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Artificial Intelligence Exposes Unexpected Byproducts of Drinking Water Treatment

Disinfecting drinking water has played a central role in protecting societies from deadly waterborne illnesses for more than a century. By killing harmful microorganisms such as bacteria, viruses, and parasites, water treatment prevents the spread of diseases that once swept rapidly through communities. Even water that appears crystal clear can contain invisible pathogens capable of causing severe and sometimes fatal illness, particularly among children, older adults, and those with weakened immune systems. Before modern sanitation systems were introduced, outbreaks of cholera, typhoid, and dysentery were frequent and devastating, claiming countless lives and crippling entire cities. For this reason, the widespread disinfection of drinking water is considered one of the most important public health achievements in human history.

However, the chemical processes that make water safer also produce unintended chemical reactions. Disinfectants such as chlorine and chloramine interact with naturally occurring organic matter found in rivers, lakes, and underground aquifers. This organic material consists of tiny particles of dissolved carbon-based compounds that are present in nearly all natural water sources. When disinfectants come into contact with this matter, they form substances known as disinfection byproducts, or DBPs, some of which have raised long-term health concerns among scientists and regulators.

Certain DBPs, including trihalomethanes and haloacetic acids, have been linked in studies to increased risks of bladder cancer and developmental problems during pregnancy. The Environmental Protection Agency has established safety limits for a small number of these compounds in public water supplies. Yet many others remain unregulated. According to Tao Ye, an assistant professor at Stevens Institute of Technology, only 11 byproducts are currently monitored under federal standards, even though researchers have already identified several hundred additional compounds that may form during water treatment. Some of these lesser-known chemicals could potentially be more harmful than those already regulated.

Testing such a vast number of substances using traditional laboratory methods is extremely difficult. Toxicity experiments require specialised equipment, long exposure periods, and significant financial resources, which limit how many chemicals can realistically be studied. To overcome this barrier, researchers are increasingly turning to artificial intelligence. Machine learning models can analyse large datasets and identify patterns between chemical structures and toxic effects, allowing scientists to predict the potential danger of compounds that have never been tested in the lab.

To advance this approach, Ye and his doctoral student, Rabbi Sikder, collaborated with Peng Gao from the Harvard T.H. Chan School of Public Health to develop an AI model focused specifically on disinfection byproducts. They compiled experimental toxicity data from previous scientific research covering more than 200 known chemicals, including their molecular structures and exposure conditions. This information was used to train the model to estimate toxicity levels for other byproducts whose health effects remain unknown.

The AI system ultimately predicted the toxicity of more than 1,100 disinfectant byproducts and identified several that may pose significantly higher risks than chemicals currently regulated. Some were estimated to be between two and ten times more toxic than existing EPA-monitored substances. The findings were published in Environmental Science & Technology Letters in January 2026, highlighting a number of compounds that could become priorities for future research and regulation.

Despite these discoveries, the researchers emphasise that drinking water remains safe for the public. The compounds identified represent a broad range of substances that may form under different environmental conditions, not a mixture present in everyday tap water. Water sources and treatment methods vary widely across regions, meaning different byproducts appear in other places. The purpose of the research is to improve understanding, guide smarter regulation, and further enhance water safety. For individuals who wish to reduce exposure even further, household water filters and boiling can help remove inevitable byproducts. As AI continues to refine these predictions, scientists hope it will become a powerful tool in ensuring clean, safe drinking water for generations to come.

More information: Rabbi Sikder et al, Multi-Endpoint Semisupervised Learning Identifies High-Priority Unregulated Disinfection Byproducts, Environmental Science & Technology Letters. DOI: 10.1021/acs.estlett.5c01145

Journal information: Environmental Science & Technology Letters Provided by Stevens Institute of Technology

Researchers Find Physical Activity May Restore Brain Health

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Caring for the brain is a lifelong process, and new research from the AdventHealth Research Institute offers encouraging evidence that everyday habits can help protect cognitive health. The study suggests that maintaining a consistent aerobic exercise routine may keep the brain biologically younger, supporting clearer thinking, stronger memory, and overall mental well-being. Rather than relying on intense training, the benefits stem from steady, manageable physical activity.

Researchers found that adults who followed a structured aerobic exercise programme for one year ended the study with brains that appeared almost a full year younger than those of participants who did not change their activity levels. While the difference may seem modest, scientists stress that even small shifts in brain ageing can accumulate over time, potentially influencing long-term brain health in meaningful ways.

