Brainwave study sheds light on cause of 'hearing voices'

A new study led by psychologists  has provided the strongest evidence yet that auditory verbal hallucinations—or hearing voices—in schizophrenia may stem from a disruption in the brain's ability to recognize its own inner voice.

In a paper published today in the journal Schizophrenia Bulletin, the researchers say the finding could also be an important step toward finding biological indicators that point to the presence of schizophrenia. This is significant, as there are currently no blood tests, brain scans, or lab-based biomarkers—signs in the body that can tell us something about our health—that are uniquely characteristic of schizophrenia.

Inner speech is the voice in your head that silently narrates your thoughts—what you're doing, planning, or noticing. Most people experience inner speech regularly, often without realizing it, though there are some who don't experience it at all.

The research shows that when we speak—even just in our heads—the part of the brain that processes sounds from the outside world becomes less active. This is because the brain predicts the sound of our own voice. But in people who hear voices, this prediction seems to go wrong, and the brain reacts as if the voice is coming from someone else.

This confirms what mental health researchers have long theorized: that auditory hallucinations in schizophrenia may be due to the person's own inner speech being misattributed as external speech.

And how do you measure it? One way is by using an EEG, which records the brain's electrical activity. Even though we can't hear inner speech, the brain still reacts to it—and in healthy people, using inner speech produces the same kind of reduction in brain activity as when they speak out loud.

But in people who hear voices, that reduction of activity doesn't happen. In fact, their brains react even more strongly to inner speech, as if it's coming from someone else. That might help explain why the voices feel so real.

Part 1

In the experiments conducted, in the healthy participants, when the sound that played in the headphones matched the syllable they imagined saying in their minds, the EEG showed reduced activity in the auditory cortex—the part of the brain that processes sound and speech. This suggests the brain was predicting the sound and dampening its response—similar to what happens when we speak out loud.

However, in the group of participants who had recently experienced AVH, the results were the reverse. In these individuals, instead of the expected suppression of brain activity when the imagined speech matched the sound heard, the EEG showed an enhanced response.
Their brains reacted more strongly to inner speech that matched the external sound, which was the exact opposite of what the researchers found in the healthy participants.
This reversal of the normal suppression effect suggests that the brain's prediction mechanism may be disrupted in people currently experiencing auditory hallucinations, which may cause their own inner voice to be misinterpreted as external speech.
Participants in the second group—people with a schizophrenia-spectrum disorder who hadn't experienced AVH recently or at all—showed a pattern that was intermediate between the healthy participants and the hallucinating participants.
The researchers say this is the strongest confirmation to date that the brains of people living with schizophrenia are misperceiving imagined speech as speech that is produced externally.

Thomas Whitford et al, Corollary discharge dysfunction to inner speech and its relationship to auditory verbal hallucinations in patients with schizophrenia spectrum disorders, Schizophrenia Bulletin (2025). DOI: 10.1093/schbul/sbaf167

Part 2

An edible fungus could make paper and fabric liquid-proof

As an alternative to single-use plastic wrap and paper cup coatings, researchers in Langmuir report a way to waterproof materials using edible fungus. Along with fibers made from wood, the fungus produced a layer that blocks water, oil and grease absorption. In a proof-of-concept study, the impervious film grew on common materials such as paper, denim, polyester felt and thin wood, revealing its potential to replace plastic coatings with sustainable, natural materials.

By providing more ways to potentially reduce our reliance on single-use plastics, we can help lessen the waste that ends up in landfills and the ocean; nature offers elegant, sustainable solutions to help us get there.

Fungi are more than their mushroom caps; underground they form an extensive, interwoven network of feathery filaments called mycelium. Recently, researchers have been inventing water-resistant materials made from these fibrous networks, including leather-like, electrically conductive gauze and spun yarn, because the surface of mycelium naturally repels water.

Additionally, films made from the fluffy wood fibers used in paper-making—specifically, a microscopic form called cellulose nanofibrils—can create barriers for oxygen, oil and grease.

The edible "turkey tail" fungus (Trametes versicolor) can grow with cellulose fibrils into a protective coating on various materials.

Part 1

To create the film, the researchers first blended T. versicolor mycelia with a nutrient-rich solution of cellulose nanofibrils. They applied thin layers of the mixture to denim, polyester felt, birch wood veneer and two types of paper, letting the fungus grow in a warm environment. Placing the samples in an oven for one day inactivated the fungus and allowed the coating to dry.

