One CRISPR treatment cut “bad” cholesterol in half for a full year

 

A single CRISPR infusion cut “bad” cholesterol and triglycerides by about half for a full year in an early human trial. Credit: Shutterstock

A first-in-human Phase 1 clinical trial from Cleveland Clinic found that a single infusion of a CRISPR-Cas9 gene-editing therapy produced lasting reductions in LDL ("bad") cholesterol and triglycerides in people with lipid disorders that had not responded adequately to medications.

The study followed 15 patients for one year to determine whether the cholesterol and triglyceride reductions previously reported after two months would continue over time. After 12 months, participants who received the highest dose had a 52.5% reduction from baseline in LDL cholesterol and a 47.8% drop in triglycerides.

No serious adverse events related to the therapy were reported during the one-year follow-up.

Cholesterol Reductions Lasted for a Year

The findings were presented at the 2026 European Society of Cardiology annual meeting and published at the same time in the New England Journal of Medicine.

"Building upon the initial data presented in November 2025, the durability of the lipid-lowering effect was impressive," said Cleveland Clinic cardiologist Luke Laffin, M.D., first author of the study."It is encouraging that there were no serious safety events related to CTX310 in the trial and in the year following treatment. We look forward to continuing to investigate this therapy in a larger number of patients."

CRISPR-Cas9 is a gene-editing technology designed to make targeted changes to specific parts of a person's DNA. Researchers are studying it as a potential way to treat serious diseases by altering genes that contribute to those conditions.

How CTX310 Targets Blood Fats

The experimental treatment tested in the trial, called CTX310, is given as a one-time infusion. It carries the CRISPR editing system to the liver, where it switches off a gene known as ANGPTL3.

ANGPTL3 helps regulate fats circulating in the blood. Disabling the gene can reduce LDL cholesterol and triglycerides, both of which are associated with cardiovascular disease.

During the study, patients received CTX310 at doses ranging from 0.1 to 0.8 mg/kg. Before the infusion, they were treated with corticosteroids and antihistamines.

Researchers then monitored participants for treatment safety and measured changes in ANGPTL3, LDL cholesterol, and triglyceride levels.

At the highest dose, CTX310 lowered both LDL cholesterol and triglycerides by about 50% on average 12 months after treatment.

Long-Term Monitoring Will Continue

Although the early results are encouraging, CTX310 remains experimental and the study involved only 15 people.

Participants were monitored for one year after treatment, and researchers plan to continue long-term safety follow-up for another 15 years, in line with FDA recommendations for gene-editing therapies.

The study was funded by CRISPR Therapeutics AG; Zug, Switzerland.

Dr. Laffin's institution has received research funding from Crispr Therapeutics.

Journal Reference:

1. Luke J. Laffin, Stephen J. Nicholls, Russell S. Scott, Peter M. Clifton, Renate Koops, Ashish Sarraju, Shweta Singh, Qiuqing Wang, Kathy Wolski, Huansheng Xu, Jen Nielsen, Naimish Patel, Jason M. Duran, Steven E. Nissen. Durability of CRISPR-Cas9 Gene Editing Targeting ANGPTL3 with CTX310. New England Journal of Medicine, 2026; DOI: 10.1056/NEJMc2609825

Courtesy:

Cleveland Clinic. "One CRISPR treatment cut “bad” cholesterol in half for a full year." ScienceDaily. ScienceDaily, 27 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260925005434.htm>. 

 

Glucosamine, a popular joint supplement, linked to faster Alzheimer’s progression

 

A widely used supplement for joint pain has been linked to a potentially concerning outcome in people with early cognitive problems.

Researchers at the University of Florida found that glucosamine use was associated with a greater likelihood that mild cognitive impairment would progress to dementia. Mild cognitive impairment, often shortened to MCI, describes measurable problems with memory or thinking that are greater than expected with normal aging but do not necessarily interfere substantially with everyday life.

The findings come from a large retrospective analysis of patient health records, supported by experiments involving human brain tissue and mouse models of Alzheimer's disease. The results remain preliminary and will need to be tested in a human clinical trial, but the researchers say they add to growing evidence that disrupted metabolism may play an important role in neurodegeneration.

The study was published in Nature Metabolism.

A Popular Supplement Comes Under Scrutiny

"In the United States, there are about 7 million people living with Alzheimer's and millions more with related dementias such as Lewy body or frontotemporal dementia," said senior author Ramon Sun, Ph.D., director of the Center for Advanced Spatial Biomolecule Research and associate director for innovation of UF's McKnight Brain Institute. "A lot of these people actively take an over-the-counter supplement that could be making their disease progression worse."