Published in the Journal of Sport and Health Science in August 2025, the study explored whether regular aerobic exercise could slow or slightly reverse “brain age,” a measure derived from MRI scans that estimates how old the brain appears compared with a person’s actual age. When the brain looks older than expected, researchers record a higher brain-predicted age difference, or brain-PAD, which previous studies have linked to poorer physical function, cognitive decline, and increased mortality risk.

Lead author Dr Lu Wan explained that following a simple exercise routine aligned with existing health guidelines was enough to produce measurable changes in brain ageing within just twelve months. Although the absolute changes were small, she noted that even a one-year improvement could become significant when considered across decades. For people concerned about protecting their brain as they age, the findings offer practical and hopeful guidance.

The clinical trial involved 130 healthy adults aged between 26 and 58. Participants were randomly assigned either to an aerobic exercise group or to a control group that continued with their habits. Those in the exercise group completed two supervised hour-long sessions each week and additional home workouts, reaching around 150 minutes of aerobic activity per week, in line with widely recommended physical activity guidelines.

After twelve months, the exercise group showed an apparent reduction in brain age, with brains appearing about 0.6 years younger on average, while the control group showed a slight increase. Although improved fitness did not directly explain the change, researchers believe exercise may influence brain ageing through factors such as reduced inflammation, better blood flow, and subtle structural changes in the brain. The team also highlighted the importance of starting in early to mid-adulthood, when preventative benefits may be most substantial, while noting that longer studies are needed to confirm long-term protection against cognitive decline.

More information: Lu Wan et al, Fitness and exercise effects on brain age: A randomized clinical trial, Journal of Sport and Health Science. DOI: 10.1016/j.jshs.2025.101079

Extensive analysis highlights the biological reasons memory fades with age

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A significant international research effort combining thousands of brain scans with extensive memory testing has provided fresh insight into how physical changes in the brain are linked to declining memory as people grow older. By drawing together data from adults across multiple countries, scientists were able to examine ageing-related brain structure in far greater detail than ever before.

Using more than 10,000 MRI scans alongside over 13,000 memory assessments from roughly 3,700 cognitively healthy participants spanning 13 separate studies, the researchers discovered that the relationship between brain shrinkage and memory decline is far from simple. Rather than progressing steadily, the link becomes much stronger in later life and follows a nonlinear pattern, meaning that faster structural loss leads to disproportionately greater cognitive decline. Crucially, these effects were not explained solely by genetic risk factors commonly associated with Alzheimer’s disease, such as the APOE ε4 variant, pointing to a far more complex biological process underlying brain ageing.

Reported in Nature Communications, the study showed that memory decline is associated with widespread structural change throughout the brain rather than damage confined to one isolated region. Although the hippocampus — long known for its central role in memory — displayed the strongest connection between volume loss and poorer memory performance, numerous cortical and subcortical areas were also involved. Together, these regions formed a gradual pattern of vulnerability, with effects tapering from the hippocampus outward but remaining meaningful across much of the brain. This suggests that cognitive ageing reflects a broad, network-level weakening of brain structure rather than the failure of a single anatomical site.

The researchers also observed substantial differences between individuals. Some people experienced relatively modest brain changes with little impact on memory, while others showed rapid tissue loss accompanied by steep cognitive decline. Once structural shrinkage passed certain thresholds, memory deterioration appeared to accelerate rather than progress in a smooth, predictable way. This pattern was consistent across multiple brain regions, reinforcing the idea that ageing-related memory decline arises from global structural vulnerability, with the hippocampus acting as a particularly sensitive — but not exclusive — indicator.

Senior author Alvaro Pascual-Leone noted that bringing together data from so many research cohorts has produced the most comprehensive picture to date of how the ageing brain changes and how those changes relate to memory. He emphasised that memory loss is not an inevitable consequence of getting older but reflects the interaction between individual biological predispositions and long-term structural processes that can enable neurodegenerative conditions.

Overall, the findings suggest that memory decline in later life is shaped by widespread biological changes accumulating across decades, rather than by one gene or one brain region alone. By recognising this broader vulnerability, researchers may be better positioned to identify people at higher risk earlier and to design more targeted, personalised strategies aimed at maintaining cognitive health and preventing disability as populations age.

