Day: April 29, 2026

Categories : Ageing Environmental EffectsTags : Leave a comment

HEPA Air Purifiers May Boost Brain Power in Adults Over 40 – New Research

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Photo by Mari Lezhava on Unsplash

Nicholas Pellegrino, University of Connecticut; Doug Brugge, University of Connecticut, and Misha Eliasziw, Tufts University

Using an in-home HEPA purifier for one month spurs a small but significant improvement in brain function in adults age 40 and older. That’s the result of a new study we co-authored in the journal Scientific Reports.

HEPA purifiers – HEPA stands for high efficiency particulate air – remove particulate matter from the air. Exposure to particulate matter has been connected to respiratory and cardiovascular illnesses as well as neurological diseases such as Alzheimer’s and Parkinson’s. Environmental health researchers increasingly recommend that people use HEPA air purifiers in their homes to lower their exposure to particulate matter, but few studies have examined whether using them boosts mental function.

We analysed data from a study of 119 people ages 30 to 74 living in Somerville, Massachusetts. Somerville sits along Interstate 93 and Route 28, two major highways, resulting in relatively high levels of traffic-related air pollution. This makes it an especially good location for testing the health effects of air purifiers.

We randomly assigned participants to one of two groups. One used a HEPA air purifier for one month and then a sham air purifier – which looked and acted like the real thing but did not contain the air-cleaning filter – for one month, with a monthlong break in between. The second group used the real and sham purifiers in reverse order.

After each month, participants took a test that measured different aspects of their mental capacity. The test probed people’s visual memory and motor speed skills by measuring how quickly they could draw lines between sequential numbers, and it tested executive function and mental flexibility by asking them to draw lines between alternating sequential numbers and letters.

We found that participants 40 years and older – about 42% of our sample – on average completed the section testing for mental flexibility and executive function 12% faster after using the HEPA purifier than after using the sham purifier. That was true even when we accounted for factors like differences in the amount of time participants spent indoors, with either filter, as well as how stressful they found the test.

This improvement may seem small, but it is similar to the cognitive benefits that people experience from increasing their daily exercise. While you may not experience a sudden increase in clarity from a 12% boost, preventing cognitive decline is vital for long-term well-being. Even small decreases in cognitive functioning may be associated with a higher risk of death.

Studies increasingly show that air pollution can be detrimental to brain health.

Why it matters

Air pollution can negatively affect mental function after just a few hours of exposure. Studies show that air purifiers are effective at reducing particulates, but it’s unclear whether these reductions can prevent cognitive harm from ongoing pollution sources like traffic. Research has been especially lacking in people living near major sources of air pollution, such as highways.

People living near highways or major roadways are exposed to more air pollution and also experience higher rates of air pollution-related diseases. These risks aren’t encountered by all Americans equally: People of color and low-income people are more likely to live near highways or areas with heavy traffic.

Our study shows that HEPA air purifiers may offer meaningful health benefits under these circumstances.

What still isn’t known

Research shows that air pollution begins to affect cognitive function especially strongly around age 40. These effects may become increasingly prominent as people age.

HEPA air purifiers may therefore be especially beneficial for older adults. Our study did not explore this possibility, as fewer than 10 of our 119 participants were over the age of 60.

Also, our participants only used a HEPA air purifier for one month. It’s possible that longer durations of air purification may sustain or even increase the improvement in cognitive function we observed in our study.

Finally, it is unclear exactly how air purifiers improve cognition. Some studies suggest that exposure to particulate matter reduces the amount of the brain’s white matter, which helps brain cells conduct electrical signals and maintains connections between brain regions. The brain regions most harmed by air pollution are the ones that control mental flexibility and executive function, the same domains in which we saw improvements in our study.

We plan to study whether reducing particulate matter by using air purifiers is indeed protecting the brain’s white matter, and whether it could reverse some cognitive decline. We will explore that possibility by studying how levels of molecules called metabolites, which cells produce as they do their jobs, change in response to breathing polluted air and air cleaned by a HEPA filter.

The Research Brief is a short take on interesting academic work.

Nicholas Pellegrino, Research Associate in Public Health Sciences, University of Connecticut; Doug Brugge, Professor of Public Health Science and Community Medicine, University of Connecticut, and Misha Eliasziw, Associate Professor of Biostatistics, Public Health and Community Medicine, Tufts University

This article is republished from The Conversation under a Creative Commons license. Read the original article.

