Category: Ageing

Categories : Ageing NeurologyTags :

Poor Sleep May Accelerate Brain Ageing

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Poor sleep may accelerate brain ageing, a new study shows. Photo by Andrea Piacquadio

People who sleep poorly are more likely than others to have brains that appear older than they actually are. This is according to a comprehensive brain imaging study from Karolinska Institutet, published in the journal eBioMedicine. Increased inflammation in the body may partly explain the association.

Poor sleep has been linked to dementia, but it is unclear whether unhealthy sleep habits contribute to the development of dementia or whether they are rather early symptoms of the disease. In a new study, researchers at Karolinska Institutet have investigated the link between sleep characteristics and how old the brain appears in relation to its chronological age. 

The study includes 27 500 middle-aged and older people from the UK Biobank who underwent magnetic resonance imaging (MRI) of the brain. Using machine learning, the researchers estimated the biological age of the brain based on over a thousand brain MRI phenotypes. 

Low-grade inflammation 

The participants’ sleep quality was scored based on five self-reported factors: chronotype (being a morning/evening person), sleep duration, insomnia, snoring, and daytime sleepiness. They were then divided into three groups: healthy (≥ 4 points), intermediate (2-3 points), or poor (≤ 1 point) sleep. 

“The gap between brain age and chronological age widened by about six months for every 1-point decrease in healthy sleep score,” explains Abigail Dove, researcher at the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, who led the study. “People with poor sleep had brains that appeared on average one year older than their actual age.” 

To understand how poor sleep can affect the brain, the researchers also examined levels of low-grade inflammation in the body. They found that inflammation could explain just over ten per cent of the link between poor sleep and older brain age. 

“Our findings provide evidence that poor sleep may contribute to accelerated brain ageing and point to inflammation as one of the underlying mechanisms,” says Abigail Dove. “Since sleep is modifiable, it may be possible to prevent accelerated brain ageing and perhaps even cognitive decline through healthier sleep.” 

Several possible explanations 

Other possible mechanisms that could explain the association are negative effects on the brain’s waste clearance system, which is active mainly during sleep, or that poor sleep affects cardiovascular health, which in turn can have a negative impact on the brain. 

Participants in the UK Biobank are healthier than the general UK population, which could limit the generalisability of the findings. Another limitation of the study is that the results are based on self-reported sleep. 

The study was conducted in collaboration with researchers from the Swedish School of Sport and Health Sciences, and Tianjin Medical University and Sichuan University in China, among others. It was funded by the Alzheimer’s Foundation, the Dementia Foundation, the Swedish Research Council, the Loo and Hans Osterman Foundation for Medical Research, and the Knowledge Foundation. The researchers report no conflicts of interest. 

Source: Karolinska Institutet

Categories : Ageing Neurodegenerative DiseasesTags :

Is Physical Frailty a Cause of Dementia?

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A new study suggests that physical frailty may contribute to the development of dementia. The study was published on September 17, 2025, in Neurology®, the medical journal of the American Academy of Neurology.

Physical frailty is defined as having three or more of these five symptoms: often feeling tired; little or no physical activity; slow walking speed; low grip strength; and unintentional weight loss.

“We’ve known that frailty is associated with a higher risk of dementia, but our study provides evidence that frailty may be an actual cause of dementia,” said study author Yacong Bo, PhD, of Zhengzhou University in China. “On the other hand, despite this new evidence, we can’t rule out the possibility that frailty is instead a marker of the early changes in the disease process.”

The study involved 489 573 people with an average age of 57 who were followed for an average of 14 years. A total of 4.6% of the participants met the definition for frailty, with three or more of the symptoms. Another 43.9% who had one or two symptoms were categorised as pre-frailty and 51.5% had no symptoms and were categorised as not frail.