It took at least three days of fungal growth for an effective water barrier to develop. And after four days, the newly grown layer didn't add much thickness to the materials (about the same as a coat of paint), but it did change their colors, forming mottled yellow, orange or tan patterns.

Water droplets placed on the fungus-treated textiles and paper formed bead-like spheres, whereas similar droplets on untreated materials either flattened out or soaked in completely. In addition, the fungal coating prevented other liquids from absorbing, including n-heptane, toluene and castor oil, suggesting that it could be a barrier to many liquids. The researchers say this work is a successful demonstration of a food-safe fungal coating and shows this technology's potential to replace single-use plastic products.

Sandro Zier et al, Growing Sustainable Barrier Coatings from Edible Fungal Mycelia, Langmuir (2025). DOI: 10.1021/acs.langmuir.5c03185

Part 2

Female bodybuilders at risk of sudden cardiac death, research indicates

Sudden cardiac death is responsible for an unusually high proportion of deaths in female bodybuilders worldwide, according to research published in the European Heart Journal.

Sudden cardiac death is when someone dies suddenly and unexpectedly due to a problem with their heart. It is generally rare in young and seemingly healthy individuals.

The study found the greatest risk among women competing professionally. It also revealed a high proportion of deaths from suicide and homicide among female bodybuilders.

Bodybuilders, both female and male, often engage in extreme training, and use fasting and dehydration strategies to achieve extreme physiques. Some also take performance-enhancing substances. These strategies can take a serious toll on the heart and blood vessels.

Over recent years, more and more women have taken up strength training and competitive bodybuilding. Despite this growing participation, most of the available research and media attention has focused exclusively on male athletes. This work counters that.

The researchers gathered the names of 9,447 female bodybuilders from the official competition records and from an unofficial online database. All the women had participated in at least one International Fitness and Bodybuilding Federation event between 2005 and 2020.

The researchers then searched for reports of deaths of any of these named competitors in five different languages across different web sources, including official media reports, social media, bodybuilding forums and blogs. Any reported deaths were then cross-referenced using multiple sources and these reports were verified and analyzed by two clinicians to establish, as far as possible, the cause of death.

The researchers found 32 deaths among the women, with an average age at death of around 42 years. Sudden cardiac death was the most common cause of death, accounting for 31% of deaths. The risk of sudden cardiac death was more than 20 times higher among professional bodybuilders, compared to amateurs.

These results indicate that the risk of sudden cardiac death seems much higher for women bodybuilders compared to other professional athletes, although it is lower than the risk for male bodybuilders.

The researchers acknowledge that the study is based on a web-based search strategy, which could have influenced their findings. For example, some deaths, especially among less-known athletes, may have gone unreported. They also found that autopsy data were available for only a small proportion of cases, meaning that sudden deaths had to be classified based on clinical interpretation rather than confirmed forensic findings.

Mortality in female bodybuilding athletes, European Heart Journal (2025). DOI: 10.1093/eurheartj/ehaf789

Blood test for more than 50 cancers brings 'exciting' results

A blood test that screens for more than 50 cancers is correct in 62% of cases where it thinks people may have the disease, a study has found.

The Galleri test, which can be given annually and is undergoing trial in the U.K.'s health system, looks for the "fingerprint" of dozens of deadly cancers, often picking up signs before symptoms even appear.

It works by identifying DNA in the bloodstream that has been shed by cancer cells, giving the earliest signs somebody may have the disease.

Now, a key U.S. trial on the test has shown that Galleri is highly accurate in ruling out cancer in people without the disease, while also picking up cancer cases at an early stage, when the disease is more treatable.

Of those people found to have a "cancer signal" detected in their blood, 61.6% went on to be diagnosed with cancer, the findings of the Pathfinder 2 study showed.

And in 92% of cases, the test could pinpoint in which organ or tissue the cancer arose, meaning time and money could be saved on other scans and other tests.

More than half (53.5%) of the new cancers detected by Galleri in the study were the earliest stage I or II, while more than two-thirds (69.3%) were detected at stages I-III.

Galleri, which has been dubbed the holy grail of cancer tests, also correctly ruled out cancer in 99.6% of people who did not have the disease.