More information: Didac Vidal-Piñeiro et al, Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change, Nature Communications. DOI: 10.1038/s41467-025-66354-y

Journal information: Nature Communications Provided by Hebrew SeniorLife Hinda and Arthur Marcus Institute for Aging Research

From gums to the brain: exploring the oral health–dementia link

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Poor oral health may raise the risk of dementia through a combination of biological processes and social factors, according to researchers from Science Tokyo. Drawing on recent epidemiological evidence, the team suggests that problems with eating and speaking may represent underappreciated social pathways that heighten risk by fostering social withdrawal and isolation. In addition, their longitudinal findings indicate that declining oral health is a strong predictor of weight loss among older adults, pointing to broader consequences for physical well-being.

As individuals age, oral health often worsens if it is not adequately cared for. Issues such as tooth loss, weakened jaw muscles, and dry mouth become increasingly common, interfering with essential functions like chewing, swallowing, and speech. Although modern healthcare offers many effective treatments to manage these conditions, poor oral health can still create a foundation for more serious health problems. What may initially seem like minor discomforts can gradually influence nutrition, communication, and overall quality of life.

A growing body of research has identified links between deteriorating oral health and dementia. However, the exact mechanisms driving this association remain uncertain, and scientists have yet to determine whether one condition directly causes the other. Much of the existing research has concentrated on biological explanations, such as the impact of chronic inflammation or the spread of oral bacteria on brain function and immune responses. These studies suggest that poor oral health may prime the body for neurodegeneration, but they leave significant gaps in understanding the whole picture.

Social dimensions of oral function have received far less attention. Difficulties with speaking clearly or eating comfortably can reduce opportunities for social interaction, leading individuals to avoid shared meals or conversations. Over time, this withdrawal may contribute to loneliness and reduced cognitive stimulation, both of which are known risk factors for dementia. Recognising this gap in the literature, a research team led by Professor Jun Aida from the Department of Dental Public Health at Science Tokyo undertook a comprehensive review of recent epidemiological studies better to clarify the relationship between oral health and cognitive decline.

Their analysis incorporated advances in causal inference methods to address long-standing uncertainties around directionality. While many studies proposed a two-way relationship between oral health and dementia, they often failed to account for baseline cognitive function before data collection began. This omission is important, as early cognitive decline may itself increase the likelihood of poor oral hygiene and dental problems, acting as a confounding factor. The researchers highlighted newer studies that have attempted to control for this issue, offering more robust insights into causation.

Crucially, the team emphasised the role of eating and speaking difficulties as potential mediators linking oral health to dementia through social isolation. These everyday functions play a central role in maintaining social connections, and impairments can gradually erode participation in communal activities. Aida noted that when considering the layered pathways leading to dementia across the lifespan, poor oral health may indirectly elevate risk by limiting social engagement through functional decline.

Complementing their review, the researchers also conducted a six-year longitudinal study involving more than 3,000 older adults in Japan. This investigation focused on oral frailty and its relationship to weight loss, revealing that difficulty chewing was the strongest predictor among factors such as dry mouth and missing teeth. The findings underline how oral health can influence nutritional status, which in turn may affect cognitive health.

Together, these studies reinforce the idea that oral health extends far beyond the mouth. It plays a meaningful role in brain function, social participation, and overall physical well-being. The researchers argue that maintaining good oral health throughout life could be an important, yet often overlooked, strategy in reducing dementia risk. Further research will be essential to untangle these complex interactions and to develop interventions that address both the biological and social consequences of declining oral function.

More information: Jun Aida et al, Oral Health and Dementia: Causal Inference and Theoretical Mechanisms, Journal of Dental Research. DOI: 10.1177/00220345251377014

Journal information: Journal of Dental Research Provided by Institute of Science Tokyo

Why Grip Strength Matters as We Grow Older

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New research has highlighted a little-known structure deep within the brain that may be essential for maintaining physical strength as people grow older. Scientists suggest this region could play a key role in identifying early signs of frailty, potentially allowing interventions before noticeable physical decline begins. Rather than focusing solely on muscles, the study points to the brain as a central driver of how well the body preserves strength with age, offering a more complete picture of the ageing process.

The research team used functional MRI scans to observe brain activity in older adults while they completed a revealing yet straightforward task: squeezing a handheld device with maximum effort. This measurement, commonly referred to as a grip strength test, is increasingly recognised as a reliable indicator of overall health and resilience. Although it seems basic, grip strength is closely linked to mobility, recovery from illness, and independence later in life.

One finding stood out clearly among the many brain regions analysed. The strongest predictor of grip strength was the caudate nucleus, a deep brain structure traditionally associated with movement control and decision-making. Until now, its involvement in physical strength and vulnerability in ageing has received little attention. The discovery suggests that this region may act as a central hub connecting neural function with muscular performance.

