Scientists uncover cancer-causing chemicals hidden in everyday foods

 

More people are paying close attention to what they eat, often tracking calories, exercising daily, and filling their plates with foods that seem naturally healthy, including fruits and vegetables. Yet even nutritious foods can carry hidden chemical concerns. Some contaminants can enter food from the environment, while others can form during high heat cooking methods such as heating, smoking, grilling, roasting, and frying.

Among the compounds of concern are polycyclic aromatic hydrocarbons, or PAHs (hydrophobic organic compounds comprising multiple fused aromatic rings). Some PAHs are known for their cancer causing potential, which makes reliable food testing an important part of protecting public health.

A Hidden Food Safety Challenge

Detecting PAHs in food is not simple. Conventional extraction methods, such as solid phase extraction, liquid liquid extraction, and accelerated solvent extraction, can be affordable, but they often require lengthy preparation, heavy hands on labor, and chemical intensive procedures that are not ideal for workers or the environment.

To solve these problems, scientists have been turning to a streamlined method known as QuEChERS (Quick, Easy, Cheap, Effective, Rugged, and Safe). The approach is designed to speed up sample preparation, reduce chemical use, improve recovery rates, and make food contaminant testing more practical for routine safety checks.

In a 2025 study, researchers from the Department of Food Science and Biotechnology at Seoul National University of Science and Technology, led by Professor Joon-Goo Lee, used QuEChERS to measure eight PAHs (Benzo[a]anthracene, Chrysene, Benzo[b]fluoranthene, Benzo[k]fluoranthene, Benzo[a]pyrene, Indeno[1,2,3-cd]pyrene, Dibenz[a,h]anthracene, and Benzo[g,h,i]perylene in food. The findings were published in the journal Food Science and Biotechnology.

Faster Testing With Strong Accuracy

The team used acetonitrile to extract PAHs from food samples, then tested several purification strategies involving different combinations of sorbents. The method was validated across multiple food matrices, showing strong performance. Calibration curves for all eight PAHs had R2 values above 0.99, indicating a highly linear and reliable measurement system.

Further analysis using gas chromatography and mass spectrometry showed that the limits of detection ranged from 0.006 to 0.035 µg/kg, while the limits of quantification ranged from 0.019 to 0.133 µg/kg. Recovery rates were also strong, ranging from 86.3 to 109.6% at 5 µg/kg, 87.7 to 100.1% at 10 µg/kg, and 89.6 to 102.9% at 20 µg/kg. Precision values stayed between 0.4 and 6.9% across all tested food matrices.

The study also reported that, among the foods tested, the highest PAH levels were found in soybean oil, followed by duck meat and canola oil.

Prof. Lee explains, "This method not only simplifies the analytical process but also demonstrates high efficiency in detection compared to conventional methods. It can be applied to a wide range of food matrices."

Why PAHs Matter

PAHs can form when food is exposed to high temperatures or smoke. According to the National Cancer Institute, PAHs can develop when fat and juices from meat drip onto a hot surface or open flame, creating smoke that deposits these compounds onto the food. PAHs can also form during smoking and may be found in sources such as cigarette smoke and car exhaust fumes.

The NCI notes that PAHs and related high temperature cooking compounds have caused cancer in animal studies, although human population studies have not established a definitive link between exposure from cooked meats and cancer. This uncertainty is one reason more accurate measurement tools are valuable. Better testing can help regulators, researchers, and food companies understand where contamination is occurring and how it can be reduced.

Newer Research Points to Broader Use

Since the SeoulTech study, other researchers have continued refining QuEChERS based methods for PAH detection. A 2025 study in Foods developed a modified QuEChERS method with a freeze out step and applied it to 302 retail food samples. That work found the highest concentration of four priority PAHs in Kezuribushi, a smoked and dried fish product, and identified grilled chicken feet as a possible health concern based on the European Food Safety Authority margin of exposure approach.

Another 2025 study focused on cereals and cereal based products. Researchers developed a modified QuEChERS method using Z Sep⁺ clean up and gas chromatography with tandem mass spectrometry. In 96 cereal samples and 18 cereal based products from the Romanian market, only chrysene was quantified in 17% of cereal samples, while no PAHs were quantified in the derived products.

Together, these newer findings suggest that QuEChERS based approaches are becoming increasingly useful for different food categories, from oils and meats to smoked products and cereals. They also show why food specific testing matters, since PAH levels can vary widely depending on ingredients, processing, cooking methods, and environmental exposure.

Safer Food Testing and Cleaner Labs

For the food industry, a faster and more efficient PAH testing method could improve safety management by making it easier to inspect products before they reach consumers. The approach may also reduce costs and improve working conditions by cutting down on time consuming procedures and limiting the use of hazardous chemicals.

"Our research can improve public health by providing safe food. It also reduces the use and emission of hazardous chemicals in laboratory testing," concludes Prof. Lee.

The broader takeaway is clear: food safety testing is becoming faster, cleaner, and more precise. By improving how scientists detect PAHs, methods like QuEChERS could help identify hidden contaminants, support safer food production, and reduce chemical waste in the lab.

About Professor Joon Goo Lee

Joon Goo Lee is a Professor at the Department of Food Science and Biotechnology, Seoul National University of Science and Technology. He is an expert in food regulation and safety assessment. He served as a scientific officer at Korea's Ministry of Food and Drug Safety and as a visiting researcher at FSANZ. He is a member of the National Food Sanitation Committee and an expert for the FAO/WHO JECFA. He also serves as the executive director of the Korean food safety societies. His research focuses on risk assessment and the reduction of contaminants in food, contributing to science based policies and improved public health.

Journal Reference:

1. Jihun Jeong, Minju Koo, Joon-Goo Lee. QuEChERS method development for the GC–MS analysis of polycyclic aromatic hydrocarbons in food. Food Science and Biotechnology, 2025; 34 (12): 2749 DOI: 10.1007/s10068-025-01910-2

Courtesy:

Seoul National University of Science & Technology. "Scientists uncover cancer-causing chemicals hidden in everyday foods." ScienceDaily. ScienceDaily, 22 May 2026. <www.sciencedaily.com/releases/2026/05/260522030853.htm>. 

 

 

 

 

Scientists discover a two-stage aging process that may cause cancer and arthritis

 

Researchers are offering a new way to understand why aging is so closely connected to chronic illness. In a review published in Aging-US titled "Aging as a multifactorial disorder with two stages," scientists from University College London and Queen Mary University of London describe a model suggesting that diseases linked to aging may develop through two separate but connected phases over the course of life.

The review was written by David Gems and Alexander Carver from University College London, along with Yuan Zhao from Queen Mary University of London. Their work combines ideas from evolutionary biology with findings from modern biomedical research to explain how early damage in the body may later contribute to diseases such as cancer, arthritis, and infections.