The findings are being presented at the European Society for Medical Oncology, or ESMO, Congress in Berlin.

https://bmjopen.bmj.com/content/15/5/e086648

People exposed to rationing in utero and during early life also showed progressively longer delays (up to two and a half years) in the age of onset of cardiovascular outcomes compared with those not exposed to rationing.

Sugar rationing was also associated with small yet meaningful increases in healthy heart function compared with those never rationed.

The authors point out that during the rationing period, sugar allowances for everyone, including pregnanat women and children, were limited to under 40 g per day—and no added sugars were permitted for infants under 2 years old—restrictions consistent with modern dietary recommendations.

Reminder: This is just an observational study, so no firm conclusions can be drawn about cause and effect.

Exposure to sugar rationing in first 1000 days after conception and long term cardiovascular outcomes: natural experiment study, The BMJ (2025). DOI: 10.1136/bmj-2024-083890

Part 2

Why the universe exists

In 1867, Lord Kelvin imagined atoms as knots in the aether. The idea was soon disproven. Atoms turned out to be something else entirely. But his discarded vision may yet hold the key to why the universe exists.

Now, for the first time, physicists have shown that knots can arise in a realistic particle physics framework, one that also tackles deep puzzles such as neutrino masses, dark matter, and the strong CP problem.

Their findings, in Physical Review Letters, suggest these "cosmic knots" could have formed and briefly dominated in the turbulent newborn universe, collapsing in ways that favored matter over antimatter and leaving behind a unique hum in spacetime that future detectors could listen for—a rarity for a physics mystery that's notoriously hard to probe.

This study addresses one of the most fundamental mysteries in physics: why our universe is made of matter and not antimatter.

This question is important because it touches directly on why stars, galaxies, and we ourselves exist at all.

The universe's missing antimatter

The Big Bang should have produced equal amounts of matter and antimatter, each particle destroying its twin until only radiation remained. Yet the universe is overwhelmingly made of matter, with almost no antimatter in sight. Calculations show that everything we see today, from atoms to galaxies, exists because just one extra particle of matter survived for every billion matter–antimatter pairs.

The Standard Model of particle physics, despite its extraordinary success, cannot account for that discrepancy. Its predictions fall many orders of magnitude short. Explaining the origin of that tiny excess of matter, known as baryogenesis, is one of physics' greatest unsolved puzzles.

In the present study, by combining a gauged Baryon Number Minus Lepton Number (B-L) symmetry, with the Peccei–Quinn (PQ) symmetry, the team showed that knots could naturally form in the early universe and generate the observed surplus.

These two long-studied extensions of the Standard Model patch some of its most puzzling gaps. The PQ symmetry solves the strong CP problem, the conundrum of why experiments don't detect the tiny electric dipole moment that theory predicts for the neutron, and in the process, introduces the axion, a leading dark matter candidate. Meanwhile, the B–L symmetry explains why neutrinos, ghostlike particles that can slip through entire planets unnoticed, have mass.

Minoru Eto et al, Tying Knots in Particle Physics, Physical Review Letters (2025). DOI: 10.1103/s3vd-brsn

Chemists discover clean and green way to recycle Teflon

New research demonstrates a simple, eco-friendly method to break down Teflon—one of the world's most durable plastics—into useful chemical building blocks.

Scientists have developed a clean and energy-efficient way to recycle Teflon (PTFE), a material best known for its use in non-stick coatings and other applications that demand high chemical and thermal stability.

The researchers discovered that Teflon waste can be broken down and repurposed using only sodium metal and mechanical energy—movement by shaking—at room temperature and without toxic solvents.

Publishing their findings in the Journal of the American Chemical Society, researchers reveal a low-energy, waste-free alternative to conventional fluorine recycling.

The process they discovered breaks the strong carbon–fluorine bonds in Teflon, converting it into sodium fluoride, which is used in fluoride toothpastes and added to drinking water.