To reach this conclusion, researchers mapped each participant’s brain communication networks and compared them with recorded grip strength levels. This approach allowed them to see which neural pathways aligned most closely with physical output. The clearest patterns consistently involved the caudate nucleus, showing that stronger connectivity and blood flow in this area were linked to better grip strength, regardless of sex or body composition.

The study involved 60 older adults who each completed multiple brain scans alongside strength testing sessions. The researchers carefully adjusted their data to remove the influence of differences in muscle mass and physical size, ensuring the results reflected brain activity rather than simple physical variation. While a few other brain regions showed weaker connections to grip performance, none matched the influence of the caudate nucleus.

These findings could have significant implications for how frailty is detected and managed. Since grip strength is already a simple clinical tool, linking it to specific brain networks may lead to earlier and more precise assessments of physical decline. In the long term, scientists hope this knowledge could support targeted therapies aimed at strengthening neural connections, much like physical exercise strengthens muscles. Although further research is needed, the study provides a promising step towards understanding ageing as an interconnected brain–body process rather than a purely physical one.

More information: Amin Ghaffari et al, Connectome-based predictive modeling of grip strength: a marker of physical frailty, Frontiers in Neuroscience. DOI: 10.3389/fnins.2025.1697908

Journal information: Frontiers in Neuroscience Provided by University of California – Riverside

Maintaining Heart Health for Older Male Sportsmen

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Veteran male endurance athletes who have spent many years training at high intensity may face a higher risk of serious heart rhythm problems during exercise, according to new research from the University of Leeds funded by the British Heart Foundation. The study suggests that this increased risk is linked not to how much or how hard these athletes train, but to whether they already have scarring in their heart muscle.

The research focused on male endurance athletes aged over 50, a group that accounts for the vast majority of sudden cardiac deaths occurring during sport. The team set out to determine whether high levels of exercise could trigger a potentially life-threatening heart rhythm disturbance known as ventricular tachycardia in these athletes. Their findings indicate that exercise itself is not inherently dangerous, but it may act as a trigger for abnormal rhythms in individuals who already have underlying heart damage.

In the study, the researchers closely monitored 106 healthy male endurance athletes who had been running or cycling for more than 10 hours a week for at least 15 years. Participants wore smart watches and heart rate monitors to track all their physical activity, while implantable loop recorders placed under the skin continuously recorded their heart rhythms. This allowed the researchers to precisely match episodes of abnormal heart rhythm with specific periods of exercise.

Over the two-year study period, around one in four participants experienced ventricular tachycardia during or shortly after exercise. Most of these episodes were non-sustained, meaning they were brief and usually less dangerous, but they can still act as warning signs for more serious events. Importantly, around three-quarters of the athletes who experienced these abnormal rhythms were found to have scarring in their hearts. The few longer and more dangerous sustained episodes of ventricular tachycardia all occurred during exercise and exclusively in athletes with heart scarring.

Crucially, the researchers found no evidence that those who developed abnormal heart rhythms were training more frequently or at higher intensity than those who did not. This reinforces the conclusion that exercise alone is not the cause of the problem. Instead, the presence of scar tissue appears to increase vulnerability, with physical exertion acting as a trigger rather than the underlying source of risk.

Many of the athletes were unaware that they had heart scarring before taking part in the study, highlighting the importance of regular cardiac health checks for older male endurance athletes. Heart scarring can result from previous heart attacks, underlying disease, or many years of intense endurance exercise, and it may remain undetected without specialist screening.

The researchers also emphasise the value of wearable technology for athletes who wish to monitor their heart health. Sudden, unexplained spikes in heart rate, especially when accompanied by symptoms such as feeling unwell or light-headed, should prompt athletes to reduce intensity or seek medical advice. The study is the first to combine long-term wearable activity data with continuous heart rhythm monitoring, and the team hopes it will inform future research in other athletic populations, including women and younger athletes.

More information: Wasim Javed et al, The Timing and Relationship of Ventricular Arrhythmia with Exercise Patterns in Veteran Male Endurance Athletes, European Journal of Preventive Cardiology. DOI: 10.1093/eurjpc/zwag021

Journal information: European Journal of Preventive Cardiology Provided by University of Leeds

Why Cooler Bedroom Temperatures Benefit the Heart While You Sleep

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Maintaining a bedroom temperature of around 24°C overnight can help reduce stress responses in older adults during sleep, according to new research from Griffith University.

