of 39 people who had experienced a stroke with that of 24 healthy adults of a similar age. By analysing these two groups side by side, the researchers aimed to uncover the neural mechanisms that support language processing and how these mechanisms are altered after stroke.

To capture brain activity in a naturalistic way, participants were asked to listen to a spoken story while their neural responses were recorded. This approach allowed the researchers to observe how the brain processes speech in real time, rather than relying on artificial tasks involving isolated sounds or words. The results revealed a striking pattern. Individuals with stroke-related difficulties in verbal speech processing were not slower than healthy listeners in responding to speech sounds. Instead, their brain responses were noticeably weaker.

This finding suggests that the core problem is not a delay in processing but a reduction in the strength or quality of that processing. In practical terms, people affected by this language disorder appear to detect sounds just as efficiently as those without brain injury. However, they struggle when it comes to combining these sounds into coherent linguistic units that carry meaning. The brain receives the auditory information, but the integration needed to understand spoken language is less effective.

The study also highlighted differences in how the brain deals with uncertainty in speech. When words were difficult to hear or ambiguous, healthy participants showed prolonged processing of speech sound features. This extended neural activity is thought to reflect the brain’s effort to resolve uncertainty and arrive at the correct interpretation. In contrast, people who had experienced a stroke showed less sustained processing in these situations. This shortened engagement with speech sounds may make it harder for them to identify words that are unclear or masked by noise successfully.

Taken together, these findings point to specific patterns of brain activity that are crucial for understanding spoken language. They suggest that successful speech comprehension relies not only on detecting sounds quickly but also on maintaining and strengthening neural processing when interpretation becomes challenging. After a stroke, this supportive processing may be reduced, contributing to persistent language difficulties.

The authors emphasise that these insights could have important clinical implications. First author Jill Kries expressed enthusiasm about continuing this line of research, particularly the use of simple, natural listening tasks such as hearing a story. Such approaches may improve the diagnosis of language processing disorders, which currently often require lengthy and demanding behavioural assessments. By focusing on how the brain responds during everyday listening, future tools could become both more efficient and more closely aligned with real-world communication challenges.

More information: Jill Kries et al, The spatio-temporal dynamics of phoneme encoding in aging and aphasia, JNeurosci. DOI: 10.1523/JNEUROSCI.1001-25.2025

Journal information: JNeurosci Provided by Society for Neuroscience

Geographic inequality shown to affect hip fracture recovery

Leave a Reply

Older adults living in economically disadvantaged neighbourhoods spend significantly fewer days at home in the year following a fall-related hip fracture than those in more affluent areas, according to an extensive national study published in JAMA Network Open. The findings highlight how recovery after a significant injury is shaped not only by medical care, but also by the social and physical conditions of the places where people live.

The researchers analysed Medicare data from more than 52,000 older adults who experienced a hip fracture. After accounting for individual factors such as age and chronic illness, they found that people living in the most economically disadvantaged neighbourhoods spent an average of 23 fewer days at home in the year after their injury compared with those in the least disadvantaged areas. Instead, they spent more time in skilled nursing facilities or long-term care settings, suggesting slower or more complicated recoveries.

The study’s senior author, Jason R. Falvey, Associate Professor of Physical Therapy and Rehabilitation Science at the University of Maryland School of Medicine, emphasised that neighbourhood context is often overlooked in hip fracture research. He noted that older adults in highly disadvantaged areas face multiple barriers to recovery, including limited access to rehabilitation services, fewer supports for caregivers, and environmental challenges such as damaged pavements that restrict safe mobility. Together, these factors make it harder for individuals to regain independence after injury.

To assess neighbourhood disadvantage, the researchers used the Area Deprivation Index, a national measure that incorporates income, education, employment, and housing quality. Participants living in the most deprived neighbourhoods were more likely to belong to racial or ethnic minority groups and to be dually eligible for Medicare and Medicaid—these overlapping forms of disadvantage point to broader structural inequalities that extend well beyond the hospital setting.

The findings matter because hip fractures are life-changing events and a leading cause of disability and loss of independence in older adults. “Days at home” is a patient-centred measure that captures quality of recovery, reflecting independence, well-being, and the ability to age in place. The study shows that even when medical factors are similar, place-based disadvantage reduces the likelihood of spending time at home after surgery, underscoring the role of environment in shaping outcomes.