During the study, 8900 people developed dementia. A total of 4.6% of those with frailty developed dementia, compared to 2.2% of those with pre-frailty and 1.3% of those without frailty. After researchers adjusted for other factors that could affect the risk of dementia, such as age, education level and physical activity, they found that the people who met the definition for frailty were nearly three times more likely to develop dementia than those who had no symptoms of frailty.

Those categorised as pre-frailty were 50% more likely to develop dementia. People with frailty who also had genes linked to dementia were nearly four times more likely to develop dementia than those without frailty or the genetic risk. The researchers also analysed the data and found evidence suggesting that frailty may potentially be a factor in causing dementia.

“These findings reinforce the importance of identifying and managing frailty as a strategy for preventing dementia,” Bo said.

Looking at the data from the other direction, the researchers found that dementia is unlikely to increase the risk of frailty. The researchers also looked at brain imaging and biological biomarkers and found that people with frailty were more likely to have changes in their brain structure related to dementia.

“These biomarkers may be a mechanism underlying the pathway from frailty to dementia,” said Bo. A limitation of the study was that four of the five symptoms of frailty were reported by the participants, so they may not have provided accurate information.

Source: American Academy of Neurology

Categories : Ageing Cardiovascular DiseaseTags :

New Research Finds Visceral Fat is Linked to Heart Ageing

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Photo by Anna Shvets

Excessive amounts of visceral fat, the hidden fat surrounding organs, is linked with faster ageing of the heart, a new study has found. Ageing is the biggest risk factor for heart disease but why some people age faster than others isn’t fully understood.

The scientists leading the research, which is published in the European Heart Journal, say that visceral body fat could play an important role in accelerating ageing of the heart and blood vessels. This type of fat is known to be harmful to health and this study now links it to faster heart ageing.

Sex differences

The study, led by scientists from the Medical Research Council (MRC) Laboratory of Medical Sciences, also found differences between men and women. They discovered that fat around the hips and thighs could potentially slow heart ageing in women. The scientists analysed data from 21 241 participants in UK Biobank, which includes whole body imaging to map the amount of fat and where it is located in the body. The study was

Determining an individual’s ‘heart age’

The UK Biobank data also includes detailed imaging of the heart and blood vessels. Artificial intelligence (AI) was used to analyse these images to capture signs of organ ageing such as tissues becoming stiff and inflamed. An individual was given a ‘heart age’ which can be compared to their actual age at the time of the scan.

The risks of ‘hidden’ fat

The researchers found that faster heart ageing was linked to having more visceral adipose tissue. Visceral adipose tissue is fat found deep inside the abdomen around organs such as the stomach, intestines, and liver. This type of fat cannot be seen from the outside, and some people can have large amounts of visceral fat despite having a healthy weight.

Premature ageing

The researchers found signs on blood tests that visceral fat is linked to increased inflammation in the body, which is a potential cause of premature ageing. They also found differences between the sexes. Male-type fat distribution, which is fat around the belly and often called ‘apple-shaped’, was particularly predictive of early ageing in men.

The role of hormones

In contrast, a genetic predisposition to female-type fat, primarily fat on the hips and thighs, often called ‘pear-shaped’, was protective against heart ageing in women. The researchers also found a link between higher oestrogen levels in pre-menopausal women and a slowing of heart ageing. They suggested that this could indicate a role for hormones in protecting against heart ageing.

Increasing healthy lifespan

Professor Declan O’Regan, who led the research at the MRC Laboratory of Medical Sciences and Imperial College London, said:

We have known about the apple and pear distinction in body fat, but it hasn’t been clear how it leads to poor health outcomes. Our research shows that ‘bad’ fat, hidden deep around the organs, accelerates ageing of the heart.

But some types of fat could protect against ageing, specifically fat around the hips and thighs in women.

We also showed that body mass index wasn’t a good way of predicting heart age which underscores the importance of knowing where fat is stored in the body and not just total body weight.

The goal of our research is to find ways to increase healthy lifespan. While being active is important, we found that hidden fat could still be harmful even in fit people.