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Alzheimer’s Risk Gene APOE4 Silently Undermines Bone Quality in Women

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Buck Institute researchers discover a surprising connection between a major risk factor for Alzheimer’s

Photo by Karolina Grabowska on Pexels

Scientists at the Buck Institute for Research on Aging, along with collaborators at UC San Francisco, have discovered that APOE4, the most common genetic risk factor for Alzheimer’s disease, causes bone quality deficits specifically in female mice, through a mechanism that is invisible to standard imaging and can emerge as early as midlife.

The findings, published in Advanced Science, reveal an unexpected biological link between Alzheimer’s risk and skeletal health, and identify a new molecular pathway that could one day inform earlier diagnosis of cognitive decline or guide treatment for bone quality loss in women who carry the APOE4 gene.

“What makes this finding so striking is that bone quality is being compromised at a molecular level that a standard bone scan simply will not catch,” says Buck professor Birgit Schilling, PhD, a senior author of the study. “APOE4 is quietly disrupting the very cells responsible for keeping bone strong, and it is doing this specifically in females, which mirrors what we see with Alzheimer’s disease risk.”

Physicians have long observed that people with Alzheimer’s disease suffer bone fractures at higher rates, and that a diagnosis of osteoporosis in women is actually the earliest known predictor for Alzheimer’s. But the underlying mechanism connecting brain and bone health has remained elusive.

To investigate this connection, researchers, led by research scientist and co-first author of the paper Charles Schurman, PhD, first performed a proteomic analysis of aged mouse bone, a comprehensive survey of all the proteins present in the tissue. “The team discovered that bone, and particularly osteocytes, the long-lived cells embedded within it, is unusually rich in proteins associated with neurological disease, including apolipoprotein E [APOE] and amyloid precursor protein,” says Schurman. “Notably, APOE expression in osteocytes was twice as high in aged female mice as in young or male mice.”

The team then turned to a humanised mouse model carrying either APOE2 (associated with reduced Alzheimer’s risk), APOE3 (considered neutral), or APOE4 (the risk variant), and analysed bone and hippocampal tissue from the same animals. APOE4 produced strong, sex-specific effects on both the bone transcriptome and proteome; researchers found the protein-level disruption in bone was actually more pronounced than the corresponding changes in the hippocampus.

Despite the protein level disruption, cortical bone structure appeared normal under imaging. Researchers found that bone quality deficits arose not from changes in bone shape or density, but from APOE4’s suppression of perilacunar/canalicular remodelling, the process by which osteocytes actively maintain the microscopic channels that keep bone mechanically resilient. When this maintenance breaks down, bone quality deteriorates even when it looks intact.

“These results suggest that osteocytes could serve as early biological sentinels for age-related cognitive decline in women carrying APOE4,” says professor Lisa Ellerby, PhD, also a senior author of the paper. The Ellerby lab studies genetic risk factors for Alzheimer’s.  “We think that targeting osteocyte function may open a new front in preserving bone quality in this population.”

Researchers say there is a larger takeaway from this research that links brain and bone science.  “While we think this work is relevant for human patients with Alzheimer’s disease or with osteoporosis, this study also highlights the need for researchers to consider the human body as an entire system without isolating organs and diseases from each other,” says Ellerby.

Source: Buck Institute for Research on Aging

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Searching for the Weak Spots in C. Diff’s Defences

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New studies reveal how Clostridioides difficile behaves inside the body

Clostridioides difficile. Credit: CDC

Bacterial infections caused by Clostridioides difficile are a serious and persistent problem for patients and hospitals alike. The bacterium can cause severe diarrhoea, life-threatening inflammation of the colon, and recurring illness that dramatically reduces quality of life – especially for older adults, who face the highest risk of complications and death.  

C. diff remains difficult to control for a combination of factors. The bacterium survives many disinfectants, allowing it to easily spread in health care settings, where it is the most common cause of infectious diarrhoea. After entering the body through the mouth, the bacterium travels to the colon, where it colonises and starts releasing toxins that damage tissues. About one in nine patients treated for C. diff will develop another infection within weeks or months, often unpredictably, with the risk of a repeat infection increasing from there. And some strains of the bacterium have become resistant to the first-line antibiotics used to treat it.

Researchers at Tufts University School of Medicine are tackling these challenges by studying C. diff at multiple levels, from how individual bacterial cells behave inside the gut to the molecular switches that help them survive and spread. Together, these approaches are revealing hidden vulnerabilities that could lead to better ways to prevent new or recurrent infections, predict severe disease, or stop the bacterium before it causes harm. 