The study, led by Dr Fergus O’Connor from Griffith’s School of Allied Health, Sport and Social Work, examined how higher night-time bedroom temperatures affect heart rate and physiological stress in people aged 65 and over. The findings suggest that keeping bedrooms at 24°C while sleeping lowers the likelihood of heightened stress responses during the night.

Dr O’Connor explained that exposure to heat triggers a natural physiological reaction in the body, causing the heart rate to rise. As temperatures increase, the heart works harder to circulate blood towards the skin in an effort to dissipate heat and cool the body. While this response is regular, prolonged periods of elevated heart activity place additional strain on the cardiovascular system and reduce the body’s ability to recover from heat exposure accumulated during the day.

When the heart continues to work harder for extended periods overnight, this added stress can interfere with the restorative functions of sleep. Over time, such strain may have implications for overall cardiovascular health, particularly in older adults who are more vulnerable to heat-related stress.

To capture real-world data, participants in the study wore fitness activity trackers on their non-dominant wrist to continuously monitor heart rate and stress indicators. Bedroom temperatures were recorded using installed temperature sensors, allowing researchers to closely track environmental conditions throughout the Australian summer-long data collection period. This approach enabled the team to assess how naturally occurring temperature variations influenced physiological responses during sleep, rather than relying on laboratory-based simulations.

The findings provide some of the first real-world evidence demonstrating how increased bedroom temperatures can affect heart rate and stress responses overnight. According to Dr O’Connor, the results highlight an often-overlooked aspect of thermal health: night-time indoor conditions.
The research also has broader implications in the context of climate change. Rising global temperatures are increasing the frequency of hot nights, which may independently contribute to higher rates of cardiovascular illness and mortality. This occurs not only through direct heat exposure but also by disrupting sleep and impairing the body’s autonomic recovery processes that generally take place overnight.

Despite the known risks associated with excessive indoor heat during the day, clear guidance for nighttime temperatures is lacking. While there are established recommendations for maximum indoor daytime temperatures, set at 26°C, no equivalent standards exist for overnight sleeping environments. The researchers suggest that developing evidence-based guidelines for nighttime bedroom temperatures could play an essential role in protecting cardiovascular health as climates continue to warm.

More information: Fergus K. O’Connor et al, Effect of nighttime bedroom temperature on heart rate variability in older adults: an observational study, BMC Medicine. DOI: 10.1186/s12916-025-04513-0

Journal information: BMC Medicine Provided by Griffith University

Beyond the Night: Researchers Point to Daytime Function as a Core Measure of Insomnia Treatment Success

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About one in nine adults experiences chronic insomnia, a condition that reaches well beyond disrupted sleep at night. Many individuals continue to struggle during the day with persistent drowsiness, slowed thinking, memory problems, and irritability. When insomnia is left untreated, it is also linked to increased long-term health risks, including diabetes and cardiovascular disease. Despite the wide range of available treatments, from prescription medications to behavioural interventions, clinicians still face a central challenge: accurately determining how effective a given treatment is for a particular patient, especially in terms of how that patient functions during waking hours.

A new study from the University of Maryland School of Medicine suggests that smartphone-based, real-time assessments provide a more precise way to evaluate the effectiveness of insomnia treatments. Rather than relying solely on traditional questionnaires that ask patients to summarise their symptoms after the fact, the researchers used a method that captured experiences as they occurred throughout the day. This approach allowed the study team to detect changes in key daytime symptoms of insomnia, including fatigue, cognitive functioning, and mood, with greater sensitivity than conventional recall-based tools. The findings were published in JAMA Network Open.

The study was designed as a randomised clinical trial involving 40 older adults aged between 60 and 85, all of whom met criteria for chronic insomnia. Participants were randomly assigned to receive either the sleep medication suvorexant or a placebo for 16 consecutive nights. Throughout the study period, participants used a smartphone app to report their daytime symptoms in real time, completing brief assessments four times per day. In parallel, they also completed standard questionnaires evaluating sleep quality and daytime functioning before and after the treatment phase, enabling a direct comparison between traditional and real-time measurement methods.

When the results were analysed, essential differences emerged between the two assessment approaches. Conventional questionnaires identified an overall improvement in insomnia severity in the treatment group compared with the placebo group, but they failed to detect meaningful differences in daytime symptoms. By contrast, the smartphone-based method, known as ecological momentary assessment, revealed subtle but clinically relevant patterns across the day. Participants taking suvorexant reported greater fatigue in the morning but less fatigue in the afternoon and evening compared with those taking a placebo. A similar pattern was seen for cognition, with reduced alertness earlier in the day that normalised as the day progressed. These time-specific effects would likely have gone unnoticed using retrospective questionnaires alone.