In the future, we plan to investigate how drug therapies, such as GLP-1 inhibitors (for example, Ozempic) could improve not just diabetes and obesity but target the ageing effects of hidden visceral fat.

Source: UK Research Institute

Categories : Ageing RheumatologyTags :

Immune Ageing Found to Drive – Not Be Driven by – Rheumatoid Arthritis

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Rheumatoid arthritis. Credit: Scientific Animations CC4.0

Features of immune system ageing can be detected in the earliest stages of rheumatoid arthritis (RA), even before clinical diagnosis, a new study has found which provides at-risk individuals with hope for early intervention.

The research led by academics at the University of Birmingham, delivered through the National Institute for Health and Care Research (NIHR) Birmingham Biomedical Research Centre, and published in the journal eBioMedicine shows that individuals with joint pain or undifferentiated arthritis already exhibit signs of a prematurely aged immune system, suggesting that immune ageing may play a direct role in the development of RA.

The study involved 224 participants across various stages of RA development and was funded by FOREUM and the European League Against Rheumatism (EULAR). It represents one of the most comprehensive analyses of immune ageing in RA to date.

Researchers found that patients with early immune ageing features were more likely to develop RA. These findings could lead to the development of predictive tools that identify at-risk individuals and enable timely treatment.

“We’ve discovered that immune ageing isn’t just a consequence of rheumatoid arthritis—it may be a driver of the disease itself,” said Dr Niharika Duggal, senior author of the study and Associate Professor in Immune Ageing at the University of Birmingham. “We found that people in the early stages of rheumatoid arthritis ie, before a clinical diagnosis show signs of faster immune system ageing.

“These findings suggest we might be able to intercept the disease development in at-risk individuals and prevent it from developing by using treatments that slow ageing, such as boosting the body’s natural process for clearing out damaged cells (autophagy).”

Key Findings

  • Hallmarks of immune ageing, including reduced naïve T cells and thymic output, were observed in patients with early joint symptoms.
  • An elevated IMM-AGE score revealed accelerated immune ageing in patients before RA diagnosis.
  • Elevated levels of inflammatory markers (such as IL-6, TNFα, and CRP) were found in preclinical stages.
  • Advanced ageing features, including senescent T cells and inflammatory Th17 cells, appeared only after RA was fully established.

The study suggests that targeting ageing pathways could offer new strategies to prevent RA. Future research should determine whether geroprotective drugs such as spermidine (autophagy booster), senolytics (clearance of senescent cells) and metformin (attenuates inflammation and boosts autophagy) may help slow or halt disease progression in high-risk individuals.

Source: University of Birmingham

Categories : AgeingTags :

Study Explains Why Influenza is More Deadly for Older People

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Scientists have discovered why older people are more likely to suffer severely from the flu, and can now use their findings to address this risk. In a new study published in PNAS, experts discovered that older people produce a glycosylated protein called apoplipoprotein D (ApoD), which is involved in lipid metabolism and inflammation, at much higher levels than in younger people. This has the effect of reducing the patient’s ability to resist virus infection, resulting in a more serious disease outcome.

The team established that highly elevated ApoD production with age in the lung drives extensive tissue damage during infection to reduce the protective antiviral type I interferon response.

The research was an international collaboration led by scientists from the China Agricultural University, University of Nottingham, Institute of Microbiology (Chinese Academy of Sciences), National Institute for Viral Disease Control and Prevention (Chinese Centre for Disease Control and Prevention) and the University of Edinburgh.

Aging is a leading risk factor in influenza-related deaths. Furthermore, the global population is aging at an unprecedented rate in human history, posing major issues for healthcare and the economy. So we need to find out why older patients often suffer more severely from influenza virus infection.”

Professor Kin-Chow Chang from the School of Veterinary Medicine and Science at the University of Nottingham, and co-author on the paper

In this new study, the team investigated the mechanisms behind increased severity of influenza virus infection with age using an aging-mouse model and appropriate donor human tissue sections.