Watching Infections Unfold, Cell by Cell

“C. diff is everywhere,” said Aimee Shen, an associate professor of molecular biology and microbiology at Tufts School of Medicine. “But infections can look very different from one patient to the next.”  

Some people carry the bacterium without ever getting sick. Others develop severe, life-disrupting illness – typically after being treated for another illness with antibiotics that wipe out beneficial gut bacteria that may have otherwise warded off an infection.  

“A bad C. diff infection is reportedly incredibly painful, like glass shards moving through your intestine,” said Shen. “And there’s some research that shows that C. diff toxins actually act on neurons in the gut.” 

To better understand why the spectrum of disease severity varies so widely, Shen, Tufts’ School of Medicine professor Carol Kumamoto, and their collaborators developed a new imaging approach that lets them track what individual C. diff cells were doing inside the body. They applied fluorescent “reporters” – microscopic glowing tags that mark gene activity – to track which genes are turned on in individual C. diff cells in tissue samples from infected mice. This allowed them to see where the bacteria hide in the gut, which cells switched on toxin genes, and how activity differed from cell to cell during infection.

Their study, recently published in Nature Communications, showed that C. diff spread throughout the entire gut, including closer to the gut’s vulnerable lining than previously thought.  

However, toxin production didn’t depend on the bacteria’s location and only some cells made toxins at any given time. Shen said this suggests that disease may be driven by a small, hard-to-detect subpopulation rather than simply how many bacteria are present.

The imaging study also revealed other unexpected findings, including that a strain of toxin-overproducing bacteria formed unusually long, filament-like shapes in the gut during the acute phase of infection. “These were not observed in later stages of an infection,” said Shen. “This suggests that bacteria producing the most destructive amounts of toxins may be particularly susceptible to certain stresses encountered during infection.”

By illuminating how infections unfold cell by cell in this way, the new imaging method may provide information that could someday help doctors predict which patients are likely to develop severe or recurrent disease. It also may help researchers develop new treatments that better target harmful subpopulations of C. diff bacteria while sparing beneficial gut microbes.

Finding a Potential Weak Spot  

One reason C. diff spreads so effectively is its ability to form tough, dormant spores that act like microscopic seeds sealed in armour. Transmitted via trace amounts of faecal matter, these spores can survive for long periods, stubbornly resisting heat and many common disinfectants, including hand sanitisers. Once ingested, C. diff spores germinate – springing back to life and thus able to spawn toxins.  

This is a pivotal moment scientists hope to block.

Shen’s lab has long studied how the bacterium recognises it has reached the right place to reawaken. Most spore-forming bacteria rely on the same standard molecular sensors, but C. diff uses a different system. Its spores respond to bile acids found in digestive fluids, along with other signals that together flip the bacterium’s switch from dormancy to active growth.

In a study recently published in PLOS Biology, Shen, Tufts’ School of Medicine professor Ekaterina Heldwein, and their collaborators identified a key part of that switch. They found that two proteins, CspC and CspA, lock together to form a signalling hub that helps spores interpret environmental cues. By mapping the structure of this protein pair and testing how it functions, the team showed the combined complex controls how sensitive spores are to germination signals.

“It’s like we’ve identified a central control panel for deciding when the spore comes back to life,” Shen says. “If we understand how that panel works, scientists someday may be able to design new drugs to keep it switched off.”

Searching for More Precise Targets

Together, the studies offer a clearer picture of both how C. diff causes disease and when it becomes dangerous.

Now, in addition to continuing their work on single-cell imaging and spore germination, Shen’s lab is working to uncover other hidden rules that govern C. diff’s behaviour. This includes how it reproduces using a division mechanism unlike those seen in other well-studied bacteria – the focus of a 2023 study published by Shen and collaborators in Nature Communications.  

“The hope is the aspects that make C. diff unique – how it spreads, reproduces, and damages tissue – will allow researchers to design ways to target it much more specifically, while keeping the rest of the gut microbiome healthy and intact,” she said.