Mood changes were also examined. Although participants in the suvorexant group reported slightly worse mood ratings at each of the four daily assessment points compared with the placebo group, these differences were not statistically significant. Importantly, participants reported high satisfaction with the smartphone-based assessments. The completion rate exceeded 93 per cent across all surveys, demonstrating that frequent, real-time symptom tracking was both feasible and well accepted, even among older adults.

“Daytime symptoms such as fatigue, cognitive impairment, and mood disturbances are core features of insomnia,” said Emerson M. Wickwire, the study’s corresponding author and section chief of sleep medicine at the University of Maryland Medical Center. He emphasised that improving sleep alone does not fully address the condition from the patient’s perspective, noting that retrospective questionnaires often miss subtle but meaningful changes in daily functioning that matter most to those living with insomnia.

As the first randomised controlled trial to incorporate smartphone-based ecological momentary assessment as an outcome measure in a sleep-focused study, this research highlights the potential of digital tools to reshape insomnia research and care. According to Mark T. Gladwin, Dean of the University of Maryland School of Medicine, real-time smartphone assessments offer valuable insights that could improve how treatments are evaluated, personalised, and ultimately delivered, benefiting millions of people affected by sleep disorders.

More information: Emerson M. Wickwire et al, Smartphone-Based Real-Time Assessment of Daytime Insomnia Symptoms With Suvorexant, JAMA Network Open. DOI: 10.1001/jamanetworkopen.2025.50186

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

Tissue repair slows with age. These proteins help restore it.

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As we grow older, the body’s ability to bounce back from injury or illness steadily weakens. Cuts heal more slowly, organs recover less completely, and the cumulative wear of time becomes harder to repair. New research from the University of California, San Francisco, suggests this decline may not be inevitable. Scientists there have identified a group of gene regulators — proteins that control when genes are switched on or off — that appear capable of restoring some of the ageing body’s lost capacity for self-repair.

The researchers focused on fibroblasts, a vital but often overlooked type of cell. Fibroblasts construct and maintain the scaffolding that sits between cells, providing shape, strength, and structural support to tissues and organs throughout the body. This cellular framework is constantly under strain from everyday wear, illness, and injury, and fibroblasts typically work continuously to repair and renew it. With advancing age, however, these cells become less active, and the tissues they support begin to deteriorate.

As fibroblasts slow down, the consequences ripple outward. Structural damage accumulates, healing becomes inefficient, and organs become more vulnerable to disease. When the scientists examined older fibroblasts, they found clear molecular signs of decline, particularly in the way these cells expressed their genes. Patterns that were once tightly regulated had become disordered, reflecting the broader breakdown in cellular function associated with ageing.

Using computational analysis, the team traced these changes back to a specific set of transcription factors — gene regulators that orchestrate large networks of genetic activity. These factors appeared to be key drivers of the ageing process in fibroblasts. By identifying which transcription factors were responsible, the researchers uncovered a potential way to reverse age-related changes at their source, rather than simply treating their downstream effects.

To test this idea, the scientists compared gene expression in young and old fibroblasts grown in laboratory dishes, then used advanced modelling to pinpoint which transcription factors were pushing cells towards an aged state. They subsequently used CRISPR-based techniques to adjust the activity of these factors in older fibroblasts. Remarkably, altering the levels of any one of thirty transcription factors was enough to trigger a youthful pattern of gene expression. In particular, changes to four of these regulators significantly improved cellular metabolism and restored the cells’ ability to multiply — two hallmarks of younger, healthier fibroblasts.

The work extended beyond cell cultures into living organisms. In collaboration with colleagues specialising in anatomy and ageing, the team showed that increasing levels of a transcription factor called EZH2 rejuvenated the livers of elderly mice. These animals, roughly equivalent in age to humans in their mid-sixties, showed dramatic improvements: liver fibrosis was reversed, fat accumulation was reduced by half, and glucose tolerance improved. Together, the findings suggest that carefully reprogramming gene regulation could one day form the basis of therapies aimed at treating, or even reversing, diseases driven by ageing rather than simply managing their symptoms.