Glucosamine is widely sold without a prescription and is especially popular among older adults who take it for joint discomfort and joint health. Because of how commonly it is used, the researchers wanted to know whether it might influence Alzheimer's disease and related dementias, known as ADRD.

Working with Yi Guo, Ph.D., and Jiang Bian, Ph.D., the team used artificial intelligence to analyze deidentified UF Health records collected from 2012 to 2024.

The researchers focused on patients diagnosed with either ADRD or mild cognitive impairment, or MCI. In both groups, 8% of patients reported using glucosamine. That included 1,896 people with ADRD and 2,750 people with MCI.

Glucosamine Linked to Dementia Progression

After accounting for age, sex and demographics, the researchers found that glucosamine use was associated with a 25% higher likelihood that mild cognitive impairment would progress to dementia.

Among people who already had ADRD, glucosamine use was also associated with a 25% higher mortality risk, meaning a greater likelihood of death during a defined period of time.

The researchers did not observe that mortality association in the MCI group. That difference suggests glucosamine may have a stronger effect once dementia is already established.

Importantly, the health record findings do not show that glucosamine itself causes dementia to progress. Observational studies can reveal associations, but other differences between people who take a supplement and those who do not may contribute to the results.

"The electronic health record data are very provocative," said Matt Gentry, Ph.D., chair of UF's Department of Biochemistry and Molecular Biology and a study co-author. "While it's an association and not proof of causality, it does raise an important clinical question that now deserves much more attention."

A Metabolic Pathway May Help Explain the Link

The researchers also uncovered evidence of a biological mechanism that could help explain the association.

Their work points to a metabolic pathway involving the attachment of sugar structures to proteins. This process is a normal and important part of cell biology, but the researchers found signs that it becomes excessively active in Alzheimer's disease.

Sun said that abnormal activity in this pathway could eventually become a target for new treatments.

"Our results suggest that altered metabolism is a significant contributor to Alzheimer's progression and, in addition, addressing the metabolic defect could be an important complement to approaches focused on Alzheimer's plaques and tangles," Sun said.

Plaques and tangles are two of the best known features of Alzheimer's disease. Plaques are abnormal deposits of a protein called amyloid beta that accumulate between brain cells, while tangles are twisted forms of the tau protein that develop inside neurons. Much Alzheimer's research has traditionally focused on these abnormalities, but scientists are increasingly studying additional processes that may contribute to the disease.

Mapping Thousands of Molecules in the Brain

A spatial technology developed in Sun's laboratory helped researchers examine the metabolic changes in much greater detail.

"This technology allows us to examine thousands and thousands of molecules created when the body breaks down food or drugs and to uncover intricate pathways that otherwise would stay hidden," Sun said.

The team then focused specifically on glucosamine. Glucosamine is a naturally occurring, sugar-related molecule that can cross the blood-brain barrier, the protective boundary that tightly controls which substances can move from the bloodstream into brain tissue.

Once inside the brain, glucosamine can enter biochemical pathways that construct complex sugar structures and attach them to proteins. Commercial glucosamine supplements can be produced from materials including shellfish shells or corn.

According to the researchers, the effects of glucosamine may depend heavily on the biological environment in which it is acting. A healthy brain and a brain affected by Alzheimer's may therefore respond differently to the same molecule.

The Alzheimer's brain appeared to be particularly vulnerable to this metabolic pathway.

Mouse Experiments Point to a Possible Mechanism

To explore the mechanism more closely, the scientists studied genetically modified mice.

Glucosamine significantly increased the attachment of sugar residues to proteins inside cells. At the same time, glucosamine-treated mice developed worse deficits in "social memory" -- or memory of recognition -- compared with the other animals.

When the researchers used a chemical treatment to suppress the sugar attachment process, memory performance improved.

That experiment suggested that excessive sugar tagging could play a direct role in the memory problems seen in the animals rather than simply occurring alongside them.

Human Alzheimer's Brain Tissue Shows the Same Pattern

The researchers next examined human brain tissue with Stefan Prokop, M.D.

Brain specimens from people with Alzheimer's disease, provided by the UF Neuromedicine Brain and Tissue Bank, showed significantly more sugar attachment than tissue from normal controls.

Combined with the mouse experiments and health record analysis, the findings suggest that abnormal metabolism may be more than a secondary consequence of Alzheimer's disease. The researchers reported that it could instead contribute to the disease process itself.