Polytetrafluoroethylene (PTFE), best known by the brand name Teflon, is prized for its resistance to heat and chemicals, making it ideal for cookware, electronics, and laboratory equipment, but those same properties make it almost impossible to recycle.
When burned or incinerated, PTFE releases persistent pollutants known as "forever chemicals" (PFAS), which remain in the environment for decades. Traditional disposal methods therefore raise major environmental and health concerns.
The research team tackled this challenge using mechanochemistry—a green approach that drives chemical reactions by applying mechanical energy instead of heat.
Inside a sealed steel container known as a ball mill, sodium metal fragments are ground with Teflon which causes them to react at room temperature. The process breaks the strong carbon–fluorine bonds in Teflon, converting it into harmless carbon and sodium fluoride, a stable inorganic salt.
The researchers then showed that the sodium fluoride recovered in this way can also be used directly, without purification, to create other valuable fluorine-containing molecules. These include compounds used in pharmaceuticals, diagnostics, and other fine chemicals.

A Reductive Mechanochemical Approach Enabling Direct Upcycling of Fluoride from Polytetrafluoroethylene (PTFE) into Fine Chemicals, Journal of the American Chemical Society (2025). DOI: 10.1021/jacs.5c14052

Dangerous E. coli strain blocks gut's defense mechanism against spreading infection

When harmful bacteria that cause food poisoning, such as E. coli, invade through the digestive tract, gut cells usually fight back by pushing infected cells out of the body to stop the infection from spreading.

In a new study published today in Nature, scientists discovered that a dangerous strain of E. coli—known for causing bloody diarrhea—can block this gut defense, allowing the bacteria to spread more easily.

The bacteria inject a special protein called NleL into gut cells, which breaks down key enzymes known as ROCK1 and ROCK2, that are needed for infected cells to be expelled. Without this process, the infected cells can't leave quickly, allowing the bacteria to spread more easily.

Usually, when harmful bacteria invade the gut, the body fights back quickly. The first line of defense is the intestinal lining—made up of tightly packed cells that absorb nutrients and keep bacteria out of the bloodstream. If one of these cells gets infected, it sacrifices itself by pushing itself out of the gut lining and into the intestines to be flushed. This helps prevent the bacteria from spreading.

This study shows that pathogenic bacteria can block infected cells from being pushed out.

It's a completely different strategy from what we've seen before. Some bacteria try to hide from being detected, but this one actually stops the cell's escape route.

This discovery could pave the way for new treatments that target how bacteria cause disease, rather than killing the bacteria outright, like antibiotics do.

Vishva Dixit, Enteropathogenic bacteria evade ROCK-driven epithelial cell extrusion, Nature (2025). DOI: 10.1038/s41586-025-09645-0. www.nature.com/articles/s41586-025-09645-0

Snakes' biting styles revealed in fine detail for the first time

Few actions in nature inspire more fear and fascination than snake bites. And the venomous reptiles have to move fast to sink their fangs into their prey before their victim flinches, which may be as little as 60 ms when hunting rodents.

Until recently, video technology was not sufficiently sophisticated to capture the deathly maneuvers in high definition, but recent improvements have made this possible, so researchers decided to get to the heart of how venomous viper, elapid and colubrid snakes sink their fangs into their dinner.

Publishing their research in the Journal of Experimental Biology, the researchers reveal how vipers sink their fangs into their victims before walking them into position to inject venom. Elapids squeeze venom into their victims by biting repeatedly. And colubrids sweep their jaws from side to side to tear a gash in their victim and deliver maximum venom.

Researchers also tempted 36 species of snake—from western diamondback rattlesnakes (Crotalus atrox) and west African carpet vipers (Echis ocellatus) to the rough-scaled death adder (Acanthophis rugosus)—to lunge at a cylinder of warm muscle-like medical gel resembling a small animal, recording the encounters with two cameras at 1000 frames/s to recreate the lightning-fast maneuvers in 3D. 

Part 1

After capturing more than 100 snake strikes in minute detail, the team saw the vipers embed their fangs in the fake prey within 100ms of launching a smooth strike—with the blunt-nosed viper (Macrovipera lebetina) accelerating up to 710m/s2 and landing its bite within 22ms; the elapid snakes bit their victims as quickly as vipers.

In addition, the vipers moved the fastest as they struck, with Bothrops asper—sometimes known as the ultimate pit-viper—reaching speeds of over 4.5m/s after hitting accelerations of more than 370m/s2, although the fastest elapid—the rough-scaled death adder—only reached speeds of 2.5m/s.

Focusing on the vipers' fangs, the team saw the needle-like teeth sink into the fake prey, but if the viper wasn't happy with the position of a fang, it pulled it out to reinsert it at a better angle, effectively walking the fang forward. Only when the fangs were comfortably in place did the vipers close their jaws and inject venom into their catch.