Original written by Genevieve Rajewski

Source: Tufts University

Categories : CancerTags : Leave a comment

Age, Sex, and Cancer Type Influence Risk of Subsequent Cancers Among Survivors

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Findings may have implications for long-term cancer survivorship surveillance

Researchers assess the risk of developing a subsequent primary cancer based on demographic factors and cancer characteristics. Tara Winstead, Pexels (CC0, https://creativecommons.org/publicdomain/zero/1.0/)

Risk of developing a subsequent primary cancer varied significantly by age at initial diagnosis, sex, and type of first cancer, according to a study by Oxana Palesh and Susan Hong and colleagues at Virginia Commonwealth University, U.S., published April 28th in the open-access journal PLOS Medicine.

Advances in cancer detection and treatment have led to a growing population of cancer survivors. In the U.S., the number of cancer survivors is expected to grow by 22% over the next decade – from 18 million in 2025 to more than 22 million by 2035. Survivors remain at higher risk for developing new primary cancers distinct from their original diagnosis. This risk may be influenced by factors such as older age, exposure to radiation and/or chemotherapy and ongoing lifestyle factors like smoking, obesity and poor diet. Understanding who is at greater risk and how this risk changes over time can help to inform prevention and monitoring strategies.

Using retrospective data from more than 3 million cancer survivors in the U.S., researchers examined how demographic factors and cancer characteristics correlate with subsequent cancer risk. Several factors were associated with developing a subsequent cancer, including older age at initial diagnosis and male sex. In addition, survivors of lung, bladder, and skin melanoma were at higher risk of developing new cancer.

These findings reinforce the importance of long‑term survivorship care and risk‑based monitoring. By identifying survivor groups at heightened risk, studies like this can help to inform tailored prevention strategies, surveillance guidelines, and survivorship care planning as the cancer survivor population continues to grow.

First author Hui Cheng adds, “By examining nearly five decades of national data, we found population-level shifts in subsequent primary cancer risk, with several survivor groups experiencing rising risks. These findings can help design more tailored surveillance and prevention strategies.”

Provided by PLOS

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Beware the Salt Trap: Why South Africa’s Heart Health Depends on More Than Regulation

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Credit: Pixabay CC0

While South Africa was among the first countries to introduce mandatory salt reduction targets in processed foods, health experts warn that hypertension remains a major public health concern. The reason is increasingly clear, the problem is no longer only what is manufactured, but how people eat every day.

As World Salt and Hypertension Awareness Week (4–29 May) approaches, the focus should shift from reformulated products to daily behaviour change. High salt intake causes the body to retain excess fluid, which increases the volume of blood in the system and places greater pressure on the artery walls, directly leading to the development of hypertension.

“While the policy has successfully reduced hidden salt in many staple foods, it has not yet shifted South African taste preferences.,” says Lizeth Kruger, Clinic Executive at Dis-Chem. “We are still reaching for the shaker out of habit, and that’s where the real danger lies.”

Hypertension remains one of South Africa’s leading risk factors for heart disease and stroke, often progressing silently until complications arise. According to the Heart and Stroke Foundation South Africa, more than one in three adults lives with high blood pressure, a ‘silent killer’ that accounts for roughly half of all strokes and 40% of heart attacks in the country.

Kruger says a shift in everyday eating habits could reduce excess salt intake

1. Automatic salt shake

Many people add salt before tasting their food, even when meals have already been seasoned during cooking or processing.

2. Hidden salt in everyday staples

Stock cubes, processed meats, margarine and sauces remain significant sodium sources, especially when used frequently in daily cooking.

3. Convenience meals and takeaways

Ultra-processed foods and fast meals are often high in sodium, with a single serving sometimes approaching or exceeding the recommended daily limit.

4. A conditioned taste for salt

Long-term high-salt diets have shaped taste preferences, making fresh, whole foods seem bland and reinforcing reliance on added seasoning.

5. Unnoticed snack intake

Savoury snacks, biltong and crackers contribute meaningful sodium but are often not counted in daily intake.

Small changes, meaningful impact

Kruger says reducing salt intake is less about strict diets and more about changing repeat behaviours.

“Small, consistent adjustments can make a real difference over time,” she explains.

  • Tasting food before adding salt is a simple first step, as many meals are already seasoned. Rinsing canned foods such as beans or corn can also reduce sodium content.
  • Flavour can be enhanced using alternatives such as garlic, lemon juice, herbs and black pepper, while checking labels for lower-sodium options helps guide better choices.

A shared responsibility

“Regulation has laid the foundation, but the final step is ours,” Kruger advises. “By becoming more aware of everyday habits, we can reduce the risk of hypertension, stroke and heart disease in our homes.”