The researchers argue that improving recovery after hip fracture will require action beyond clinical care alone. For clinicians, this means considering neighbourhood and social factors when planning discharge and rehabilitation. For health systems and policymakers, it points to the need for investment in community-based supports, transportation, caregiver resources, home health services, and safer neighbourhood infrastructure. Future research will focus on developing care models that address these barriers and help more older adults recover and remain at home, regardless of where they live.

More information: Alyssa M. Baginski et al, Neighborhood Deprivation and Days Spent at Home After Fall-Related Hip Fracture, JAMA Network Open. DOI: 10.1001/jamanetworkopen.2025.49118

Journal information: JAMA Network Open Provided by University of Maryland School of Medicine

An AI-Driven Review of a Century of Ageing Research Reveals Trends and Gaps

Leave a Reply

A research article published in Volume 17, Issue 11 of Aging-US on 25 November 2025 presents a large-scale, AI-based analysis of how ageing research has evolved over the past century. Titled “A natural language processing–driven map of the aging research landscape, the paper adopts a meta-research perspective, using computational tools to examine not a single biological problem, but the structure, priorities, and blind spots of ageing science as a whole. It aims to provide a clear, data-driven overview of where the field has come from and where it may need to go next.

The study was led by Jose Perez-Maletzki, affiliated with Universidad Europea de Valencia and Universitat de València, in collaboration with Jorge Sanz-Ros from Stanford University School of Medicine. Together, the authors used artificial intelligence to analyse global ageing research output, seeking to identify long-term trends, shifts in emphasis, and areas that remain underexplored. Their approach reflects a growing recognition that understanding the organisation of scientific knowledge is itself essential for accelerating progress.

To conduct the analysis, the team examined more than 460,000 scientific abstracts published between 1925 and 2023. This massive dataset allowed them to capture nearly a century of research across basic biology, clinical medicine, and population health. By focusing on abstracts, the authors were able to include a broad range of disciplines and journals, producing a more comprehensive and less selective overview than is typically possible with traditional narrative reviews.

Using natural language processing and machine-learning techniques, the researchers grouped publications into thematic clusters and tracked how interest in each topic changed over time. Their methodology combined Latent Dirichlet Allocation, term frequency–inverse document frequency analysis, dimensionality reduction, and clustering to generate a structured thematic map of ageing research. This enabled them to visualise both dominant research areas and weaker connections between topics, revealing patterns that are difficult to detect through manual review alone.

One key finding was a clear historical shift in focus. Early ageing research was primarily centred on fundamental cellular processes and animal models, whereas more recent decades show a strong move towards clinical and disease-oriented studies. In particular, research on Alzheimer’s disease, dementia, and geriatric healthcare has grown rapidly. While this reflects the realities of ageing populations, the analysis also indicates a widening gap between basic biological research and clinical application.

The study shows that basic and clinical ageing research often develops in parallel, with limited integration. Clinical studies tend to focus on care, neurodegeneration, and age-related disease, while basic science emphasises mechanisms such as mitochondrial dysfunction, telomere shortening, oxidative stress, and cellular senescence. Emerging areas like autophagy, RNA biology, and nutrient sensing are expanding quickly but remain weakly connected to clinical research. The authors argue that these gaps represent missed opportunities and potential directions for future interdisciplinary work.

Overall, this AI-driven analysis provides a powerful tool for reflecting on how ageing research is organised and prioritised. By identifying both strong connections and neglected links, the study offers guidance for shaping more integrated and translational research strategies. As global populations continue to age, such a comprehensive and critical overview may help ensure that future research is not only productive but also better aligned with real-world health outcomes.

More information: Jose Perez-Maletzki et al, A natural language processing–driven map of the aging research landscape, Aging-US. DOI: 10.18632/aging.206340

Journal information: Aging-US Provided by Impact Journals LLC

As neuron death increases with ageing, a natural human protein treatment shows potential to halt Alzheimer’s-related brain cell loss

Leave a Reply

Scientists at the University of Colorado Anschutz have found that changes in brain neurons, including gradual cell loss, may begin much earlier in life than previously thought. Their research also suggests that a drug already approved for other medical uses could potentially be repurposed to slow this damage, offering fresh hope for people living with Alzheimer’s disease and other cognitive disorders. The findings highlight a possible new direction in tackling neurodegeneration, an area where effective treatments remain limited.

