Category: Ageing

Categories : Ageing CancerTags :

Global Study Challenges Age-Based Treatment Decisions in Leukaemia

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Study of 2,800 patients suggests moving beyond chronological cut-offs in cancer care

SAG Leukaemia. Credit: Scientific Animations CC0

An international study conducted by the Alliance for Clinical Trials in Oncology and the Acute Myeloid Leukemia Cooperative Group reveals that age-based classifications in the treatment of acute myeloid leukaemia (AML) may be outdated and overly simplistic.

AML is a fast-growing cancer of the blood and bone marrow that disproportionately affects older adults. Historically, age has been a key factor in determining treatment intensity, eligibility for clinical trials, and access to targeted therapies. However, this new research suggests that age alone is not a reliable indicator of disease biology or prognosis.

“Our findings support a more flexible, biology-driven approach to AML treatment and trial design. Age alone should not be a gatekeeper to potentially life-saving therapies,” said Alliance researcher and lead author Ann-Kathrin Eisfeld, MD, associate professor of Internal Medicine and director of the Clara D. Bloomfield Center for Leukemia Outcomes Research at The Ohio State University. “Our results suggest reconsidering age-based eligibility criteria for treatments. By focusing on molecular and genetic profiles rather than chronological age, clinicians may better tailor treatments to individual patients, improving outcomes and expanding access to novel therapies.”

Published in Leukemia, the study analysed data from 2823 adult AML patients treated in the setting of large cooperative group frontline trials across the United States (CALGB/Alliance) and Germany (AMLCG), uncovering nuanced age-related trends in genetic mutations and survival outcomes that challenge current clinical practices. This research is the first large-scale, cross continental study to analyse the mutational patterns and outcomes among patients of all age groups with AML.

The analysis included patients treated with frontline cytarabine-based chemotherapy between 1986 and 2017. Molecular profiling was conducted using targeted sequencing platforms, and survival outcomes were assessed using the 2022 European LeukemiaNet (ELN) genetic-risk classification.

The study found no clear age threshold that could biologically or prognostically separate patients into distinct groups. Instead, genetic mutations and survival outcomes varied continuously across the age spectrum. This challenges the long-standing practice of using arbitrary age cut-offs, such as 60 or 65 years, to guide treatment decisions.

Survival outcomes also declined steadily with age, even among patients classified as having favourable genetic risk. For example, patients aged 18 to 24 with favourable-risk AML had a five-year overall survival rate of 73%, while those aged 75 and older had a survival rate of just 21%. This trend was consistent across all risk categories, indicating that age negatively impacts prognosis regardless of genetic classification.

“This research arrives at a critical moment in oncology, as precision medicine continues to transform cancer care,” added Dr Eisfeld. “Most targeted treatment options are still only available for patients above a certain age threshold that is dictated by corresponding inclusion criteria of pivotal clinical trials, even though patients outside of that age range might equally benefit from these often less toxic treatments.”

Source: Alliance for Clinical Trials in Oncology

Categories : Ageing Metabolic DisordersTags :

Small Reductions in Cholesterol Could Slash Risk of Dementia for Those with Certain Genetics

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Photo by Kampus Production: https://www.pexels.com/photo/a-man-in-blue-sweater-sitting-beside-man-in-white-long-sleeves-7551646/

Low cholesterol can reduce the risk of dementia, a new University of Bristol-led study with more than a million participants has shown.

The research, led by Dr Liv Tybjærg Nordestgaard while at the University of Bristol and the Department of Clinical Biochemistry at Copenhagen University Hospital – Herlev and Gentofte, found that people with certain genetic variants that naturally lower cholesterol have a lower risk of developing dementia.

The study, which is based on data from over a million people in Denmark, England, and Finland, has been published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. 

Some people are born with genetic variants that naturally affect the same proteins targeted by cholesterol-lowering drugs, such as statins and ezetimibe. To test the effect of cholesterol-lowering medication on the risk of dementia, the researchers used a method called Mendelian Randomisation – this genetic analysis technique allowed them to mimic the effects of these drugs to investigate how they influence the risk of dementia, while minimising the influence of confounding factors like weight, diet, and other lifestyle habits.

By comparing these individuals to individuals without these genetic variants, the researchers were able to measure differences in the risk of dementia. They found reducing the amount of cholesterol in the blood by a small amount (one millimole per litre) to be associated with up to 80% reduction in risk of developing dementia for certain drug targets.

“What our study indicates is that if you have these variants that lower your cholesterol, it looks like you have a significantly lower risk of developing dementia,” said Dr Nordestgaard, who now works in the Department of Clinical Biochemistry at Copenhagen University Hospital – Bispebjerg and Frederiksberg hospital.

The results suggest that having low cholesterol, whether due to genes or medical treatment, can help reduce the risk of dementia. However, the study does not say anything definitive about the effect of the medicine itself.  

One of the challenges is that dementia typically does not appear until late in life, and therefore research in the area typically requires a very long period of follow-up. 

It is still not known exactly why high cholesterol can increase the risk of dementia, but one possible explanation proposed by Dr Nordestgaard is that high cholesterol can lead to atherosclerosis. 

“Atherosclerosis is a result of the accumulation of cholesterol in your blood vessels,” Dr Nordestgaard said.  “It can be in both the body and the brain and increases the risk of forming small blood clots – one of the causes of dementia. 