How Early-Life Damage May Shape Health Decades Later

According to the researchers, the first stage begins earlier in life when the body experiences various forms of disruption. These can include infections, physical injuries, or genetic mutations. While the body is often able to repair or contain much of this damage, some of it may remain hidden rather than being fully removed.

The second stage occurs later in life as normal genetic activity starts changing in ways that are no longer beneficial to the body. These late-life biological changes can weaken the body's ability to keep earlier damage under control. As a result, previously contained problems may gradually develop into disease.

The scientists argue that this process helps explain why many illnesses appear mainly in older adults even though their origins may trace back much earlier.

Why Diseases Like Shingles and Arthritis Appear With Age

The review highlights aging as a multifactorial process, meaning it is driven by many interacting biological factors instead of a single cause. The proposed model suggests that the combination of earlier damage and later-life genetic changes plays a major role in age-related disease.

For example, dormant viruses that remain inactive for years can become active again when the immune system weakens with age, leading to conditions such as shingles. In a similar way, injuries sustained in youth may eventually contribute to osteoarthritis as aging tissues become less resilient over time.

Inherited genetic mutations may also stay silent for decades before increasing the risk of diseases such as cancer or fibrosis later in life.

Evolutionary Biology and Aging Research

The researchers say their model builds on long-standing evolutionary theories of aging. One influential idea is that natural selection becomes weaker later in life, allowing harmful biological processes to emerge with age because they have less impact on reproduction and survival earlier in life.

The review also references studies involving the roundworm Caenorhabditis elegans. In these experiments, early mechanical damage in the worms eventually led to fatal infections in old age. The scientists suggest similar patterns may also occur in humans.

A New Framework for Healthier Aging

Overall, the review presents aging as a process shaped by multiple interacting causes that unfold over time. By separating aging into two major stages, early-life damage and later-life genetic activity, the researchers believe their framework could help guide future strategies aimed at disease prevention and healthier aging.

The findings also raise the possibility that reducing damage earlier in life or targeting harmful late-life biological changes could help lower the risk of chronic disease in older adults.

Journal Reference:

1. David Gems, Alexander Carver, Yuan Zhao. Aging as a multifactorial disorder with two stages. Aging, 2025; 17 (12): 2989 DOI: 10.18632/aging.206339

Courtesy:

Impact Journals LLC. "Scientists discover a two-stage aging process that may cause cancer and arthritis." ScienceDaily. ScienceDaily, 21 May 2026. <www.sciencedaily.com/releases/2026/05/260521072420.htm>. 

 

 

 

Scientists successfully transfer longevity gene and extend lifespan

 

Naked mole rats are not much to look at, but their biology has made them one of the most fascinating animals in aging research. These small, wrinkled rodents can live for decades, rarely develop cancer, and seem unusually protected from many of the diseases that normally arrive with age.

Researchers at the University of Rochester showed that one of those biological advantages can be moved into another mammal. By transferring a gene linked to the naked mole rat's unusually high levels of high molecular weight hyaluronic acid (HMW-HA), the team improved health and modestly extended lifespan in mice.

The work, published in Nature in 2023, suggested that at least some longevity traits that evolved in long-lived animals may be adaptable beyond the species that developed them. The genetically modified mice lived healthier lives and had an approximate 4.4 percent increase in median lifespan compared with ordinary mice.

"Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals," says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester.

Gorbunova, along with Andrei Seluanov, a professor of biology, and their colleagues, focused on a gene that helps produce HMW-HA. This substance is abundant in naked mole rats and has been tied to their striking resistance to cancer, inflammation, and age-related decline.

Why Naked Mole Rats Fascinate Aging Scientists

Naked mole rats are about the size of mice, yet their lifespans are extraordinary for rodents. They can live up to 41 years, nearly ten times longer than similarly sized rodents.

Their long lives are not the only reason scientists study them. As they age, naked mole rats appear to avoid many conditions that commonly affect other mammals, including neurodegeneration, cardiovascular disease, arthritis, and cancer. For decades, Gorbunova, Seluanov, and other researchers have been investigating how these animals stay so resilient.

One major clue is HMW-HA. Naked mole rats carry roughly ten times more of it than mice and humans. In earlier work, researchers found that when HMW-HA was removed from naked mole rat cells, those cells became more likely to form tumors.

That finding raised a powerful question. If HMW-HA helps naked mole rats resist cancer and age-related damage, could the same mechanism work in a different animal?

Transferring a Naked Mole Rat Longevity Gene

To test the idea, the Rochester team engineered mice to carry the naked mole rat version of the hyaluronan synthase 2 gene. This gene helps make the protein that produces HMW-HA.

All mammals have a version of hyaluronan synthase 2, but the naked mole rat version appears to be especially active. It seems to drive stronger gene expression, leading to greater production of the protective molecule.

The modified mice developed higher levels of hyaluronan in several tissues. They also showed stronger protection against spontaneous tumors and chemically induced skin cancer.

The effects were not limited to cancer resistance. The mice carrying the naked mole rat gene stayed healthier overall, lived longer than regular mice, had less inflammation in multiple tissues as they aged, and maintained better gut health.

Because chronic inflammation is one of the major biological features of aging, the reduction in inflammation was especially important. The researchers believe HMW-HA may work partly by directly influencing the immune system, although more research is needed to explain exactly how it produces such broad benefits.

A Small Lifespan Gain With Big Implications

The increase in median lifespan was about 4.4 percent, which is modest. But the larger significance is that a longevity mechanism from one mammal was successfully transferred to another.

That makes the finding more than a mouse study about a single gene. It supports the idea that nature's long-lived species may contain biological tools that can be studied, adapted, and possibly used to improve health in other animals.

"It took us 10 years from the discovery of HMW-HA in the naked mole rat to showing that HMW-HA improves health in mice," Gorbunova says. "Our next goal is to transfer this benefit to humans."

The researchers believe there may be two main ways to pursue that goal. One would be to slow the breakdown of HMW-HA in the body. Another would be to increase its production.

"We already have identified molecules that slow down hyaluronan degradation and are testing them in pre-clinical trials," Seluanov says. "We hope that our findings will provide the first, but not the last, example of how longevity adaptations from a long-lived species can be adapted to benefit human longevity and health."

Newer Research Adds to the Naked Mole Rat Story

Since the 2023 Nature study, naked mole rats have continued to offer new clues about why they age so differently from other mammals. A 2025 study in Science reported another potential longevity mechanism involving cGAS, a protein better known for its role in immune defense. In humans and mice, cGAS can interfere with some forms of DNA repair, but the naked mole rat version appears to help cells repair DNA damage more effectively. That study found that specific changes in the naked mole rat protein improved genome stability and delayed signs of aging in experimental models.

This newer work does not replace the HMW-HA finding. Instead, it strengthens a broader pattern. Naked mole rats likely owe their unusually long, healthy lives to several overlapping defenses, including cancer resistance, inflammation control, DNA repair, and tissue protection.