They identified ApoD as an age-related cell factor that impairs the activation of the immune system’s antiviral response to influenza virus infection by causing extensive breakdown of mitochondria (mitophagy) resulting in greater production of virus and lung damage during infection. Mitochondria are essential for cellular production of energy and for induction of protective interferons.

ApoD is therefore a target for therapeutic intervention to protect against severe influenza virus infection in the elderly which would have a major impact on reducing morbidity and mortality in the aging population.

Professor Chang, added: “There is now an exciting opportunity to therapeutically ameliorate disease severity of the elderly from influenza virus infection by the inhibitory targeting of ApoD.”

Source: University of Nottingham

Categories : AgeingTags :

Centenarians Develop Diseases More Slowly

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Reaching the age of 100 does not necessarily mean a life fraught with illness. A new study from Karolinska Institutet shows that centenarians not only live longer, they also stay healthier than other older people, with fewer diseases that develop more slowly.

The study, published in eClinicalMedicine, compared people who reached the age of 100 with those who died earlier. The results show that centenarians not only suffer from fewer diseases, they also develop them more slowly.

While many older people accumulate several diagnoses quickly during their final years, the disease burden of centenarians seems to level off from around the age of 90. They more often have diseases that are limited to a single organ system and significantly fewer concurrent conditions.

The study also shows that cardiovascular disease is less common and occurs later in life among centenarians. Neuropsychiatric diseases are also less prevalent among those who live the longest.

”Our results challenge the widespread belief that a longer life inevitably means more diseases. We show that centenarians follow a distinct ageing curve, with slower disease progression and greater resistance to common age-related diseases,” says last author Karin Modig, associate professor at the Institute of Environmental Medicine, Karolinska Institutet.

Ages in a different ways

The study covered the entire Swedish birth cohort between 1920 and 1922, totalling over 270,000 individuals. The researchers followed the participants’ health from the age of 70 and up to three decades. The progression of disease in centenarians was compared with those who lived shorter lives using national health registers. The results show that centenarians not only delay disease – they seem to age in a fundamentally different way.

”We show that exceptional longevity is not just about delaying ill health. It reflects a unique pattern of ageing. The results suggest that centenarians have preserved homeostasis and resistance to disease despite ageing and physiological stresses – something that may be due to a favourable combination of genes, lifestyle and environment,” says Karin Modig.

The study was funded by Karolinska Institutet. No conflicts of interest have been reported.

Publikation

”Disease accumulation and distribution across the lifespan in Swedish centenarians and non-centenarians: a nationwide life course comparison of longevity and health resilience”, Yuge Zhang, Shunsuke Murata, Katharina Schmidt-Mende, Marcus Ebeling, Karin Modig, eClinicalMedicine, online August 4, 2025, doi: 10.1016/j.eclinm.2025.103396

Source: Karolinska Institutet

Categories : Ageing Expert OpinionTags :

From Lifespan to Healthspan: Why Preventive Healthcare Matters Now More Than Ever

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South Africa is facing a major health transition. While the average life expectancy has nearly doubled over the past century, the quality of those additional years, commonly referred to as one’s ‘healthspan,’ remains under threat from non-communicable diseases (NCDs). This threat calls for a renewed national focus on prevention and early intervention to address the rapidly growing challenge.

The Healthspan Imperative

According to health data presented at the 2025 Momentum Healthcare Insights Summit, NCDs such as heart disease, cancer, diabetes and neurodegenerative disorders now account for 51% of all deaths in South Africa. In contrast, communicable diseases make up around 40% and non-natural causes (like accidents and violence) account for a mere 9%. This shift reflects a global trend, although some challenges remain; infectious diseases become more manageable, while chronic conditions associated with lifestyle and ageing take centre stage.