“It would be a really good next step to carry out randomised clinical trials over 10 or 30 years, for example, where you give the participants cholesterol-lowering medication and then look at the risk of developing dementia,” Dr Nordestgaard added. 

The study used data from the UK Biobank, the Copenhagen General Population Study, the Copenhagen City Heart Study, the FinnGen study, and the Global Lipids Genetics Consortium.

Source: University of Bristol

Categories : AgeingTags :

Age-related Macular Degeneration Reversed in Mice with Polyunsaturated Fatty Acid

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Retina showing reticular pseudodrusen. Although they can infrequently appear in individuals with no other apparent pathology, their highest rates of occurrence are in association with age-related macular degeneration (AMD), for which they hold clinical significance by being highly correlated with end-stage disease sub-types, choroidal neovascularisation and geographic atrophy. Credit: National Eye Institute

In a new study, UC Irvine researchers explore a possible therapy for addressing “aging” in the eye and for preventing diseases such as age-related macular degeneration (AMD).

“We show the potential for reversing age-related vision loss,” says Dorota Skowronska-Krawczyk, PhD, an associate professor in the Department of Physiology and Biophysics and the Department of Ophthalmology and Visual Sciences. The study was a collaboration between researchers from UC Irvine, the Polish Academy of Sciences, and the Health and Medical University in Potsdam, Germany.

They outline their findings in a paper published in Science Translational Medicine.

Understanding the “Aging” Gene

The work is a follow-up to an earlier study on Elongation of Very Long Chain Fatty Acids Protein 2 (ELOVL2), an established biomarker of age. “We showed that we have lower vision when this ELOVL2 enzyme isn’t active,” says Skowronska-Krawczyk, also a faculty member in the Robert M. Brunson Center for Translational Vision Research at the UC Irvine School of Medicine. In that work, the researchers found that enhancing ELOVL2 gene expression in aging mice boosted levels of the omega−3 fatty acid docosahexaenoic acid (DHA) in the eye and improved vision.

The more recent study sought to identify a way to bypass the need for the ELOVL2 enzyme.

As we age, changes in lipid metabolism lead to a decline in very-long-chain polyunsaturated fatty acids (VLC-PUFAs) in the retina, which in turn affects our vision and can lead to AMD. The ELOVL2 gene is a key enzyme in the production of VLC-PUFAs as well as DHA.

Injecting aged mice with the polyunsaturated fatty acid improved visual function. “It’s a proof-of-concept for turning lipid injection into a possible therapy,” says Skowronska-Krawczyk. “What is important is that we didn’t see the same effect with DHA.” Others have also questioned the ability of DHA to slow AMD progression.

“Our work really confirms the fact that DHA alone cannot do the work, but we have this other fatty acid that is seemingly working and improving vision in aged animals,” says Skowronska-Krawczyk. “We have also shown on a molecular level that it actually reverses the aging features.”

Furthermore, the researchers found genetic variants in the ELOVL2 enzyme that correlate with faster progression of AMD. “Now we actually have a genetic connection to the disease and its aging aspect,” says Skowronska-Krawczyk, “so we could potentially identify people at higher risk for vision loss progression.” This could lead to not only therapeutic treatment options but also targeted interventions for prevention.

These findings have only further solidified Skowronska-Krawczyk’s view of the importance of the ELOVL2 enzyme. “I am pretty convinced it’s one of the top aging genes that we should look at when we think about anti-aging therapies.”

Looking Beyond the Retina

In a collaboration with researchers from UC San Diego, Skowronska-Krawczyk has also started to explore the role of lipid metabolism in immune system aging. That study found that the lack of ELOVL2 enzyme induces accelerated aging of immune cells, suggesting that systemic lipid supplementation could potentially counteract the effects of age on the immune system. It also suggested that lipid metabolism might play a role in blood cancers.

“Our first study explored a potential therapy to address vision loss,” says Skowronska-Krawczyk, “but with the information we’ve since learned about immune aging, we are hopeful the supplementation therapy will boost the immune system as well.”

Source: University of California – Irvine

Categories : Ageing Ethics and LawTags :

Does Prior Incarceration Contribute to Poor Health Later in Life?

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A recent analysis reveals that older adults with prior incarceration report worse physical and mental health than their peers, even if they were incarcerated in the distant past. The findings are published in the Journal of the American Geriatrics Society.

Among the 1318 US adults aged 50 years and older who responded to the Family History of Incarceration Survey, 21% had been incarcerated. Formerly incarcerated older adults were more likely to be men, non-Hispanic Black or “other” race/ethnicity, meet criteria for disability, be unmarried, and have lower income and education compared with those never incarcerated.

After adjusting for potentially confounding factors like demographics and socioeconomics, prior incarceration was associated with an approximately 90% higher odds of reporting “fair” or “poor” physical health. Length of time since incarceration did not moderate the association, meaning that even those incarcerated more than 10 years ago had equally poor self-reported health. The association with mental health was explained in part by income and employment.

The findings suggest that clinicians could consider screening for incarceration history and connecting formerly incarcerated patients to services and organisations that serve this community.

“Mass incarceration began in 1973, so older adults have spent most of their adult lives in this era and millions have been incarcerated in the past. It is critical to understand how incarceration – even in the distant past – may affect the health of older adults and what we can do to improve their health,” said corresponding author Louisa W. Holaday, MD, MHS, of the Icahn School of Medicine at Mount Sinai.

Source: Wiley

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