For human aging research, that matters. A single molecule is unlikely to become a simple fountain of youth. But each discovery gives scientists another possible route for targeting the biological processes that drive age-related disease.

The 2023 gene transfer study remains a striking proof of concept. A survival strategy that evolved in one of nature's strangest mammals helped mice resist disease, age more smoothly, and live longer. The next challenge is determining whether those same biological tricks can be safely adapted to improve human healthspan.

Journal Reference:

1. Zhihui Zhang, Xiao Tian, J. Yuyang Lu, Kathryn Boit, Julia Ablaeva, Frances Tolibzoda Zakusilo, Stephan Emmrich, Denis Firsanov, Elena Rydkina, Seyed Ali Biashad, Quan Lu, Alexander Tyshkovskiy, Vadim N. Gladyshev, Steve Horvath, Andrei Seluanov, Vera Gorbunova. Increased hyaluronan by naked mole-rat Has2 improves healthspan in mice. Nature, 2023; 621 (7977): 196 DOI: 10.1038/s41586-023-06463-0

Courtesy:

University of Rochester. "Scientists successfully transfer longevity gene and extend lifespan." ScienceDaily. ScienceDaily, 10 May 2026. <www.sciencedaily.com/releases/2026/05/260510030948.htm>. 

 

 

 

 

A rare cancer-fighting plant compound has been decoded

 

Researchers at UBC Okanagan have uncovered the process plants use to create mitraphylline, a rare natural compound that has attracted attention for its possible cancer fighting properties.

Mitraphylline belongs to a unique class of plant chemicals known as spirooxindole alkaloids. These molecules are recognized for their unusual twisted ring structures and their powerful biological effects, including anti inflammatory and anti tumor activity.

Even though scientists have studied these compounds for years, the exact molecular steps plants use to produce them had remained unknown.

Breakthrough Discovery in Plant Chemistry

That mystery began to unravel in 2023 when Dr. Thu-Thuy Dang's team in UBC Okanagan's Irving K. Barber Faculty of Science identified the first known plant enzyme capable of twisting a molecule into the distinctive spiro shape.

Building on that earlier finding, doctoral student Tuan-Anh Nguyen led new research that uncovered two critical enzymes involved in the production of mitraphylline. One enzyme organizes the molecule into the correct three dimensional structure, while the second transforms it into mitraphylline itself.

"This is similar to finding the missing links in an assembly line," says Dr. Dang, UBC Okanagan Principal's Research Chair in Natural Products Biotechnology. "It answers a long-standing question about how nature builds these complex molecules and gives us a new way to replicate that process."

Why Mitraphylline Is So Valuable

Many promising natural compounds are found only in tiny amounts inside plants, making them difficult and expensive to recreate in laboratories. Mitraphylline is one of those rare substances. It exists only in trace quantities in tropical trees such as Mitragyna (kratom) and Uncaria (cat's claw), both members of the coffee family.

Now that researchers have identified the enzymes responsible for shaping and assembling mitraphylline, they have a clearer path toward producing the compound and related molecules in more sustainable ways.

"With this discovery, we have a green chemistry approach to accessing compounds with enormous pharmaceutical value," says Nguyen. "This is a result of UBC Okanagan's research environment, where students and faculty work closely to solve problems with global reach."

Nguyen also reflected on the experience of contributing to the breakthrough.

"Being part of the team that uncovered the enzymes behind spirooxindole compounds has been amazing," Nguyen adds. "UBC Okanagan's mentorship and support made this possible, and I'm excited to keep growing as a researcher here in Canada."

International Collaboration Fuels the Research

The project brought together Dr. Dang's laboratory at UBC Okanagan and Dr. Satya Nadakuduti's research group at the University of Florida.

Funding for the work came from Canada's Natural Sciences and Engineering Research Council's Alliance International Collaboration program, the Canada Foundation for Innovation, and the Michael Smith Health Research BC Scholar Program. Additional support was provided by the United States Department of Agriculture's National Institute of Food and Agriculture.

"We are proud of this discovery coming from UBC Okanagan. Plants are fantastic natural chemists," Dr. Dang says. "Our next steps will focus on adapting their molecular tools to create a wider range of therapeutic compounds."

Journal Reference:

1. Larissa C Laforest, Tuan-Anh M Nguyen, Gabriel Oliveira Matsumoto, Pavithra Ramachandria, Andre Chanderbali, Siva Rama Raju Kanumuri, Abhisheak Sharma, Christopher R McCurdy, Thu-Thuy T Dang, Satya Swathi Nadakuduti. A chromosome-level Mitragyna parvifolia genome unveils spirooxindole alkaloid diversification and mitraphylline biosynthesis. The Plant Cell, 2025; 37 (9) DOI: 10.1093/plcell/koaf207

Courtesy:

University of British Columbia Okanagan. "A rare cancer-fighting plant compound has been decoded." ScienceDaily. ScienceDaily, 12 May 2026. <www.sciencedaily.com/releases/2026/05/260512213836.htm>. 

 

 

 

Scientists reverse Alzheimer’s in mice with breakthrough nanotechnology

 

An international team of researchers has reported a striking Alzheimer's breakthrough in mice using specially engineered nanoparticles that do much more than deliver medicine. These microscopic particles act as drugs themselves, helping the brain restore its own natural cleaning system and dramatically reducing toxic protein buildup linked to Alzheimer's disease.

The work was led by scientists from the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital Sichuan University (WCHSU), together with collaborators in the United Kingdom. Their findings were published in Signal Transduction and Targeted Therapy.

Instead of focusing directly on damaged neurons, the scientists targeted the blood-brain barrier (BBB), a protective network of cells and blood vessels that controls what enters and leaves the brain. In Alzheimer's disease, this system gradually breaks down, allowing harmful proteins to accumulate and damaging brain function over time.

The researchers designed bioactive nanoparticles called "supramolecular drugs" to help restore this barrier and restart the brain's ability to remove waste.

Repairing the Brain's Cleanup System

The human brain uses enormous amounts of energy. In adults, it consumes around 20% of the body's total energy supply, and in children the figure can reach 60%. To meet those demands, the brain depends on an extremely dense network of blood vessels. Scientists estimate the brain contains roughly one billion capillaries, with nearly every neuron connected to its own blood supply.

Growing evidence suggests these blood vessels play a far larger role in dementia than previously thought. Many researchers now believe vascular damage is not simply a side effect of Alzheimer's disease but may actively drive its progression. Recent studies have also linked blood-brain barrier breakdown to early cognitive decline and increased buildup of toxic proteins.

Under healthy conditions, the blood-brain barrier helps clear waste products from the brain while blocking harmful substances such as toxins and pathogens. One of the most important waste proteins is amyloid-β (Aβ), the sticky material that forms plaques associated with Alzheimer's disease.

In Alzheimer's patients, the brain's waste disposal system begins to fail. As amyloid-β accumulates, neurons become damaged and memory problems worsen.