Damian McHugh, Chief Marketing Officer at Momentum Health

“Medical advances have added years to our lives, but not necessarily life to our years. More and more, there is growing evidence to support the fact that prevention offers the greatest potential to reduce the burden as well as cost of chronic disease and improve quality of life,” says Damian McHugh, Chief Marketing Officer at Momentum Health.

Prevention Outperforms Treatment

The summit highlighted compelling evidence that prevention is more effective than treatment for advanced disease. For example, research from the American Cancer Society shows that tobacco control measures, such as smoking bans and taxes, have prevented 3.8 million lung cancer deaths in the United States since 1970. The most effective way to save lives from late-stage lung cancer has not been through treatment, but through reducing or eliminating smoking altogether.

The same principle applies to other chronic diseases. Managing risk factors such as high blood pressure, obesity, high blood glucose, and abnormal cholesterol can actively prevent or delay the onset of disease. These factors are strongly influenced by behaviours such as a lack of physical activity, poor nutrition, unmanaged stress levels, and even excessive alcohol use or smoking.

Investing in regular health check-ups and preventative care can mitigate the risk of serious health problems, ultimately reducing the incidence of costly, advanced illnesses. Simple lifestyle changes, such as prioritising rest and recovery, making time to connect with loved ones, maintaining balanced nutrition, practicing mindfulness, and engaging in regular exercise not only promotes physical and mental health, but can also translate into significant long-term savings in healthcare costs.

“Making quality healthcare more accessible, while enabling and rewarding healthy, preventative habits can lead to complete physical and mental health and wellbeing. Investing in access and wellbeing is a powerful pathway to realising more wealth and more health for more South Africans,” says McHugh.

Measuring and Managing Healthspan within the South African Context

Momentum Health’s data reveals that many South Africans are living longer, but the average age of medical scheme beneficiaries has increased by nearly three years over the past decade, and the proportion of pensioners in medical schemes is rising. Without proactive measures, our nation’s ailing healthcare system will face increasing claims and costs as the population ages and chronic diseases become more prevalent.

Momentum Health believes that the solution lies in taking measures to improve access to both quality medical care and reliable health information and empowering individuals to take responsibility for their own health.

South Africa’s rising NCD burden is not inevitable. With early detection, healthy lifestyle choices, and consistent engagement with preventative healthcare, individuals can not only extend their lifespan but also improve the years lived in good health.

“Prevention isn’t just a personal choice; it’s a public health imperative. By investing in wellness now, we can reduce the future burden on our healthcare system and help more South Africans enjoy longer, healthier lives,” concludes McHugh.

Categories : AgeingTags :

Psilocybin Byproduct Delays Aging and Extends Lifespan, New Study Suggests

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Photo by Marek Piwnicki

As revenues from the anti-aging market – riddled with hope and thousands of supplements – surged past $500 million last year, Emory University researchers identified a compound that actively delays aging in cells and organisms.

A newly published study in Nature Partner Journals’ Aging demonstrates that psilocin, a byproduct of consuming psilocybin, the active ingredient in psychedelic mushrooms, extended the cellular lifespan of human skin and lung cells by more than 50%.

In parallel, researchers also conducted the first long-term in vivo study evaluating the systemic effects of psilocybin in aged mice of 19 months, or the equivalent of 60–65 human years. Results indicated that the mice that received an initial low dose of psilocybin of 5mg/kg, followed by a monthly high dose of 15mg/kg for 10 months, had a 30% increase in survival compared to controls. These mice also displayed healthier physical features, such as improved fur quality, fewer white hairs and hair regrowth.

While traditionally researched for its mental health benefits, this study suggests that psilocybin impacts multiple hallmarks of aging by reducing oxidative stress, improving DNA repair responses, and preserving telomere length. Telomeres are the structured ends of a chromosome, protecting it from damage that could lead to the formation of age-related diseases, such as cancer, neurodegeneration or cardiovascular disease. These foundational processes influence human aging and the onset of these chronic diseases.

The study concludes that psilocybin may have the potential to revolutionize anti-aging therapies and could be an impactful intervention in an aging population.