The study, published in Cell Reports Medicine, builds on earlier clinical work involving sargramostim, also known as Leukine. According to senior author Professor Huntington Potter, director of the University of Colorado Alzheimer’s and Cognition Center, the drug showed encouraging effects in its first clinical trial. Over a relatively short period, sargramostim reduced a blood-based marker of neuron death in people with Alzheimer’s disease and improved performance on one established cognitive test. These findings are notable because they link biological evidence of reduced neuronal damage with measurable cognitive benefit.

Sargramostim is a synthetic version of GM-CSF, a natural human protein that stimulates the immune system. It has been used safely for around 30 years, particularly in cancer care, to promote the production of immune cells. In early neurological studies, the drug improved blood biomarkers associated with brain pathology. While these biomarker improvements were only maintained during active treatment, gains in one measure of memory persisted beyond the treatment period, suggesting longer-lasting effects on brain function.

In the new cross-sectional study, researchers examined blood samples from individuals across a wide age range. They focused on proteins released when neurons are damaged or die, including UCH-L1 and neurofilament light chain (NfL). Levels of both proteins were low in early life but increased exponentially with age, reaching much higher concentrations in later adulthood. While modest increases earlier in life likely reflect normal ageing, higher levels in older age were associated with poorer outcomes, pointing to accelerated neuronal damage as a contributor to cognitive decline and Alzheimer’s disease.

The team also measured glial fibrillary acidic protein (GFAP), a marker of brain inflammation believed to play a central role in cognitive deterioration. GFAP levels rose significantly from around age 40, supporting the idea that neuroinflammation intensifies in midlife and may drive later neuronal loss. Interestingly, age-related levels of GFAP and UCH-L1 were higher in women than in men, although the reasons for this difference remain unclear.

Results from the clinical trial were particularly striking. People with Alzheimer’s disease who received sargramostim showed a roughly 40 per cent reduction in blood levels of UCH-L1, comparable to levels typically seen much earlier in life. They also performed better on the Mini-Mental State Examination than those receiving a placebo. Although UCH-L1 levels returned to pre-treatment values after the drug was stopped, the cognitive improvement persisted, raising essential questions about how the treatment works and how long its benefits might last.

The authors caution that these findings are still preliminary. Blood markers of neuronal damage change naturally with age, and more research is needed to determine whether sargramostim can slow normal age-related cognitive decline or requires continuous use to maintain its effects. A larger, longer clinical trial in people with mild-to-moderate Alzheimer’s disease is currently underway. Until regulatory review is complete, the drug should not be used outside its approved indications.

More information: Stefan H. Sillau et al, Blood measure of neuronal death is exponentially higher with age, especially in females, and halted in Alzheimer’s disease by GM-CSF treatment, Cell Reports Medicine. DOI: 10.1016/j.xcrm.2025.102525

Journal information: Cell Reports Medicine Provided by University of Colorado Anschutz

How a brain care score can predict stroke risk across racial groups, study finds

Leave a Reply

A new study led by researchers at Mass General Brigham has found that the Brain Care Score (BCS) is a strong predictor of stroke risk across racial groups in the United States. The findings, published in Neurology, the medical journal of the American Academy of Neurology, suggest that this composite measure of brain health may be especially valuable for addressing long-standing disparities in stroke risk. In particular, the results indicate that improvements in the Brain Care Score could yield meaningful benefits for stroke prevention among Black adults.

Black adults in the United States face a two- to threefold higher risk of stroke compared with white adults, a disparity that has persisted despite decades of research and public health efforts. Senior author Sanjula Dhillon Singh, a principal investigator in the Brain Care Labs within the Mass General Brigham Department of Neurology, explained that the Brain Care Score offers a practical way to understand better and address this gap. By focusing on modifiable behaviours, the score provides a framework for identifying concrete actions that can lower stroke risk, rather than treating such disparities as inevitable or purely genetic.

The Brain Care Score was initially developed at the McCance Center for Brain Health as a holistic tool that brings together multiple dimensions of brain health into a single metric. It incorporates physical, lifestyle, and social-emotional factors, including blood pressure and blood sugar control, nutrition, alcohol intake, physical activity, stress levels, and social relationships. Scores range from 0 to 21, with higher values reflecting healthier behaviours and a lower risk of age-related brain diseases such as stroke, dementia, and depression.