Alzheimer's Plaques Dropped Within Hours

To test the new therapy, researchers used genetically engineered mice that develop high levels of amyloid-β and progressive cognitive decline similar to Alzheimer's disease in humans.

The animals received only 3 doses of the nanoparticles. The effects appeared quickly.

"Only 1h after the injection we observed a reduction of 50-60% in Aβ amount inside the brain," explains Junyang Chen, first co-author of the study, researcher at the West China Hospital of Sichuan University and PhD student at the University College London (UCL).

The long-term results were even more dramatic. Scientists tracked the animals for months using behavioral and memory tests covering different stages of disease progression.

In one experiment, researchers treated a 12-month-old mouse (equivalent to a 60-year-old human) and evaluated it six months later. By that point, the animal was roughly comparable to a 90-year-old human. Despite its age, the mouse behaved similarly to a healthy animal with no signs of Alzheimer's-related decline.

"The long-term effect comes from restoring the brain's vasculature. We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses. But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What's remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels," said Giuseppe Battaglia, ICREA Research Professor at IBEC, Principal Investigator of the Molecular Bionics Group and leader of the study.

How the Nanoparticles Work

A major focus of the study was a protein called LRP1, which acts like a molecular transport system at the blood-brain barrier. Normally, LRP1 recognizes amyloid-β, binds to it, and moves it out of the brain and into the bloodstream for disposal.

But the process is delicate. If LRP1 binds amyloid-β too strongly, the transport machinery becomes overloaded and breaks down. If the interaction is too weak, waste removal does not occur efficiently enough. Either way, amyloid-β starts piling up in the brain.

The supramolecular nanoparticles were engineered to mimic the natural molecules that interact with LRP1. By doing this, the particles appear to "reset" the transport system, allowing amyloid-β to move out of the brain again.

Researchers say this strategy differs from many traditional Alzheimer's therapies because it focuses on repairing the brain's own infrastructure instead of simply attacking plaques directly.

That idea has gained momentum in recent years. Scientists increasingly view Alzheimer's as both a neurological and vascular disease, with disrupted blood flow and blood-brain barrier damage contributing to the spread of toxic proteins.

A Different Kind of Nanomedicine

Most nanomedicine approaches use nanoparticles as delivery vehicles to carry drugs into the body. In this case, the nanoparticles themselves are the therapy.

The research team created the particles using a bottom-up molecular engineering process that allowed them to precisely control their size and the number of ligands on their surface. This precision helped the particles interact with receptors on cell membranes in highly specific ways.

By influencing how these receptors move and function, the nanoparticles improved amyloid-β clearance and helped restore healthier blood vessel activity in the brain.

Researchers say this approach could eventually complement other Alzheimer's treatments, including anti-amyloid antibody drugs. One of the biggest problems facing current therapies is getting enough medicine across the blood-brain barrier safely and efficiently.

Other experimental technologies are also exploring ways to overcome this challenge, including ultrasound-based delivery systems, "brain shuttle" molecules, and additional nanoparticle platforms designed to cross the barrier more effectively.

What Happens Next

Although the findings are promising, the research remains in the animal-testing stage. Many Alzheimer's therapies that worked in mice have later failed in human clinical trials.

Still, experts say the study highlights an increasingly important area of Alzheimer's research: restoring the health of the brain's blood vessels and waste-removal systems.

"Our study demonstrated remarkable efficacy in achieving rapid Aβ clearance, restoring healthy function in the blood-brain barrier and leading to a striking reversal of Alzheimer's pathology," concludes Lorena Ruiz Perez, researcher at the Molecular Bionics group from the Institute for Bioengineering of Catalonia (IBEC) and Serra Hunter Assistant Professor at the University of Barcelona (UB).

The project involved researchers from the Institute for Bioengineering of Catalunya (IBEC), West China Hospital of Sichuan University, West China Xiamen Hospital of Sichuan University, University College London, the Xiamen Key Laboratory of Psychoradiology and Neuromodulation, the University of Barcelona, the Chinese Academy of Medical Sciences, and the Catalan Institution for Research and Advanced Studies (ICREA).

Journal Reference:

1. Junyang Chen, Pan Xiang, Aroa Duro-Castano, Huawei Cai, Bin Guo, Xiqin Liu, Yifan Yu, Su Lui, Kui Luo, Bowen Ke, Lorena Ruiz-Pérez, Qiyong Gong, Xiaohe Tian, Giuseppe Battaglia. Rapid amyloid-β clearance and cognitive recovery through multivalent modulation of blood–brain barrier transport. Signal Transduction and Targeted Therapy, 2025; 10 (1) DOI: 10.1038/s41392-025-02426-1

Courtesy:

Institute for Bioengineering of Catalonia (IBEC). "Scientists reverse Alzheimer’s in mice with breakthrough nanotechnology." ScienceDaily. ScienceDaily, 17 May 2026. <www.sciencedaily.com/releases/2026/05/260517030326.htm>. 

 

 

 

 

 

Scientists found the “holy grail” gene that could one day help humans regrow limbs

Scientists studying axolotls, zebrafish, and mice have uncovered a shared set of genes that could someday help researchers develop therapies for regrowing human limbs. The findings, published in the Proceedings of the National Academy of Sciences, point to a possible new direction for regenerative medicine and gene therapy.

"This significant research brought together three labs, working across three organisms to compare regeneration," said Wake Forest Assistant Professor of Biology Josh Currie, whose lab studies the Mexican axolotl salamander. "It showed us that there are universal, unifying genetic programs that are driving regeneration in very different types of organisms, salamanders, zebrafish and mice."

The project also included Duke University plastic surgeon David A. Brown, who studies digit regeneration in mice, and Kenneth D. Poss of the University of Wisconsin-Madison, whose research focuses on fin regeneration in zebrafish.

Shared Regeneration Genes Across Species

Around the world, more than 1 million amputations occur every year due to diabetes-related vascular disease, traumatic injuries, infections, and cancer, according to Global Burden of Disease statistics. Researchers expect that number to climb as populations age and diabetes becomes more common.

For years, scientists have searched for ways to move beyond prosthetic limbs and toward treatments capable of restoring natural movement, sensation, and function. This new study suggests that a group of genes known as SP genes may play a central role in that effort.

Researchers selected axolotls, zebrafish, and mice because each species offers unique insights into regeneration.

Axolotls are famous for their extraordinary ability to regrow entire limbs along with tails, spinal cord tissue, and parts of organs including the heart, brain, lungs, liver, and jaw.

Zebrafish are another powerful regeneration model because they can repeatedly regrow damaged tail fins. They are also capable of repairing the heart, brain, spinal cord, kidneys, retinas, and pancreas.

Mice were included because, like humans, they are mammals. Mice can regenerate the tips of their digits, and humans can sometimes regrow fingertips if the nailbed remains intact after injury, allowing skin, flesh, and bone to regenerate.