More information: Janine Sengstack et al, Systematic identification of single transcription factor perturbations that drive cellular and tissue rejuvenation, Proceedings of the National Academy of Sciences. DOI: 0.1073/pnas.2515183123

Journal information: Proceedings of the National Academy of Sciences Provided by University of California – San Francisco

Greenland Shark Research Could Unlock New Approaches to Protecting Ageing Vision

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Dorota Skowronska-Krawczyk sits in her office, her gaze fixed on the computer monitor in front of her. On the screen, a Greenland shark glides slowly through the dark, clouded waters of the Arctic Ocean. She points to the image as it plays. “You can see the eye move,” says the UC Irvine associate professor of physiology and biophysics. “It’s tracking the light. That’s what’s so fascinating.” What looks like a sluggish, indifferent animal reveals a subtle awareness that immediately challenges long-standing assumptions.

The video shows the world’s longest-living vertebrate: a thick, grey shark with a heavy body, small head and blunt snout. Its eyes appear opaque and lifeless, further obscured by a parasite attached to one eyeball. For years, scientists believed Greenland sharks were functionally blind, citing both the frequent presence of these parasites and the extremely dim, murky environment in which the animals live. Vision, it was assumed, was not necessary. Yet the deliberate movement of the eye towards light tells a different story, hinting at an unexpected sensory resilience.

New research led by Skowronska-Krawczyk is now reshaping what scientists understand about ageing, vision and longevity. Co-authored with Walter Salzburger and Lily G. Fogg from the University of Basel, the study examines Greenland shark vision through an evolutionary lens. Published in Nature Communications on 5 January, the findings suggest that these sharks rely on a powerful DNA repair mechanism that allows them to preserve retinal health over centuries. Some Greenland sharks are estimated to live for as long as 400 years, yet their eyes show no signs of retinal degeneration and appear finely adapted to extreme low-light conditions.

Skowronska-Krawczyk traces her interest in the Greenland shark’s visual system to a 2016 paper by marine biologist John Fleng Steffensen. That study noted how commonly parasites attach themselves to the sharks’ eyes, raising an evolutionary puzzle. “You don’t keep an organ you don’t need,” she explains. After watching numerous videos, she noticed something others had missed: the sharks actively moved their eyeballs towards light. That observation prompted a deeper investigation and ultimately led to the current study.

The sharks used in the research were caught between 2020 and 2024 using scientific long lines near the University of Copenhagen’s Arctic Station on Disko Island, Greenland. Their eyeballs were dissected, preserved and sent for analysis to Skowronska-Krawczyk’s lab. Emily Tom, a PhD student and physician-scientist in training, remembers opening the package to find a massive, centuries-old eyeball resting on dry ice. Used to working with mouse eyes, she had to adapt quickly. Through careful histological analysis, Tom found no signs of cell death and confirmed that rhodopsin, a protein crucial for low-light vision, remained active. For Skowronska-Krawczyk, these findings offer promising insights into how vision might be preserved as humans age.

More information: Lily G. Fogg et al, The visual system of the longest-living vertebrate, the Greenland shark, Nature Communications. DOI: 10.1038/s41467-025-67429-6

Journal information: Nature Communications Provided by University of California – Irvine

Links Between Reproductive History and Biological Ageing

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Researchers at the University of Helsinki and the Minerva Foundation Institute for Medical Research report that both the number of children a woman has and the timing of her pregnancies are associated with health in adulthood and overall life expectancy. Their findings suggest that reproductive history is reflected not only in later-life outcomes such as longevity, but also in broader patterns of ageing across the life course.

The analysis is based on a long-running twin cohort study in which participants were first invited to complete a comprehensive questionnaire in 1975. Since then, their lives have been followed at regular intervals for several decades. This extensive follow-up has allowed researchers to link early and midlife reproductive patterns with long-term health trajectories, making it possible to examine ageing and mortality outcomes in considerable detail.

Drawing on data from nearly 15,000 participants, the researchers found that women with two or three children tended, on average, to live the longest. The timing of pregnancies also appeared to be important. Women whose pregnancies occurred roughly between the ages of 24 and 38 showed more favourable ageing profiles and greater longevity than those whose pregnancies fell outside this range. These results point to a complex relationship between reproduction and ageing rather than a simple linear effect.

In contrast, women with an above-average number of children—defined in this study as more than four—were found to have shorter lifespans and signs of accelerated biological ageing. According to the researchers, this pattern is consistent with life history theory in evolutionary biology, which emphasises trade-offs in how organisms allocate limited resources. “From an evolutionary biology perspective, organisms have finite resources such as time and energy,” explains doctoral researcher Mikaela Hukkanen. “When a large share of these resources is invested in reproduction, fewer remain available for bodily maintenance and repair, which may ultimately reduce lifespan.”