Part 2

In contrast, the elapid snakes, such as the Cape coral cobra (Aspidelaps lubricus) and the forest cobra (Naja melanoleuca), used a stealthier strategy, creeping closer to their victim before lunging and biting repeatedly as their jaw muscles tensed to squeeze the venom into their dinner.

The colubrid snakes, with fangs further back in their mouths, lunge over the greatest distances before clamping their jaws around their meal, sweeping their jaws from side-to-side to tear a crescent-shaped gash in the victim to deliver the maximum dose of venom. And on one occasion, a blunt-nosed viper misjudged the distance to its prey, hitting the right fang and breaking it off. But the team suspects that this occurs more than you'd think, with fangs turning up in snake scats after being swallowed.

Venomous snakes use dramatically different strategies to deliver their deadly bites. Vipers and elapids strike elegantly before victims are even aware of their presence and colubrid bites inflict the maximum damage. These creatures don't pull any punches when they mean business.

Cleuren, S. G. C., et al. Kinematics of feeding strikes in venomous snakes., Journal of Experimental Biology (2025). DOI: 10.1242/jeb.250347

Part 3

Peatlands' 'huge reservoir' of carbon at risk of release, researchers warn

Peatlands make up just 3% of Earth's land surface but store more than 30% of the world's soil carbon, preserving organic matter and sequestering its carbon for tens of thousands of years. A new study sounds the alarm that an extreme drought event could quadruple peatland carbon loss in a warming climate.

In the study, published in Science, researchers find that, under conditions that mimic a future climate (with warmer temperatures and elevated carbon dioxide), extreme drought dramatically increases the release of carbon in peatlands by nearly three times. This means that droughts in future climate conditions could turn a valuable carbon sink into a carbon source, erasing between 90 and 250 years of carbon stores in a matter of months.

As temperatures increase, drought events become more frequent and severe, making peatlands more vulnerable than before. These extreme drought events can wipe out hundreds of years of accumulated carbon, so this has a huge implication.

The researchers found that the lowered water table during drought took longer to recover at higher temperatures and elevated carbon dioxide levels, which led to more carbon release.

Quan Quan et al, Drought-induced peatland carbon loss exacerbated by elevated CO₂ and warming, Science (2025). DOI: 10.1126/science.adv7104. www.science.org/doi/10.1126/science.adv7104

Hitchhiking DNA picked up by a gene may save a species from extinction

An international research team  has solved a genetic mystery and revealed a previously unknown way that DNA can control what cells do.

Published in Science, the study reveals that in the roundworm C. elegans, vital RNA needed to keep the ends of chromosomes intact does not have its own gene. Instead, it hitchhikes inside another one. DNA hitchhiking could be a common strategy in the animal kingdom, and has implications for anti-aging therapies and regenerative medicine in humans.

Telomeres are DNA caps that protect the ends of chromosomes, much like the plastic tips of shoelaces. As we age, the cells of our bodies—called somatic cells—divide when we need new tissue, and every time that happens the telomeres lose some of their DNA.

Some signs of aging are related to this process. For example, skin cells with shorter telomeres make less collagen and skin becomes wrinkled. When they are too short, cells self-destruct.

Sperm and egg precursor cells—collectively called germ cells—are an exception to this rule. When they divide, an enzyme called telomerase adds replacement DNA to the ends of shortened telomeres. Because of this, telomere length doesn't get shorter with each generation, and species do not become extinct.

Part 1

Telomerase contains an RNA template that is used to make the replacement DNA. In humans and other mammals, this RNA comes from the TERC gene. C. elegans has working telomerase, but it doesn't seem to have a TERC gene.
This mystery has stumped scientists for more than 20 years, and some have assumed that the gene was lost during evolution. In their study, the team at RIKEN BDR discovered how C. elegans can exist without a standalone TERC gene.

Because telomerase levels are normally very low, the researchers genetically engineered C. elegans to overproduce the telomerase protein, which made it possible to collect large amounts of the whole telomerase complex, including the RNA template.

They then used all the collected template RNA to search the genome for matching DNA. Unlike in mammals, instead of being located in its own gene, they found it inside another gene's intron.

Usually, the instructions in DNA within genes are used to build proteins. But some parts of genes, called introns, are not used to build proteins and are usually removed and discarded once the gene's protein is made.