Currie said the team discovered that the regenerating epidermis, or skin tissue, in all three species activated two genes called SP6 and SP8. Researchers then began investigating exactly how those genes contribute to regeneration.

Biology Ph.D. student Tim Curtis Jr. participated in the work in Currie's lab, along with undergraduate Elena Singer-Freeman, a Goldwater Scholar and 2025 Wake Forest graduate in biochemistry and molecular biology.

CRISPR Experiments Reveal Key Limb Regrowth Role

The researchers found that SP8 is especially important for limb regeneration in salamanders. Using CRISPR gene-editing technology, Currie's team removed SP8 from the axolotl genome.

Without the gene, axolotls were unable to properly regenerate limb bones. Scientists observed similar problems in mice when SP6 and SP8 were missing from regenerating digits.

Using those findings, Brown's lab designed a viral gene therapy based on a tissue regeneration enhancer previously identified in zebrafish.

The therapy delivered a signaling molecule called FGF8, which is normally activated by SP8. In mice, the treatment encouraged bone regrowth in damaged digits and partially restored some regenerative abilities lost when the SP genes were absent.

Human limbs cannot naturally regenerate the way salamander limbs do, but researchers believe future therapies could potentially imitate some of the biological mechanisms controlled by SP genes.

"We can use this as a kind of proof of principle that we might be able to deliver therapies to substitute for this regenerative style of epidermis in regrowing tissue in humans," Currie explained.

Building Toward Future Human Limb Regeneration

Researchers caution that the work is still at an early stage, and far more studies will be needed before discoveries in mice could translate into therapies for humans. Even so, Currie described the research as an important foundation for future regenerative treatments.

"Scientists are pursuing many solutions for replacing limbs, including bioengineered scaffolds and stem cell therapies," Currie explained. "The gene-therapy approach in this study is a new avenue that can complement and potentially augment what will surely be a multi-disciplinary solution to one day regenerate human limbs."

Currie also emphasized the importance of collaboration between scientists working on very different animals and biological systems.

"Many times, scientists work in their silos: we're just working in axolotl, or we're just working in mouse, or just working in fish," Currie said. "A real standout feature of this research is that we work across all these different organisms. That is really powerful, and it's something that I hope we'll see more of in the field."

Journal Reference:

1. David A. Brown, Katja K. Koll, Erin Brush, Grant Darner, Timothy Curtis, Thomas Dvergsten, Melissa Tran, Colleen Milligan, David W. Wolfson, Trevor J. Gonzalez, Sydney Jeffs, Alyssa Ehrhardt, Rochelle Bitolas, Madeleine Landau, Kendall Reitz, David S. Salven, Leslie A. Slota-Burtt, Isabel Snee, Elena Singer-Freeman, Sayuri Bhatia, Jianhong Ou, Aravind Asokan, Joshua D. Currie, Kenneth D. Poss. Enhancer-directed gene delivery for digit regeneration based on conserved epidermal factors. Proceedings of the National Academy of Sciences, 2026; 123 (17) DOI: 10.1073/pnas.2532804123

Courtesy:

Wake Forest University. "Scientists found the “holy grail” gene that could one day help humans regrow limbs." ScienceDaily. ScienceDaily, 9 May 2026. <www.sciencedaily.com/releases/2026/05/260508003121.htm>.

 

 

 

 

 

New obesity discovery rewrites decades of fat science

For decades, scientists believed they understood one of the body's key fat-burning proteins. Known as hormone-sensitive lipase, or HSL, the enzyme was thought to work mainly as the body's emergency fuel switch, helping release stored fat when energy runs low.

But researchers uncovered something unexpected. HSL was not just working on the surface of fat droplets inside fat cells. It was also operating deep inside the nucleus of those cells, where DNA is stored and important genetic activity is controlled. The discovery revealed an entirely different side to a protein scientists had studied since the 1960s.

The findings, published in Cell Metabolism, helped solve a long-standing mystery in obesity research and opened new directions for understanding diabetes, heart disease, and other metabolic disorders.

Fat Cells Do Far More Than Store Calories

Fat cells, also called adipocytes, are often viewed as passive storage containers for excess calories. In reality, they are highly active cells that help regulate the body's entire energy system.

Inside adipocytes, fat is stored in structures called lipid droplets. When the body needs fuel between meals or during fasting, hormones such as adrenaline trigger the release of that stored energy. HSL plays a central role in this process by breaking down triglycerides into fatty acids that other organs can use for fuel.

Scientists long assumed that removing HSL would prevent fat breakdown and lead to obesity. Surprisingly, that is not what happened.

Studies in both mice and people with mutations in the HSL gene showed the opposite effect. Instead of accumulating extra fat, they developed lipodystrophy, a rare condition in which the body loses healthy fat tissue.

That contradiction puzzled researchers for years.

Obesity and Dangerous Fat Loss Share Similar Problems

Although obesity and lipodystrophy seem completely different, they can produce many of the same health complications.

In obesity, fat tissue becomes enlarged and dysfunctional. In lipodystrophy, the body lacks enough properly functioning fat tissue. In both cases, adipocytes fail to regulate energy normally, which can contribute to insulin resistance, type 2 diabetes, fatty liver disease, inflammation, and cardiovascular problems.

This overlap suggested that healthy fat tissue is not simply about how much fat the body carries. The quality and function of fat cells may be just as important.

Researchers at the Institute of Cardiovascular and Metabolic Diseases (I2MC) at the University of Toulouse wanted to understand why the loss of HSL caused fat tissue to break down instead of build up. What they found changed the scientific picture of fat metabolism.

Scientists Discover HSL Inside the Cell Nucleus

The research team, led by Dominique Langin, discovered that HSL was located in an unexpected place inside adipocytes: the nucleus.

The nucleus acts as the cell's control center. It contains DNA and regulates which genes are switched on or off. Proteins found in the nucleus often help control cell growth, repair, metabolism, and communication.

"In the nucleus of adipocytes, HSL is able to associate with many other proteins and take part in a program that maintains an optimal amount of adipose tissue and keeps adipocytes 'healthy'," explained Jérémy Dufau, co-author of the study.

Researchers found that nuclear HSL appears to help regulate important cellular systems, including mitochondrial activity and the extracellular matrix, which provides structural support for tissues.

Mitochondria are often called the power plants of cells because they generate energy. The extracellular matrix helps maintain the shape and integrity of tissues. Problems in either system have been linked to obesity, inflammation, and metabolic disease.

A Protein With Two Very Different Jobs

The study showed that HSL behaves differently depending on where it is located inside the cell.

On lipid droplets, HSL acts as an enzyme that helps release stored fat during fasting or exercise. In the nucleus, however, it appears to work more like a regulator that helps maintain healthy adipose tissue.

Researchers also discovered that the amount of HSL inside the nucleus changes in response to the body's metabolic state.

During fasting, adrenaline activates HSL and pushes it out of the nucleus so it can help mobilize fat stores. In obese mice fed a high-fat diet, nuclear HSL levels increased.