“Most cells in the body express serotonin receptors, and this study opens a new frontier for how psilocybin could influence systemic aging processes, particularly when administered later in life,” says Louise Hecker, PhD, senior author on the study, and former associate professor at Emory, where the research was initiated and funded.

While much of what researchers know about psilocybin relates to the brain, few studies have examined its systemic impacts. Many people associate psilocybin with the hallucinogenic impacts, but the majority of the cells in the body express serotonin receptors.

“Our study opens new questions about what long-term treatments can do. Additionally, even when the intervention is initiated late in life in mice, it still leads to improved survival, which is clinically relevant in healthy aging,” adds Hecker, currently an associate professor at Baylor College of Medicine.

Not just a longer life, but a healthier life

“This study provides strong preclinical evidence that psilocybin may contribute to healthier aging – not just a longer lifespan, but a better quality of life in later years,” says Ali John Zarrabi, MD, director of psychedelic research at Emory’s Department of Psychiatry. “As a palliative care physician-scientist, one of my biggest concerns is prolonging life at the cost of dignity and function. But these mice weren’t just surviving longer – they experienced better aging,” adds Zarrabi, co-investigator of the study. 

Zarrabi emphasises the importance of further research in older adults, as well as the well-documented overlap between physical and mental health.

“Emory is actively involved in Phase II and III clinical trials of psilocybin-assisted therapy for depression, and these results suggest we also need to understand psilocybin’s systemic effects in aging populations,” says Zarrabi. “My hope is also that if psilocybin-assisted therapy is approved as an intervention for depression by the FDA in 2027, then having a better quality of life would also translate into a longer, healthier life.”

Source: Emory Health Sciences

Categories : AgeingTags :

New Study Highlights the Hidden Risk of Polypharmacy for Older Adults

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Inappropriate polypharmacy – the excessive or unnecessary use of multiple medications – is a major driver of emergency hospital admissions among adults aged 65 and over, according to a new study from the Department of Life Sciences at the University of Bath.

The researchers hope their findings will pave the way for the development of a digital tool – such as an app – to proactively identify older adults at risk of medication-related harm and intervene before a hospital visit becomes necessary.

The study, published in Age and Ageing, is the first of its kind to use data-driven methods to explore how potentially inappropriate polypharmacy contributes to short-term hospitalisation in older adults. With this population growing rapidly and facing increased risks of complications from being hospitalised, the findings reinforce concerns in geriatric care over the dangers of overprescribing.

The hidden dangers of overprescribing

Older adults often take multiple medications to manage chronic conditions such as diabetes, hypertension and arthritis. This can lead to prescribing cascades, where side effects from one drug are treated with additional medications, creating a cycle of escalating complexity and risk.

For instance, a patient might be prescribed a drug for pain management, develop high blood pressure as a side effect and then receive another medication to manage that new symptom. Over time, this can lead to a complex web of prescriptions, carrying the risk of harmful interactions.

PhD researcher Robert Olender, who led the study under the supervision of Dr Prasad Nishtala (primary supervisor, from the Department of Life Sciences) and Dr Sandipan Roy (secondary supervisor, from the Depatment of Mathematics) from Bath, said: “With more older adults on complex drug regimens, we need proactive ways to reduce preventable emergency hospitalisations.”

Though the new research is focused on data from the UK, polypharmacy among older adults is known to be a growing problem globally, with studies from countries that include the US, Australia, New Zealand and across Europe consistently linking polypharmacy to increased risks of hospitalisation, adverse drug reactions and reduced quality of life.

In an earlier study based on a New Zealand dataset, also carried out by the team at Bath, a strong correlation was found in older people between a high drug burden, alcohol consumption and smoking with an increased risk of 30-day hospitalisations.

Using machine learning to predict hospitalisation

The study used a large UK dataset to develop three machine learning models capable of predicting 30-day emergency hospitalisation in older adults with around 75% accuracy.