It was surprising to find that the key RNA—which 's named terc-1—was hidden inside an intron of the gene called nmy-2, which is expressed only in germ cells.
Indeed, the discovery that the essential telomerase RNA was hidden within an intron was completely unexpected.
Experiments showed that in C. elegans lacking terc-1, telomeres became shorter each generation, and within 15 generations, the animals became extinct. Inserting terc-1 inside introns of other genes that are expressed in germ cells created roundworms that had normal telomeres and did not become extinct.

In contrast, when terc-1 was inserted into introns of genes that only activate in somatic cells, the animals did become extinct. Thus, by hitching a ride inside genes activated in germ cells, terc-1 is produced where it is needed—the germ cells. There, it helps ensure that future generations do not receive shortened telomeres, thus supporting the survival of the species.
Beyond its evolutionary significance, this discovery will help us better understand how telomerase is regulated in healthy cells and could transform approaches to aging, fertility, and regenerative medicine.

 Yutaka Takeda et al, Nematode telomerase RNA hitchhikes on introns of germline–up-regulated genes, Science (2025). DOI: 10.1126/science.ads7778. www.science.org/doi/10.1126/science.ads7778

Part 2

Tigers in trouble as Malaysian big cat numbers dwindle

Malaysia's national animal is in trouble.

Poaching, food loss and diminishing habitat have slashed the population from 3,000 in the 1950s to less than 150 roaming free today, according to official estimates.

The government said last month it was ramping up efforts to combat wildlife crime, introducing AI-enabled camera traps and methods to detect smuggling at airports.

But experts and officials admit that resources fall far short of what is needed to protect the country's famed big cat, listed as critically endangered.

The next 10 years will decide whether we can bring back the roar of the Malayan tiger.

Source: News agencies

Not all gas is bad: Hydrogen gas found to play key role in supporting gut health

 Scientists have revealed how hydrogen is made and used in the human gut. Though infamous for making flatulence ignite, hydrogen also has a positive role supporting gut health.

In a study published in Nature Microbiology, researchers  analyzed how microbes control hydrogen levels in the gut.

Hydrogen gas is naturally produced in the gut when bacteria ferment undigested carbohydrates from our diets. Some of this gas is exhaled, much is recycled by other gut bacteria, and the rest exits the body as flatulence.

The results revealed hydrogen had an even bigger role in gut function than previously thought.

Most people release about a liter of gas per day and half of that is hydrogen. But hydrogen is more than just the gas behind flatulence—it's a hidden driver of gut health.

Gas production in the gut is a normal process. Hydrogen is made in large amounts when gut bacteria break down food and is then used by other microbes for energy.

The study shows hydrogen shapes the gut microbiome in surprising and varied ways. It helps some beneficial bacteria thrive in the gut and keeps digestion going.

However, excessive hydrogen production can signal gut problems. Abnormal hydrogen levels are associated with infections, digestive disorders, and even cancer, and are often measured in breath tests to assess gut health.

They also  saw signs that hydrogen production was disrupted in people with gut disorders, but it's unclear if this is a cause or consequence of disease.

The researchers' work was focused on understanding the fundamental role of hydrogen in gut function, rather than improving diagnostics or developing therapies.

The study found that a specific enzyme called Group B [FeFe]-hydrogenase was mainly responsible for making hydrogen in the gut. This enzyme is found in many gut bacteria and is very active.

The researchers studied bacteria from stool samples and gut tissue and found that this enzyme helps bacteria grow and produce hydrogen, especially in the primary health associated groups. They also discovered that this enzyme works by using a specific chemical reaction involving iron and another protein called ferredoxin.

As an example, healthy people have a lot of these enzymes in their gut, but people with Crohn's disease have fewer of them and more of the other types of hydrogen-producing enzymes.

The researchers hope their discovery will highlight the need to expand fundamental knowledge of how our gut works so it can be used to design new treatments for gastrointestinal issues.

 Caitlin Welsh et al, A widespread hydrogenase supports fermentative growth of gut bacteria in healthy people, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02154-w

Scientists find ways to boost memory in aging brains

Memory loss may not simply be a symptom of getting older. New research  shows that it's tied to specific molecular changes in the brain and that adjusting those processes can improve memory.