The protein's movement appears to be controlled by signaling pathways involving TGF-β and SMAD3, molecules already known to influence inflammation, tissue remodeling, and metabolic disease.

Scientists also found evidence that nuclear HSL interacts with proteins involved in gene expression and RNA processing, suggesting it may directly influence how fat cells function at a genetic level.

Why the Discovery Matters

The findings helped explain why complete HSL deficiency causes lipodystrophy instead of obesity. Without HSL in the nucleus, fat cells may lose their ability to stay healthy and properly maintain adipose tissue.

"HSL has been known since the 1960s as a fat-mobilizing enzyme. But we now know that it also plays an essential role in the nucleus of adipocytes, where it helps maintain healthy adipose tissue," Langin said.

The discovery may also help researchers better understand why some obesity treatments succeed while others fail. Many current therapies focus mainly on reducing fat mass. But the study suggests preserving healthy fat tissue function could be equally important.

Scientists are increasingly recognizing that adipose tissue acts as a complex endocrine organ that communicates with the brain, liver, muscles, and immune system through hormones and signaling molecules. Dysfunctional fat tissue can disrupt the body far beyond weight gain alone.

Obesity Remains a Global Health Challenge

The research arrives as obesity rates continue to rise worldwide. According to global estimates, billions of people are now overweight or obese, increasing the risk of diabetes, heart disease, stroke, sleep apnea, and some cancers.

Researchers hope that understanding how proteins like HSL regulate fat cell health could eventually lead to more targeted therapies for metabolic disease.

Instead of simply trying to eliminate fat, future treatments may focus on restoring the normal function of adipocytes and protecting the biological systems that keep fat tissue healthy in the first place.

Journal Reference:

1. Jérémy Dufau, Emeline Recazens, Laura Bottin, Camille Bergoglio, Aline Mairal, Karima Chaoui, Marie-Adeline Marques, Veronica Jimenez, Miquel García, Tongtong Wang, Henrik Laurell, Jason S. Iacovoni, Remy Flores-Flores, Pierre-Damien Denechaud, Khalil Acheikh Ibn Oumar, Ez-Zoubir Amri, Catherine Postic, Jean-Paul Concordet, Pierre Gourdy, Niklas Mejhert, Mikael Rydén, Odile Burlet-Schiltz, Fatima Bosch, Christian Wolfrum, Etienne Mouisel, Genevieve Tavernier, Dominique Langin. Nuclear hormone-sensitive lipase regulates adipose tissue mass and adipocyte metabolism. Cell Metabolism, 2025; 37 (11): 2250 DOI: 10.1016/j.cmet.2025.09.014

Courtesy:

Université de Toulouse. "New obesity discovery rewrites decades of fat science." ScienceDaily. ScienceDaily, 8 May 2026. <www.sciencedaily.com/releases/2026/05/260508171123.htm>. 

 

 

 

 

Scientists reversed liver aging with young gut bacteria in stunning study

Scientists may have discovered a powerful new link between the gut microbiome, aging, and liver cancer. New research presented at Digestive Disease Week® (DDW) 2026 suggests that restoring gut bacteria to a more youthful state could help protect the liver, reduce age related damage, and potentially lower cancer risk.

The findings come from a mouse study focused on the microbiome, the vast community of bacteria and other microbes living in the digestive system. Researchers found that giving older mice back their own younger gut microbes produced striking effects throughout the body, especially in the liver.

Young Gut Microbiome Protected Aging Mice

To test the idea, scientists collected fecal samples from eight young mice and preserved them for later use. As the mice aged, the researchers transplanted the stored samples back into the same animals through a process known as fecal microbiota transplantation, or FMT.

Another group of eight aging mice served as controls and received sterilized fecal material instead. Researchers also included a small group of young mice to provide baseline comparisons.

By the end of the study, none of the mice that received their restored youthful microbiome developed liver cancer. In contrast, liver cancer appeared in 2 out of 8 untreated aging mice. The treated mice also showed lower levels of inflammation and reduced liver injury.

"We're learning from this work that the aging microbiome actively contributes to liver dysfunction and cancer risk rather than simply reflecting the aging process," said Qingjie Li, PhD, associate professor in the Division of Gastroenterology and Hepatology at The University of Texas Medical Branch, and lead researcher on the study. "The microbiome has a broader influence on the body's cancer defenses than previously understood."

Researchers Found Changes in a Cancer Related Gene

After completing the in vivo study, the research team closely examined liver tissue from the mice. They discovered important differences involving MDM2, a gene already associated with liver cancer development.

Young mice showed low levels of the MDM2 protein, while untreated older mice had much higher levels. Older mice that received the restored microbiome had suppressed MDM2 levels that more closely resembled those seen in younger animals.

"Restoring a more youthful microbiome can reverse several core features of aging at both the molecular and functional level, including inflammation, fibrosis, mitochondrial decline, telomere attrition, and DNA damage," Dr. Li said.

Earlier Heart Research Led to the Discovery

The liver findings emerged unexpectedly from previous research examining the microbiome's effects on heart health. In that earlier cardiac study, scientists observed that altering gut bacteria appeared to improve heart function.

However, when the researchers later analyzed tissue samples, they noticed even stronger effects in the liver. That observation prompted the team to investigate the connection more deeply.

To reduce the chances of immune complications or infection, the researchers used each mouse's own preserved microbiome rather than relying on donor samples. They said this approach also creates a clearer proof of concept for possible future human studies.

Dr. Li stressed that the findings are limited to animal research and cannot yet be applied to people. Still, he said the team hopes to begin first in human clinical trials in the near future.

Courtesy:

Digestive Disease Week. "Scientists reversed liver aging with young gut bacteria in stunning study." ScienceDaily. ScienceDaily, 9 May 2026. <www.sciencedaily.com/releases/2026/05/260509210643.htm>. 

 

 

This simple blood test might detect depression before symptoms appear

 

Blood tests that track how certain white blood cells age may help identify depression by focusing on emotional and cognitive symptoms rather than physical ones.

The research, published in The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences, moves scientists closer to finding a reliable biological marker for depression, a condition that affects nearly one in five adults in the United States.

Blood-Based Clues Could Improve Depression Diagnosis

Today, depression is diagnosed based on what patients report about their symptoms. Doctors may order lab tests to rule out other illnesses, but there is still no objective biological test that can confirm depression or detect it early.

Part of the challenge is that depression does not look the same for everyone. While some people experience physical (or somatic) symptoms such as fatigue, appetite changes, or restlessness, others mainly struggle with emotional and cognitive effects. These can include hopelessness, difficulty thinking clearly, or anhedonia -- the inability to feel pleasure and loss of interest in previously enjoyed activities.