"Proteins are the cell's molecular machines, and many of them need sugar tags added in just the right way to fold correctly, travel to the right place and do their jobs," Gentry said. "What we found in Alzheimer's is that this sugar-tagging system appears to be overactive. The Alzheimer's brain is adding too many of these sugar structures, and this seems to contribute to the disease rather than protect against it."

The results raise a potentially important question about glucosamine use among people with cognitive impairment or dementia, but they do not yet establish that people should stop taking the supplement. A controlled human clinical trial will be needed to determine whether glucosamine directly accelerates Alzheimer's progression and, if so, which patients may be most vulnerable.

Journal Reference:

1. Tara R. Hawkinson, Zizhen Liu, Roberto A. Ribas, Terrymar Medina, Rikke S. Nielsen, Harrison A. Clarke, Xin Ma, Angela C. Mueller, Adrielle F. Plasencia, Alexander L. Sheer, Samantha T. Simpson, Charles M. Soto, Jessica Sudderth, Feng Cai, Alex R. Cantrell, Matthieu G. Colpaert, Cameron J. Shedlock, Lei Wu, Lyndsay E. A. Young, Damon D. Kooser, Li Chen, Alison M. Ryan, Sadi Quinones, Jihye Son, Parastoo Azadi, Ralph J. Deberardinis, Stefan Prokop, Derek Allison, Shuang Yang, Hongyu Chen, Yu Huang, Xing He, Kimberly M. Alonge, Jingchuan Guo, Yi Guo, Jiang Bian, Craig W. Vander Kooi, Matthew S. Gentry, Ramon C. Sun. Hyperglycosylation is a metabolic driver of Alzheimer’s disease. Nature Metabolism, 2026; 8 (6): 1410 DOI: 10.1038/s42255-026-01538-4

Courtesy:

UF Health. "Glucosamine, a popular joint supplement, linked to faster Alzheimer’s progression." ScienceDaily. ScienceDaily, 27 September 2026. <www.sciencedaily.com/releases/2026/09/260927033754.htm>.

 

 

 

 

A massive genetic study of cat tumors reveals striking similarities to human cancer and could open new paths to treatment for both species

 

Scientists have taken a major step toward understanding cancer in cats, opening what researchers once described as a genetic "black box."

In a large international study published in Science, researchers genetically analyzed cat cancers on a scale that had not been attempted before. The work could improve cancer care for cats while also helping scientists better understand how some cancers develop in humans and other animals.

The researchers also created a freely available resource that other scientists can use to study the genetics of feline cancer.

Cancer is one of the leading causes of illness and death in cats, yet scientists have historically known far less about the genetic changes behind feline tumors than they do about cancers in humans or dogs.

Dr. Geoffrey Wood, a University of Guelph pathobiology professor and co-senior author of the study, said that gap has now begun to close.

"Despite domestic cats being common pets, there was very little known about the genetics of cancer in these animals," Wood says, "until now."

Cat and Human Cancers Share Key Genetic Changes

Researchers examined tumor samples from almost 500 domestic cats in five countries, searching for mutations and other genetic changes that help cancers form and grow.

Many cancers are driven by changes in certain genes that normally help control how cells grow, divide, repair damage, or die. When these genes are altered, cells can begin multiplying uncontrollably. Scientists often refer to genes that contribute directly to tumor growth as cancer driver genes.

The team found that many of the driver genes involved in cat cancers were also familiar from human and dog cancers.

One of the clearest examples appeared in aggressive mammary cancers, which arise in breast tissue.

The most common driver gene found in cat mammary tumors was FBXW7. More than 50 percent of the tumors examined carried a mutation in this gene.

FBXW7 normally helps regulate proteins involved in cell growth and division. When the gene is damaged, some of those growth promoting proteins can accumulate, potentially helping cancer cells survive and spread.

In humans, mutations in the FBXW7 gene in breast cancer are associated with worse prognosis - paralleling the change seen in cats.

Researchers also identified similarities between cat and human cancers affecting the blood, bones, lungs, skin, gastrointestinal system and central nervous system.

Shared Environments May Offer Cancer Clues

The similarities may be especially useful because domestic cats often live in the same environments as people.

Cats can encounter some of the same environmental factors as their owners, including household chemicals, air pollutants, smoke and other exposures that may influence cancer risk. Studying naturally occurring cancer in pets could therefore help researchers investigate how genetics and the surrounding environment interact.

"This study can help us understand more about why cancer develops in cats and humans, how the world around us influences cancer risk, and possibly find new ways to prevent and treat it," says Wood.

The genetic findings could also have implications for treatment.

Researchers found that certain chemotherapy drugs were more effective against cat mammary tumors carrying the mutated FBXW7 gene.