In two complementary studies, researchers used gene-editing tools to target those age-related changes to improve memory performance in older subjects. The work was conducted on rats, a standard model for studying how memory changes with age.

Memory loss affects more than a third of people over 70, and it's a major risk factor for Alzheimer's disease. 

This work shows that memory decline is linked to specific molecular changes that can be targeted and studied. If we can understand what's driving it at the molecular level, we can start to understand what goes wrong in dementia and eventually use that knowledge to guide new approaches to treatment.

In the first study, published in the journal Neuroscience one research team examined a process called K63 polyubiquitination. This process acts as a molecular tagging system that tells proteins inside the brain how to behave. When the system functions normally, it helps brain cells communicate and form memories.

They found that aging disrupts K63 polyubiquitination in two distinct areas of the brain. In the hippocampus, which helps form and retrieve memories, levels of K63 polyubiquitination increase with age. Using the CRISPR-dCas13 RNA editing system to reduce these levels, the researchers were able to improve memory in older rats.

In the amygdala, which is important for emotional memory, the researchers noted that K63 polyubiquitination declines with age. By reducing it even further, they were able to boost memory in older rats.

Together, these findings reveal the important functions of K63 polyubiquitination in the brain's aging process. In both regions, adjusting this one molecular process helped improve memory.

Part 1

A second study, published in the Brain Research Bulletin

focused on IGF2, a growth-factor gene that supports memory formation. As the brain ages, IGF2 activity drops as the gene becomes chemically silenced in the hippocampus.

IGF2 is one of a small number of genes in our DNA that's imprinted, which means it's expressed from only one parental copy. When that single copy starts to shut down with age, you lose its benefit.

The researchers found that this silencing happens through DNA methylation, a natural process in which chemical tags accumulate on the gene and switch it off. Using a precise gene-editing tool, CRISPR-dCas9, they removed those tags and reactivated the gene. The result was better memory in older rats.

Together, the two studies show that memory loss is not caused by a single molecule or pathway and that multiple molecular systems likely contribute to how the brain ages.

 Yeeun Bae et al, Age-related dysregulation of proteasome-independent K63 polyubiquitination in the hippocampus and amygdala, Neuroscience (2025). DOI: 10.1016/j.neuroscience.2025.06.032

Shannon Kincaid et al, Increased DNA methylation of Igf2 in the male hippocampus regulates age-related deficits in synaptic plasticity and memory, Brain Research Bulletin (2025). DOI: 10.1016/j.brainresbull.2025.111509

Part 2

Nighttime light exposure linked to higher heart attack and stroke rates

A new study has found that being exposed to bright light at night can significantly increase the chances of developing serious heart problems, including heart attacks, strokes and heart failure.

Published in JAMA Network Open, the research is the largest study of its kind to explore how personal light exposure affects heart health using data from nearly 89,000 people.

Using wrist-worn sensors, researchers from FHMRI Sleep Health tracked over 13 million hours of light exposure and followed participants for up to 9.5 years.
The study found that people who were exposed to the brightest light at night were much more likely to develop heart problems, with a 56% higher chance of heart failure and 47% more likely to have a heart attack.

These risks remained high even after accounting for other factors like exercise, diet, sleep habits and genetics.

the study highlights a risk factor that many people aren't aware of, but one that's easy to address.

This is the first large-scale study to show that simply being exposed to light at night is a strong and independent risk factor for heart disease.

Disrupting your body's internal circadian clock by repeatedly exposing yourself to bright light at night, when it would typically be dark otherwise, will put you at a higher risk of developing dangerous heart issues, say the researchers.

By using blackout curtains, dimming lights, and avoiding screens before bed, we can help to reduce the health risks associated with light at night.

The study also found that women and younger people were especially vulnerable to the impact of light exposure at night.

Women may be more sensitive to the effects of light disrupting their body clock.

In fact, women exposed to high levels of night light had similar heart failure risks to men, which is unusual because women typically have some natural protection against heart disease.

We need to take our body clocks seriously. Protecting our natural sleep rhythms could be a powerful way to fight heart disease, the researchers conclude.

Light Exposure at Night and Cardiovascular Disease Incidence, JAMA Network Open (2025). DOI: 10.1001/jamanetworkopen.2025.39031

A new human clinical trial has shown that a special procedure to deliver oxygen through the rectum is safe.