"Depression is not a one-size-fits-all disorder -- it can look really different from person to person, which is why it's so important to consider varied presentations and not just a clinical label," said study author Nicole Beaulieu Perez, assistant professor at NYU Rory Meyers College of Nursing. "Our study reveals unique biological underpinnings of mental health that are often obscured by broad diagnostic categories."

Depression, Immune Health, and HIV

Depression is especially common among people with immune-related conditions such as HIV. This higher risk may stem from a combination of chronic inflammation, social stigma, and economic challenges. Women living with HIV are particularly affected, and depression can interfere with their ability to stay engaged in care and consistently take antiretroviral medications.

"For women with HIV who may be experiencing depression, we want to better understand what's going on and catch it earlier so that it doesn't harm their whole overall health," said Perez.

Studying Biological Aging With Epigenetic Clocks

To better understand the biology behind depression, researchers examined signs of accelerated aging in the body. Biological age, which does not always match a person's chronological age, can be estimated using "epigenetic clocks." These tools measure chemical changes to DNA that occur over time.

The study included 440 women -- 261 living with HIV and 179 without HIV -- from the Women's Interagency HIV Study. Depression symptoms were assessed using the Center for Epidemiologic Studies Depression Scale (CES-D), a 20-item questionnaire that evaluates both somatic and non-somatic symptoms.

Blood samples were also analyzed to measure biological aging using two types of epigenetic clocks. One assessed aging across multiple cell types and tissues, while the other focused specifically on monocytes, a type of white blood cell involved in immune responses. Monocytes play an important role in HIV infection and are often elevated in people with depression.

Aging Immune Cells Linked to Emotional Symptoms

The findings showed that aging in monocytes was strongly associated with non-somatic symptoms of depression. These included anhedonia, feelings of hopelessness, and a sense of failure, in both women with and without HIV.

"This is particularly interesting because people with HIV often have physical symptoms like fatigue that are attributed to their chronic illness rather than a depression diagnosis. But this flips that on its head because we found that these measures are associated with mood and cognitive symptoms, not somatic symptoms," said Perez.

In contrast, the broader epigenetic clock that measured multiple cell types did not show a link to depression symptoms.

Toward Earlier Detection and Personalized Treatment

Perez emphasized that more research is needed before these findings can be used in clinical care. Still, the results point to a future where depression could be detected earlier and more precisely through biological testing.

Such advances could eventually support more personalized treatment approaches, including identifying which medications are most likely to work for a specific individual.

"I think about the adage, 'What gets measured gets managed.' An aspirational goal in mental health would be to combine subjective experience with objective biological testing," said Perez. "Our findings bring us a step closer to this goal of precision mental health care, especially for high-risk populations, by providing a biological framework that could guide future diagnosis and treatment."

Additional study authors include Ke Xu of Yale University; Yanxun Xu, Lang Lang, Gypsyamber D'Souza, and Leah Rubin of Johns Hopkins University; Kathryn Anastos of Albert Einstein College of Medicine; Maria Alcaide of the University of Miami Miller School of Medicine; Mardge Cohen of Stroger Hospital of Cook County Health System; Sadeep Shrestha of the University of Alabama at Birmingham; Andrew Edmonds of UNC Chapel Hill; Jacquelyn Meyers of Downstate Health Sciences University; Seble Kassaye of Georgetown University; Igho Ofotokun of Emory University; and Bradley Aouizerat of NYU.

The research was supported by the National Institute of Mental Health (F32MH129151, P30MH075673) and the National Institute on Minority Health and Health Disparities (K08MD019998).

Journal Reference:

1. Nicole Beaulieu Perez, Ke Xu, Yanxun Xu, Lang Lang, Kathryn Anastos, Maria L Alcaide, Mardge Cohen, Sadeep Shrestha, Andrew Edmonds, Jacquelyn Meyers, Seble Kassaye, Igho Ofotokun, Gypsyamber D’Souza, Bradley Aouizerat, Leah H Rubin. Monocyte Epigenetic Age Acceleration is Linked to Non-Somatic Depressive Symptoms in Women with and Without HIV. The Journals of Gerontology, Series A: Biological Sciences and Medical Sciences, 2026; DOI: 10.1093/gerona/glag083

Courtesy:

New York University. "This simple blood test might detect depression before symptoms appear." ScienceDaily. ScienceDaily, 4 May 2026. <www.sciencedaily.com/releases/2026/05/260504023827.htm>.

 

 

 

 

 

MIT scientists discover millions of “silent synapses” in the adult brain

 

MIT neuroscientists have uncovered a surprising feature of the adult brain. It contains millions of "silent synapses," which are immature connections between neurons that remain inactive until they are needed to help form new memories.

For many years, scientists believed these silent synapses existed only during early development, when the brain is rapidly learning about the world. But the MIT team found that in adult mice, roughly 30 percent of synapses in the brain's cortex are still silent. This suggests the adult brain holds a large reserve of unused connections that can be activated when new information arrives.

Researchers say this hidden pool of synapses may explain how the brain continues to learn throughout life without disrupting existing memories.

"These silent synapses are looking for new connections, and when important new information is presented, connections between the relevant neurons are strengthened. This lets the brain create new memories without overwriting the important memories stored in mature synapses, which are harder to change," says Dimitra Vardalaki, an MIT graduate student and the lead author of the study.

Mark Harnett, an associate professor of brain and cognitive sciences, is the senior author of the paper, published in Nature. Kwanghun Chung, an associate professor of chemical engineering at MIT, is also an author.

Rethinking How Memory Works in the Adult Brain

Silent synapses were first identified decades ago, mostly in young animals. During early development, they are thought to help the brain absorb large amounts of new information about the environment. In mice, scientists believed these synapses disappeared by about 12 days of age (equivalent to the first months of human life).

However, some researchers suspected they might persist into adulthood. Clues came from studies of addiction, which is often considered a form of maladaptive learning. These studies hinted that silent synapses could reappear or remain in the adult brain.

Theoretical work by neuroscientists Stefano Fusi and Larry Abbott also suggested the brain needs a mix of flexible and stable synapses. Some connections must be easy to change to support new learning, while others must remain steady to preserve long-term memories.

A Chance Discovery Using Advanced Imaging

The MIT team was not initially searching for silent synapses. They were following up on earlier work showing that dendrites, the branch-like extensions of neurons, process signals differently depending on their location.

To explore this further, the researchers measured neurotransmitter receptors along dendrites using a technique called eMAP (epitope-preserving Magnified Analysis of the Proteome). This method physically expands brain tissue, allowing scientists to label proteins and view them in extremely high detail.

During this imaging, the researchers noticed something unexpected.

"The first thing we saw, which was super bizarre and we didn't expect, was that there were filopodia everywhere," Harnett says.

Filopodia are tiny protrusions that extend from dendrites. Although they had been observed before, their function was unclear because they are so small and difficult to study with traditional tools.

Filopodia and the Signature of Silent Synapses

Using the eMAP technique, the team found filopodia across multiple regions of the adult mouse brain, including the visual cortex, at levels far higher than previously reported. These structures contained NMDA receptors but lacked AMPA receptors.