The result was observed only in tissue samples, so it does not yet show that the same approach will work in living cats or people. Still, the finding suggests that genetic information could eventually help doctors and veterinarians identify treatments that work better for particular tumors.

This type of approach is known as precision oncology. Instead of treating every cancer of the same general type in exactly the same way, precision oncology uses the molecular and genetic features of an individual tumor to help guide therapy.

"Having access to such a large set of donated tissues allowed us to assess drug responses across tumor types," says Dr. Sven Rottenberg, co-senior author at the University of Bern, "in a way that hasn't been possible at this scale before."

Bailey Francis, co-first author at the Wellcome Sanger Institute, said the findings could also have implications for dogs.

"When knowledge and data flows between different disciplines, we can all benefit."

Using Cat Cancer Research to Help Pets and People

The project brought together researchers from the Wellcome Sanger Institute, U of G's Ontario Veterinary College, the University of Bern and other institutions.

Rather than collecting all new samples, the team sequenced DNA from tissues that veterinarians had already obtained for diagnostic purposes.

That allowed scientists to study naturally occurring cancers from a large number of cats and compare the genetic patterns among different tumor types.

The findings also support a broader research strategy known as One Medicine.

The One Medicine approach emphasizes that human and veterinary medicine can inform one another. Cancer treatments developed for humans could potentially be evaluated in cats with naturally occurring tumors, while discoveries made during feline cancer studies and clinical trials could provide clues that help shape future human research.

That two way exchange is especially valuable because pets naturally develop many of the same diseases as people while sharing many aspects of the same environment.

Researchers hope the new genetic database will ultimately help bring more personalized cancer care to cats.

Dr. Louise Van Der Weyden, senior author at the Wellcome Sanger Institute, said the study provides a foundation for the next stage of feline cancer research.

"We can now begin to take the next steps forwards towards precision feline oncology, to catch up with the diagnostic and therapeutic options that are available for dogs with cancer, and ultimately one day, humans."

The research was funded in part by EveryCat Health Foundation, the CVS Group, Wellcome, the Natural Sciences and Engineering Research Council of Canada and the Swiss National Science Foundation.

Journal Reference:

1. Bailey A. Francis, Latasha Ludwig, Chang He, Melanie Dobromylskyj, Christof A. Bertram, Heike Aupperle-Lellbach, Hannah Wong, Aiden P. Foster, Mark J. Arends, Alejandro Suárez-Bonnet, Simon L. Priestnall, Laetitia Tatiersky, Fernanda Castillo-Alcala, Angie Rupp, Arlene Khachadoorian, Eda Parlak, Marine Inglebert, Shevaniee Umamaheswaran, Saamin Cheema, Martin Del Castillo Velasco-Herrera, Kim Wong, Ian C. Vermes, Jamie Billington, Sven Rottenberg, Geoffrey A. Wood, David J. Adams, Louise van der Weyden. The oncogenome of the domestic cat. Science, 2026; 391 (6787): 793 DOI: 10.1126/science.ady6651

Courtesy:

University of Guelph. "Scientists say house cats could help unlock better cancer treatments for humans." ScienceDaily. ScienceDaily, 26 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260924231826.htm>.

 

 

Cancer is rising in younger adults. Faster biological aging may help explain why

Younger generations may be aging faster on the inside, a biological shift researchers have linked to a higher risk of cancers diagnosed before age 55. Credit: Shutterstock

Cancer is strongly associated with age. The longer people live, the more opportunities their cells have to accumulate damage that can contribute to tumor growth. But cancer is increasingly being diagnosed in younger adults, and each newer generation appears to face a greater risk than the one before it.

That trend has prompted researchers to investigate a provocative possibility: Are younger generations accumulating biological damage more quickly, causing their bodies to age faster than expected?

A study led by researchers at Washington University School of Medicine in St. Louis offers evidence that this may be happening. The team found signs that younger generations are aging more rapidly on a biological level than older generations did at comparable ages.

Scientists are still working to understand what is driving these changes. The question is being investigated through international efforts involving research members of Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine, and Cancer Grand Challenges, a global initiative co-founded by the National Cancer Institute and Cancer Research U.K.

Importantly, the researchers also found that accelerated biological aging was associated with a greater risk of early-onset cancers among younger generations. In general, early-onset cancers are those diagnosed at age 55 or younger.

A Gap Between Biological Age and Actual Age

Chronological age simply measures how many years a person has been alive. Biological age, by contrast, reflects how old the body appears based on measurable changes in cells, organs, metabolism, and other physiological systems.