To assess the predictive value of the BCS, the researchers analysed data from 10,861 participants in the federally funded Reasons for Geographic and Racial Differences in Stroke (REGARDS) study. This large national cohort included Black and white adults aged 45 and older who had no history of stroke at baseline and complete data for all components of the Brain Care Score. Participants were followed for a median of 15.9 years, allowing the researchers to examine long-term stroke outcomes in relation to baseline brain health.

Over the follow-up period, higher Brain Care Scores were consistently associated with lower stroke risk in both racial groups. A five-point increase in the BCS was linked to a 53 per cent reduction in stroke risk among Black participants and a 25 per cent reduction among white participants, even after adjusting for demographic and socioeconomic factors. These findings suggest that while the Brain Care Score is predictive across groups, its potential benefits may be particularly pronounced for those at higher baseline risk.

The study was observational and cannot establish causality, but the results reinforce the importance of addressing behavioural and social determinants of health in efforts to reduce stroke disparities. As Jonathan Rosand, Director of the Brain Care Labs at Mass General Brigham and Founder of the Global Brain Care Coalition, noted, confirming the predictive power of the Brain Care Score in diverse populations is a critical step towards ensuring that everyone has the opportunity to protect and improve their brain health.

More information: Evy M. Reinders et al, Association of Modifiable Risk Factors Measured With the Brain Care Score and Incident Stroke in the REGARDS Cohort, Neurology. DOI: 10.1212/WNL.0000000000214488

Journal information: Neurology Provided by Mass General Brigham

A genetic blind spot: how ‘junk’ DNA might hold Alzheimer’s clues

Leave a Reply

When most people think about DNA, they tend to picture genes that determine physical traits, influence behaviour, and keep the body’s cells and organs functioning properly. This familiar image is useful, but it captures only a small slice of what our genetic material actually does. The reality is that genes themselves make up only a minor fraction of the human genome.

In fact, only about 2% of our DNA encodes the roughly 20,000 genes that code for proteins. The remaining 98% belongs to the non-coding genome, long dismissed as “junk” DNA. Scientists now know that much of this DNA is anything but useless, as it contains regulatory elements that act like switches, controlling when genes are activated and how strongly they are expressed.

Researchers from UNSW Sydney have recently identified important DNA switches that regulate astrocytes, specialised brain cells that support neurons and help maintain normal brain function. Astrocytes are increasingly recognised as playing a key role in Alzheimer’s disease, making them an essential target for understanding how genetic regulation contributes to neurodegeneration.

In a study published in Nature Neuroscience, scientists from UNSW’s School of Biotechnology and Biomolecular Sciences examined nearly 1,000 potential switches, known as enhancers, in human astrocytes grown in the laboratory. Enhancers are challenging to study because they can be located far from the genes they regulate, sometimes hundreds of thousands of DNA base pairs apart. To overcome this challenge, the team combined CRISPR interference, which allows sections of DNA to be switched off without cutting them, with single-cell RNA sequencing to measure changes in gene expression.

This approach enabled the researchers to test the function of almost 1,000 enhancers simultaneously. By turning off each candidate enhancer and observing whether gene activity changed, they identified around 150 that functioned as genuine switches. Strikingly, many of these enhancers controlled genes already linked to Alzheimer’s disease, sharply narrowing the regions of the genome that scientists need to examine when searching for genetic risk factors.

Although the findings do not immediately translate into treatments, they provide a crucial foundation for future work. The results offer a detailed map of gene regulation in astrocytes, helping researchers interpret genetic changes found outside of genes themselves. The dataset can also be used to train artificial intelligence tools to predict enhancer function, potentially accelerating future research. In the longer term, the cell-type specificity of enhancers raises the possibility of precisely controlling gene activity in astrocytes, opening new directions for understanding and eventually treating Alzheimer’s disease.

More information: Nicole F. O. Green et al, CRISPRi screening in cultured human astrocytes uncovers distal enhancers controlling genes dysregulated in Alzheimer’s disease, Nature Neuroscience. DOI: 10.1038/s41593-025-02154-3

Journal information: Nature Neuroscience Provided by University of New South Wales