This detail is crucial. Active synapses typically have both receptor types, which work together to transmit signals using the neurotransmitter glutamate. NMDA receptors alone cannot pass electrical signals under normal conditions because they are blocked by magnesium ions. Without AMPA receptors, these connections remain electrically inactive, which is why they are called "silent."

Turning Silent Synapses On

To test whether these filopodia function as silent synapses, the researchers used a modified patch clamping technique. This allowed them to measure electrical activity at individual filopodia while simulating the release of glutamate.

They found that glutamate alone did not produce a signal unless the NMDA receptors were experimentally unblocked. This provided strong evidence that these structures behave as silent synapses.

The team then showed it is possible to activate, or "unsilence," these connections. By pairing glutamate release with an electrical signal from the neuron, AMPA receptors accumulated at the synapse. This transformed the silent connection into a fully functional one capable of transmitting signals.

Importantly, this process was much easier than modifying already active synapses.

"If you start with an already functional synapse, that plasticity protocol doesn't work," Harnett says. "The synapses in the adult brain have a much higher threshold, presumably because you want those memories to be pretty resilient. You don't want them constantly being overwritten. Filopodia, on the other hand, can be captured to form new memories."

A Brain That Is Both Flexible and Stable

These findings support the idea that the brain balances flexibility and stability by maintaining a reserve of highly adaptable synapses.

"This paper is, as far as I know, the first real evidence that this is how it actually works in a mammalian brain," Harnett says. "Filopodia allow a memory system to be both flexible and robust. You need flexibility to acquire new information, but you also need stability to retain the important information."

What This Means for Aging and Brain Health

The researchers are now investigating whether similar silent synapses exist in human brains. They also want to understand how these connections change with age or in neurological conditions.

"It's entirely possible that by changing the amount of flexibility you've got in a memory system, it could become much harder to change your behaviors and habits or incorporate new information," Harnett says. "You could also imagine finding some of the molecular players that are involved in filopodia and trying to manipulate some of those things to try to restore flexible memory as we age."

More recent neuroscience research has continued to explore how synaptic plasticity supports lifelong learning. Studies on aging brains suggest that reduced synaptic flexibility may contribute to memory decline, while work in neurodegenerative diseases like Alzheimer's points to disruptions in synapse formation and function. There is also growing interest in targeting synaptic mechanisms to improve cognitive resilience and learning capacity later in life.

Together, these findings paint a picture of the brain as far more dynamic than once believed. Rather than being fixed, it appears to maintain a hidden запас of connections, ready to be activated when new experiences demand it.

The research was funded by the Boehringer Ingelheim Fonds, the National Institutes of Health, the James W. and Patricia T. Poitras Fund at MIT, a Klingenstein-Simons Fellowship, and Vallee Foundation Scholarship, and a McKnight Scholarship.

Journal Reference:

1. Dimitra Vardalaki, Kwanghun Chung, Mark T. Harnett. Filopodia are a structural substrate for silent synapses in adult neocortex. Nature, 2022; 612 (7939): 323 DOI: 10.1038/s41586-022-05483-6

Courtesy:

Massachusetts Institute of Technology. "MIT scientists discover millions of “silent synapses” in the adult brain." ScienceDaily. ScienceDaily, 6 May 2026. <www.sciencedaily.com/releases/2026/05/260504211848.htm>. 

 

 

 

 

 

Your DNA may predict your future success more than your upbringing

A major twin study is shedding new light on the long running debate over nature versus nurture, suggesting that genetics may play a far larger role in future success than many people realize.

Researchers found that IQ measured at age 23 was strongly connected to socioeconomic status by age 27, including education, occupation, and income. According to the study, much of that connection appears to be tied to genetics rather than upbringing alone.

The findings come from the German TwinLife project, a long term research effort designed to examine how genes and environment shape people's lives over time.

Twin Study Explores IQ and Life Outcomes

The research followed about 880 people, including both identical and fraternal twins. Roughly half of the participants were identical twins, who share all of their genes, while the others were fraternal twins, who share about half.

Because the twins were raised in the same households, researchers could compare how much of the differences between them came from genetics versus environment.

The participants took IQ tests at age 23. Four years later, researchers evaluated their socioeconomic status by looking at factors such as education level, occupation, and income.

The results were striking. The researchers estimated that IQ was about 75 percent genetically predicted. They also found that the link between IQ and socioeconomic status was largely explained by genetics, ranging from 69 percent to 98%.

"We knew this before, but this study shows even more clearly that we are driven by our genes and become who we are largely because of them," says personality psychologist Petri Kajonius, whose study was published in Scientific Reports.

Rethinking the "Silver Spoon" Idea

The findings challenge the familiar idea that success mainly comes from growing up in a wealthy or highly educated family.

"The so-called 'silver spoon' isn't as big as you might think. Your home life also depends on your genes," Kajonius explains.

That does not mean family environment has no influence. Instead, the research suggests that inherited traits may shape how people respond to opportunities, education, and life experiences.

The study also raises difficult questions about social mobility and public policy. If genetics strongly influence life outcomes, how much can educational programs and social interventions really change a person's long term trajectory?

 "The study shows that we are born with different genetic predispositions and that it is difficult to bring about long-term change in this regard through policy measures."

What the Findings Mean for Parents and Young Adults

Kajonius says the results may actually offer some reassurance to parents.

Many parents worry that mistakes in raising their children could permanently affect their future success. But the findings suggest parents may have less control over long term socioeconomic outcomes than commonly believed.

That does not mean parenting or educational support are unimportant. Targeted interventions can still help people succeed. However, the research suggests there may be limits to how much external factors can reshape deeply rooted traits over time.

For young adults, the findings may encourage a different perspective on career choices and achievement.

Rather than focusing only on maximizing status or income, Kajonius suggests people may benefit more from pursuing the things they naturally enjoy and excel at.

Important Limitations of the Study

The researchers note several important caveats.

One limitation is that the study did not directly control for parents' IQ or socioeconomic status. Another issue is that studies like this can struggle to fully separate genetics from environment because the two often interact in complex ways.

For example, genetic traits may express themselves differently depending on a person's upbringing or life circumstances. The researchers say this interaction could partly inflate the estimated genetic influence of IQ, potentially by as much as 15 percentage points.

Even with those limitations, the study adds to growing evidence that genetics plays a powerful role in shaping intelligence, opportunity, and life outcomes.

Journal Reference:

1. Petri J. Kajonius. Longitudinal associations between cognitive ability and socioeconomic status are partially genetic in nature. Scientific Reports, 2026; 16 (1) DOI: 10.1038/s41598-026-37786-3

Courtesy:

Lund University. "Your DNA may predict your future success more than your upbringing." ScienceDaily. ScienceDaily, 6 May 2026. <www.sciencedaily.com/releases/2026/05/260505234624.htm>.