According to the researchers, cancer risk increased as the difference between biological age and chronological age grew. People from more recent generations tended to have larger gaps than those born earlier, suggesting their bodies appeared biologically older at the same chronological age.

That generational shift could help explain at least part of the rise in cancer among younger adults.

The team also found that aging did not appear to affect every organ system in the same way. Faster aging in specific parts of the body was associated with particular cancers. An immune system that appeared biologically older, for example, was linked to early-onset lung cancer. Older-appearing fat tissue was associated with early-onset colorectal cancer.

The findings were published in the journal Nature Medicine.

Researchers say measurements of accelerated aging could eventually help doctors identify younger people who face unusually high cancer risks, potentially allowing prevention or screening to begin earlier.

"Our ultimate goal is to decode how modern environments become biologically embedded to drive cancer risk, transforming prevention from broad recommendations to personalized interventions," said Yin Cao, ScD, a molecular epidemiologist and an associate professor of surgery and of medicine at WashU Medicine. "This brings us closer to identifying risk earlier and developing prevention strategies that are tailored to an individual's biology."

Looking Beyond Individual Cancer Risk Factors

Cao's team has previously studied numerous factors that can shape cancer risk over a person's lifetime, including obesity, metabolic dysregulation, alcohol consumption, sedentary behavior, poor diet quality and cesarean delivery.

Each of these factors can provide clues about why cancer develops at younger ages. However, no single factor appears to explain very much of the overall trend on its own.

That led Cao, who is also a research member of Siteman, and her colleagues to look for a broader way of measuring how many different influences may work together over time to increase cancer susceptibility.

Support from Cancer Grand Challenges has allowed Cao, as co-lead of Team PROSPECT, to investigate this question on a much larger scale.

For the new study, the researchers examined data from more than 154,000 young adults enrolled in the UK Biobank, which contains extensive biological, health, and lifestyle information.

They also analyzed more than 10,000 participants in the United States who are part of the National Institutes of Health's (NIH) All of Us Research Program, an initiative designed to create a comprehensive health database involving more than 1 million people living in the U.S.

Measuring How Fast the Body Is Aging

To determine biological aging, the researchers, including first author Ruiyi Tian, a doctoral student in the Cao lab, looked at two different scales.

One was systemic aging, which measures aging across the body as a whole. The other was organ-specific aging, which estimates how rapidly individual organs or biological systems are aging.

For systemic aging, the researchers relied on established approaches that use clinical biomarkers, including PhenoAge and the Klemera-Doubal Method. They also used a metabolomic age score designed to capture age-related patterns in a person's metabolism.

PhenoAge, for example, uses nine blood biochemistry markers to estimate biological aging. These include albumin, made by the liver, and creatinine, a waste product removed by the kidneys.

For organ-specific aging, the researchers analyzed blood proteomic data, which measure levels of numerous proteins associated with specific organ systems. Those protein patterns were then used to estimate the biological age of individual organs.

The team calculated the average difference between biological and chronological age within each birth cohort. They then used standard deviation to measure how far each group differed from the overall study average. Standard deviation is a measure of how spread out data points are around the average.

Younger Generations Show Older Biological Profiles

The generational differences were apparent in both the UK and U.S. populations.

Among UK participants, people born between 1965 and 1974 had systemic aging that was 23% of one standard deviation higher than people born between 1950 and 1954, even after chronological age was taken into account.

Put more simply, members of the younger generation tended to have slightly older biological profiles than members of the older generation when researchers compared them at the same chronological age.

An even larger difference appeared in the U.S. data.

Participants born between 1990 and 1999 had systemic aging that was 92% of one standard deviation higher than those born between 1965 and 1969.

The researchers then examined whether these biological aging differences were connected to cancer.

Faster Aging Linked to Early-Onset Cancer

Greater systemic aging in the younger group was associated with an 8% increased risk of early-onset solid cancers. The strongest associations involved lung, gastrointestinal, and uterine cancers.

When the participants were separated into three groups according to their level of systemic aging, another pattern emerged.

People with the most advanced systemic aging had a 15% increased risk of early-onset solid cancer compared with participants showing the least advanced aging.

The association remained even after researchers accounted for inherited genetic cancer risks and genetic susceptibility to accelerated aging.

Looking at individual biological systems revealed more specific connections.

Advanced immune system aging was associated with a higher risk of early-onset lung cancer. Advanced adipose (fat) tissue aging was linked to a higher risk of early-onset colorectal cancer.