A key variable in these models was the Drug Burden Index (DBI), which measures the cumulative effect of medications with sedative and anticholinergic properties. Anticholinergics are a class of drug used to treat various chronic conditions such as dementia, depression, urinary incontinence and chronic obstructive pulmonary disease (COPD).

The cumulative effects of these drugs consistently emerged as one of the strongest predictors of a person being at risk of emergency hospitalisation. Other predictors included impaired mobility, a history of fractures and falls, smoking and excessive alcohol consumption.

What makes this study unique is its focus on a previously underexplored dataset and age group, offering new insights into a long-standing issue. While the dangers of polypharmacy are well known, this research highlights the link between polypharmacy and short-term hospitalisation. It also lays the groundwork for a potential tool to identify at-risk patients and guide them toward safer care.

From research to real-life impact

The research team envisions an app for clinicians that uses a simple questionnaire to assess a patient’s risk of hospitalisation. Questions might include current prescriptions, lifestyle factors (e.g. smoking and alcohol use) and chronic conditions like cancer or hypertension. The tool would then generate a risk score, allowing clinicians to make informed decisions in real time.

Such a tool could serve as a low-cost, high-impact intervention to keep patients safe and create savings for the NHS. By identifying high-risk patients early, clinicians may adjust medication regimens, encourage physical activity or address modifiable lifestyle factors – simple steps that could significantly reduce an individual’s risk of an emergency hospital admission.

While the app could be developed relatively quickly, integrating it into clinical workflows would require regulatory approval and trials. However, the potential benefits – fewer hospital admissions, improved patient safety, and reduced healthcare costs – make this a compelling investment, the researchers believe.

The team hopes such a tool would raise awareness among healthcare professionals, particularly those in primary care, community pharmacies and hospices, where early intervention could help prevent emergency hospital admissions.

Source: University of Bath

Categories : AgeingTags :

How Aging Quiets Lupus and Brings Relief to Some Older Patients

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A woman with Systemic Lupus Erythematosus. Source: Wikimedia CC0

Researchers have found that certain antiviral genes become less active over time in lupus, revealing why some patients see their symptoms fade as they age.

It causes the immune system’s first-line viral defences, known as interferons, to attack the body. Nearly every organ is at risk, leading to conditions like kidney and heart disease.

But unlike many other autoimmune or chronic illnesses, lupus can improve as patients reach their 60s and 70s. University of California San Francisco researchers have now found a potential explanation.

“I see my younger lupus patients in their 20s, 30s, and 40s every few months, monitoring them closely for signs of severe disease, but many of my older patients just once a year to touch base,” said Sarah Patterson, MD, assistant professor of medicine in the division of rheumatology at UCSF. “If patients make it through those risky decades, they sometimes see a dramatic improvement.”

Now, Patterson and colleagues have published a study in Science Translational Medicine that reveals how this works.

By analysing blood samples from patients across the age spectrum, the team discovered that aging turns down the activity of certain immune genes in people with lupus, leading to fewer interferons and other inflammatory proteins in the body.

The study found that in healthy adults, inflammation-related genes and proteins rose slowly over the years, a process that has been dubbed “inflammaging.” In patients with lupus, however, the expression of these genes and proteins were abnormally high in mid-life but decreased as the decades went by.

“Inflammaging seemed to be reversed in the lupus patients,” said Chaz Langelier, MD, PhD, associate professor of medicine at UCSF and senior author of the paper. “But it wasn’t fully reversed. The lupus patients still had a greater level of inflammatory signaling compared to healthy adults in older age.”

That reversal reflected what Patterson has seen in her patients — a return to something approaching healthy older age.

Next, the team intends to test whether drugs that block interferons are more or less effective in lupus patients at different ages. They also hope to extend the approach to understand other inflammation-related conditions, such as rheumatoid arthritis, COPD, and atherosclerosis.

Source: University of California San Francisco