One unexpected finding was that childless women also showed faster ageing than women with a small number of children. The authors caution that this association may be influenced by other lifestyle, social, or health-related factors that could not be fully controlled for in the analyses. They also stress that the results apply only at the population level. The study does not establish cause-and-effect relationships and should not be interpreted as guidance for individual reproductive decisions, particularly given that family size and age at first birth have changed substantially since the period covered by the data. “An individual woman should not consider changing her own plans or wishes regarding children based on these findings,” says study lead Dr Miina Ollikainen.

A novel aspect of the research was the inclusion of biological measures of ageing alongside mortality data. Epigenetic clocks were calculated from blood samples provided by more than one thousand participants, allowing researchers to estimate biological ageing by measuring molecular changes linked to the gradual deterioration of cells and tissues. These measures supported the mortality findings: women with either many children or no children at all were biologically older than their chronological age. “People who are biologically older than their calendar age face a higher risk of death,” Ollikainen notes. “Our results show that life history choices leave lasting biological imprints that can be detected long before old age.”

More information: Mikaela Hukkanen et al, Epigenetic aging and lifespan reflect reproductive history in the Finnish Twin Cohort, Nature Communications. DOI: 10.1038/s41467-025-67798-y

Journal information: Nature Communications Provided by University of Helsinki

Brazil’s blueprint for long life: genetic insights from the world’s oldest citizens

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A Viewpoint published today in Genomic Psychiatry by Dr Mayana Zatz and colleagues from the Human Genome and Stem Cell Research Center at the University of São Paulo explores why Brazil stands out as one of the world’s most promising yet underexplored settings for research into extreme human longevity. Drawing on the team’s long-running national study of exceptionally old individuals, the article situates Brazilian findings within the rapidly evolving field of supercentenarian biology, arguing that current models of ageing remain incomplete without greater ancestral diversity.

Why a small minority of humans live well beyond 110 years while most never reach 100 remains one of biomedicine’s most persistent puzzles. According to the authors, a central obstacle lies not in methodology but geography. The overwhelming majority of genomic datasets are drawn from relatively homogeneous populations, leaving admixed groups largely absent. This imbalance is particularly damaging in longevity research, where rare protective variants may be enriched in genetically diverse individuals yet remain invisible in standard reference populations.

Brazil’s population history provides a uniquely powerful counterpoint to this limitation. Centuries of admixture shaped by Indigenous ancestry, Portuguese colonisation, the forced migration of millions of enslaved Africans, and later European and Japanese immigration have produced extraordinary genomic diversity. Large-scale studies of older Brazilians have already revealed millions of previously undocumented genetic variants, including mobile element insertions and immune-related alleles missing from global databases, many of which may influence ageing, disease resistance, and resilience.

Against this backdrop, the research team has assembled an exceptional longitudinal cohort comprising more than 160 centenarians, including 20 validated supercentenarians from diverse regions and socioeconomic backgrounds. Several participants remained cognitively intact and functionally independent well into extreme old age, despite having lived most of their lives with limited access to modern healthcare. The cohort includes globally recognised longevity outliers, offering rare insight into survival mechanisms that appear to operate independently of sustained medical intervention.

Familial clustering within the cohort further strengthens the case for a genetic contribution to exceptional longevity. One family includes a 110-year-old woman alongside nieces aged 100, 104, and 106, reflecting patterns seen in earlier studies showing markedly increased longevity among siblings of centenarians. Such lineages provide a valuable opportunity to examine how polygenic inheritance and epigenetic regulation may interact to promote long-term physiological resilience.

The Viewpoint also synthesises emerging biological signatures of supercentenarians, highlighting preserved immune competence, efficient protein maintenance, and adaptive immune cell profiles more typical of younger individuals. These traits help explain striking observations such as survival from COVID-19 before vaccination in several cohort members. Collectively, the authors argue that supercentenarians exemplify not delayed decline but active resistance to ageing, and that Brazil’s unparalleled genetic landscape offers a critical opportunity to advance global understanding of healthy human longevity while addressing long-standing inequities in biomedical research.

More information: Mateus V. de Castro et al, Insights from Brazilian supercentenarians, Genomic Psychiatry. DOI: 10.61373/gp026v.0009

Journal information: Genomic Psychiatry Provided by Genomic Press