"If we can identify younger people with the highest cancer risk when they are still healthy, we can focus on prevention and early-detection strategies for the individuals who will benefit most from early interventions," Cao said.

Searching for the Causes of Cancer in Younger Adults

The research is part of Team PROSPECT, a Cancer Grand Challenges team co-led by Cao.

Cancer Grand Challenges is an international research funding initiative co-founded by Cancer Research UK and the National Cancer Institute (NCI). It brings together scientists from different specialties and countries to investigate some of the most difficult problems in cancer research.

One of those problems is explaining why early-onset cancers are becoming more common.

"Right now, we don't have a definitive answer to what's driving the rise of early-onset cancers around the world, but studies like this are helping us piece together the bigger picture, showing that cancer may be influenced not just by changes inside individual cells, but by wider changes happening across the body as a whole," said David Scott, PhD, director of Cancer Grand Challenges. "Research on this scale is possible through Cancer Grand Challenges, which brings together scientists from different fields around the world to tackle these complex questions together."

Cao and her colleagues are now working to better understand why cancer is increasingly affecting younger generations.

A major focus is determining how changes in the environment, lifestyle and society may leave long-lasting biological marks on the body. Those effects could include accelerated aging as well as other signs that make some people more vulnerable to disease.

By tracing how these risks accumulate throughout life, researchers hope to uncover more of the biological origins of early-onset cancers.

The ultimate goal is not simply to understand why cancer develops earlier, but to identify people at elevated risk while they are still healthy. That could make it possible to move prevention and screening earlier and tailor interventions to an individual's biology, shifting cancer care toward stopping disease before it begins.

This work was part of the PROSPECT team supported by the Cancer Grand Challenges initiative funded by Cancer Research UK, grant numbers CGCATF-2023/100043 and CGCATF-2023/100037; the National Cancer Institute of the NIH, grant numbers OT2CA297577 and OT2CA297576; the French National Cancer Institute; and the Bowelbabe Fund for Cancer Research UK. The project was also supported by grants from NIH/National Cancer Institute, grant number R37CA246175; the NIH/National Institute of Diabetes and Digestive and Kidney Diseases, grant number P30DK052574; the Alvin J. Siteman Cancer Center through the Foundation for Barnes-Jewish Hospital. Further support was provided by a pre-doctoral fellowship in the Cancer Biology pathway supported by NIH Molecular Oncology Training Grant T32CA113275 to Washington University School of Medicine in St. Louis; the Pediatric Gastroenterology Research Training Program grant T32DK077653 to Washington University School of Medicine in St. Louis; the Washington University School of Medicine in St. Louis Institute of Clinical and Translational Sciences, grant number UL1TR002345; and the Foundation for Barnes-Jewish Hospital. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.

Journal Reference:

1. Ruiyi Tian, Xiaoyu Zong, Duo Ren, Stefani Tica, Daniel Hong, Oluseye Oduyale, Jason D. Buenrostro, Ramaswamy Govindan, Yin Cao. Biological aging and generational shifts in early-onset cancer risk. Nature Medicine, 2026; 32 (8): 2983 DOI: 10.1038/s41591-026-04448-w

Courtesy:

WashU Medicine. "Cancer is rising in younger adults. Faster biological aging may help explain why." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913082200.htm>.

 

 

Scientists find a hidden cause of high blood pressure that routine tests can miss

A hidden nighttime hormone pattern may reveal one of the most commonly missed causes of high blood pressure. Credit: Shutterstock

A common and frequently missed cause of high blood pressure may be easier to detect with help from a wearable device that tracks hormone changes throughout the day and night.

New research published in Science Translational Medicine focuses on primary aldosteronism, a hormone disorder that may affect up to one in five people with high blood pressure. The condition is associated with an increased risk of heart disease, stroke, diabetes, and other serious health problems.

Researchers from the University of Bristol and the University of Manchester in the UK, the University of Bergen in Norway, and collaborators in Stockholm and Athens found that people with primary aldosteronism can experience bursts of hormone production both during the day and while asleep at night. Those nighttime surges are especially important because routine blood tests are rarely performed during sleep.

A Wearable Device Tracks Hormones Around the Clock

To capture these hidden changes, the research team used a portable device developed at the University of Bristol that allowed patients to have their hormone levels monitored continuously while living normally at home rather than staying in a hospital or research facility.

This type of continuous monitoring could reveal abnormalities that may be missed by conventional testing, potentially helping doctors identify hormone-related conditions earlier.

Study co-lead author Dr. Thomas Upton, Clinical Research Fellow in Automated Sampling Clinical Fellow at the University of Bristol, and Senior Clinical Fellow at Bristol Hospitals NHS Foundation Trust said: "Primary aldosteronism is an important cause of high blood pressure and the most common cause of secondary hypertension we see in our blood pressure clinic. It could be affecting millions of people in the UK. However, due to the way hormones change during the day and the current complexity of the diagnostic process, diagnosis is often delayed or never made at all.

"In our study, patients were monitored at home during normal activity, and this allowed us to see how hormones changed over time in realistic settings. This approach could potentially revolutionize how we diagnose hypertension and ultimately reduce cardiovascular disease - particularly heart disease and strokes - that could have been prevented."

Measuring Hormones Every 20 Minutes

The proof-of-concept study followed 60 patients in Bristol, Bergen, Stockholm, and Athens over a 24-hour period. Hormone levels were measured every 20 minutes using a lightweight wearable device about the size of a mobile phone that attaches at the waist.

Because the device samples hormones from the skin, participants were able to continue with their usual activities, including sleeping at night, while researchers collected detailed hormone data.

The technology, known as U-RHYTHM, was adopted and further developed by the spinout company Dynamic Therapeutics in 2023.

Study senior author Dr. Eder Zavala, UKRI Future Leader Fellow at the University of Manchester, said: "By continuously monitoring hormones over 24 hours, we were able to reveal a previously hidden pattern of nocturnal hormone bursts. This gives us a much clearer understanding of the disease and could ultimately help doctors detect it earlier and treat patients more effectively.

"A more detailed mathematical and computational analysis of daily hormonal profiles could eventually also help uncover earlier and more subtle forms of the disease, opening new opportunities to improve outcomes for patients living with high blood pressure."

Why Standard Blood Tests May Miss the Disorder

Researchers used computational analysis to study changes in aldosterone, a hormone that helps control salt and water balance in the body. They also tracked two closely related hormones, 18-hydroxycortisol and 18-oxocortisol.

The results suggest that current diagnostic approaches may miss some patients because aldosterone does not remain consistently elevated.

Even in some of the most severe cases, hormone levels sometimes dropped below the minimum thresholds typically used to diagnose primary aldosteronism. A single blood test taken at one moment could therefore capture a period when hormone levels appear relatively normal.

Instead of remaining constantly high, aldosterone showed repeated bursts of secretion at night while the overall day-night rhythm of hormone activity remained intact.

Nighttime Hormone Bursts Offer a New Clue

The hormone spikes came from the adrenal glands and were especially pronounced in patients whose primary aldosteronism was caused by a problem affecting only one adrenal gland rather than both.

Importantly, the unusual hormone patterns disappeared after the affected adrenal gland was surgically removed. That finding provided additional evidence that the bursts were directly associated with the disease.

Study co-author Prof Stafford Lightman, Professor of Medicine at the University of Bristol and inventor of the U-RHYTHM technology, added: "The findings suggest that clinicians may need to rethink how they look for the disorder, which the Endocrine Society clinical practice guidelines now recommend should be considered for all people with hypertension, also known as high blood pressure.

"Future diagnosis could move away from single time point blood tests and towards tracking the body's hormone rhythms over time, particularly the overnight patterns that appear to hold crucial clues to disease. Further research is needed to define the best clinical pathways, using dynamic hormone measurement, to ensure early diagnosis of this common and potentially curable cause of high blood pressure."

Toward Earlier Detection of High Blood Pressure Causes

The findings raise the possibility that future testing for primary aldosteronism could rely less on a single blood sample and more on monitoring how hormones change over time.

Because the disorder can be treated and, in some cases, potentially cured, detecting it earlier could help reduce the risk of preventable cardiovascular complications.

The research was funded by EU Horizon 2020, the Trond Mohn Foundation, the UKRI Biotechnology and Biological Sciences Research Council (BBSRC), Medical Research Council, University Hospitals Bristol and Weston NHS Foundation, the Swedish Medical Research Council and Knut and Alice Wallenberg Foundation.

The findings support the University of Bristol's research 'Grand Challenge' focus on Understanding and Preventing Cardiovascular Disease and builds on NIHR-funded initiatives aimed at earlier identification of people with hypertension and other cardiovascular risk factors.

 

Journal Reference:

1. Marianne A. Grytaas, Thomas Upton, Isabella Marinelli, Paal Methlie, Marianne Øksnes, Dimitra A. Vassiliadi, Sophie Bensing, Georgina Russell, Kristian Løvås, Dimitris Margaritopoulos, Ileana R. Botusan, Katerina Simunkova, Maria Balomenaki, Katarina Berinder, Belinda Lombard, Thea Sjøgren, Ida Løvik, Bergithe E. Oftedal, Anette Heie, Grethe Å. Ueland, Olle Kämpe, Stylianos Tsagarakis, Stafford L. Lightman, Eder Zavala, Eystein S. Husebye. Tissue corticosteroid rhythms are dysregulated predominantly during sleep in primary aldosteronism. Science Translational Medicine, 2026; 18 (864) DOI: 10.1126/scitranslmed.aeb7517

Courtesy:

University of Bristol. "Scientists find a hidden cause of high blood pressure that routine tests can miss." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260913081916.htm>. 

 

Scientists finally see DNA “zip” itself together for the first time

 

DNA strands zipping together. Credit: Professor Agnes Noy, University of York

DNA carries a negative electrical charge. Because objects with the same charge normally push away from each other, DNA molecules might be expected to repel one another. Yet inside living cells, DNA must sometimes come into close contact and recognize matching sequences. These interactions are essential for processes including genetic recombination and gene silencing, and they can also play a role in cancer.

Scientists have now captured a remarkably detailed view of how this happens. Using powerful atomic force microscopy, researchers watched short pieces of DNA align with extraordinary precision, matching one another groove for groove. Computer simulations then revealed what appears to make this close contact possible: positively charged metal ions can settle into the grooves of DNA and serve as tiny molecular bridges between the two molecules.

Tiny Ions Help DNA Overcome Repulsion

Professor Agnes Noy, from the School of Physics, Engineering and Technology at the University of York, co-led the research. She said: "This discovery could help researchers identify regions of the genome specially involved in DNA pairing. These regions may become particularly important when mutations disrupt normal cellular processes and contribute to cancer."

The results provide experimental support for an idea proposed about twenty years ago called the "DNA zipper" model. Professor Alexey Kornyshev from Imperial College London and his collaborators originally suggested that salt ions surrounding DNA could produce alternating patterns of electrical charge. Those patterns, according to the model, would help neighboring DNA molecules align with one another much like two interlocking spiral staircases.

Until now, directly observing this proposed mechanism had proved difficult.

Scientists Put the "DNA Zipper" to the Test

To investigate the process, the researchers scanned DNA samples with atomic force microscopy, a technique capable of mapping surfaces at extremely small scales. These scans allowed the team to construct detailed topographical maps showing how the DNA molecules were positioned.

At the same time, sophisticated computer simulations followed individual atoms and ions as they moved around the DNA. Combining the two approaches gave researchers both a direct view of DNA pairing and a way to understand the molecular forces responsible for it.

The simulations showed that double-charged metal ions can effectively behave like two charged arms. Each ion can interact with both DNA molecules at once, forming a bridge across the space separating them and helping hold the two strands in alignment.

Dr. Thomas Catley, co-lead author from the School of Chemical Materials and Biological Engineering at the University of Sheffield, said: "It was incredible to be able to directly visualize the long-hypothesized mechanism for the first time. The advanced imaging techniques at our disposal are allowing us to uncover these key DNA interactions which have implications in many key cellular processes."

Dr. Victor Velasco-Berrelleza from the University of Sheffield, who performed the simulations, added: "Microscopy shows us what happens, but the simulations allow us to uncover the molecular mechanism behind it."

Some DNA Sequences Pair More Strongly

The researchers also found that DNA does not pair equally well along every sequence. Some stretches of DNA created much stronger contacts than others, producing distinct hotspots where two helices were especially likely to line up.

That finding could help researchers pinpoint parts of the genome that are particularly involved in DNA recognition and pairing. Such regions may become especially significant when mutations interfere with normal cellular activity and contribute to cancer.

The discovery could also have uses beyond medicine. Because some DNA sequences can be programmed to interact more strongly than others, scientists may eventually be able to take advantage of these properties to build customized DNA structures for biotechnology.

The study, "Imaging and mechanism of DNA-DNA recognition mediated by divalent ions," was published in the journal Nucleic Acids Research.

 

Journal Reference:

1. Thomas E Catley, Victor Velasco-Berrelleza, Daniel E Rollins, Alice L B Pyne, Agnes Noy. Imaging and mechanism of DNA–DNA recognition mediated by divalent ions. Nucleic Acids Research, 2026; 54 (16) DOI: 10.1093/nar/gkag817

Courtesy:

University of York. "Scientists finally see DNA “zip” itself together for the first time." ScienceDaily. ScienceDaily, 14 September 2026. <www.sciencedaily.com / releases / 2026 / 09 / 260909231717.htm>.