The study involved 27 healthy male volunteers in Japan who were tasked with holding between 25 and 1,500 milliliters of perfluorocarbon liquid in their rectum for an hour.

The ‘butt-breathing’ procedure passed its first safety hurdle with flying colors.
Now researchers hope to test what happens when that liquid contains a very high concentration of oxygen.

The hope is that one day, a procedure like this could help people who are struggling to get enough oxygen through their lungs.

Pigs, rodents, turtles, and some fish can breathe through their butts, so why not us?

linkinghub.elsevier.com/retrieve/pii/S2666634025003149

Pathogen disables plant ‘alarm’ to break in
Phytophthora infestans — a fungus-like mold that causes the devastating disease potato blight — infects plants by disabling their ‘alarm system’. Researchers found that P. infestans secretes enzymes called AA7 oxidases. These enzymes damage the molecules plant cells produce to alert the immune system of an infection, which lets the microbe sneak in without being detected. “It’s like burglars cutting the wires to your home alarm before breaking in,” says biochemist and study co-author Federico Sabbadin. “The microbe has learned the plant’s own language and uses it against it.”

https://www.nature.com/articles/s41467-025-64189-1?utm_source=Live+...

'Forever Chemicals' in Mothers' Blood Linked to Brain Changes in Their Kids

'Forever chemicals' already have a shocking reputation, and now new research has linked these substances – named for the way they stick around in the environment for so long – to brain changes in children born to mothers exposed to common PFAS (per- and polyfluoroalkyl substances).
To reach that conclusion, researchers looked at 51 mother-and-child pairs, measuring PFAS levels in the mother's blood during pregnancy, and then running brain scans on the kids once they reached 5 years old.
These records meant the research team was able to compare different types of PFAS against changes in brain structure and connections between brain regions. Several distinct patterns were revealed, enough to suggest (but not prove) a strong influence.
They were able to measure seven different PFAS in this study, and found that individual compounds had specific associations with offspring brain structure.
In some cases two different PFAS had opposite relationships with the same brain region
For example, perfluorononanoic acid (PFNA) and perfluorooctanoic acid (PFOA) were linked to changes in the corpus callosum, the tract of white matter that connects the brain's left and right hemispheres.
Substantial changes connected to PFAS levels were also detected in the hypothalamus, a part of the brain that controls many of the body's core functions, and in the volume and surface area of posterior grey matter in the occipital lobe, the brain's visual processing centre.
The researchers also found certain types of PFAS more likely to influence brain structure and brain connectivity than others, based on their chemical composition. It's not immediately evident what these changes might mean – but the changes are there.

https://www.thelancet.com/journals/lanplh/article/PIIS2542-5196(25)00187-1/fulltext

Astrocyte-derived vesicles could link stress to intestinal inflammation

Inflammatory bowel diseases (IBDs), such as Crohn's disease and ulcerative colitis, are chronic and autoimmune conditions characterized by the inflammation of the intestinal tract. This inflammation can cause nausea or vomiting, diarrhea, abdominal pain and cramping, fatigue, fever, and various other debilitating symptoms.

While the underpinnings of IBDs have been widely investigated, the factors that can contribute to its emergence have not yet been clearly elucidated. Past findings suggest that the symptoms of these diseases are often exacerbated by psychological and emotional stress.

Researchers recently carried out a study aimed at shedding new light on the neurobiological mechanisms via which stress could worsen IBDs. Their findings, published in Molecular Psychiatry, hint at the existence of a brain-to-gut communication pathway that is mediated by small communication vehicles known as small extracellular vesicles (sEVs), which are released by astrocytes.

The researchers now hypothesize that psychological stress regulates intestinal inflammation through the release of small extracellular vesicles derived from astrocytes (AsEVs).

The researchers carried out various experiments involving rats, aimed at understanding how stress affected immune responses in their gut. Their study specifically focused on the role of astrocytes, star-shaped glial cells that help to maintain a balanced and healthy environment in the brain, and of small EVs released by these cells.

They  marked astrocytes with a special "tag" protein, using a technique known as in-utero electroporation. This technique allowed them to monitor where signals originating from these cells traveled within the rats' body.

"In-utero electroporation performed to selectively express an AsEV-associated membrane recombinant protein in rat forebrain astrocytes reveals that this protein is transferred to the gut-associated lymphoid tissue (GALT)," wrote the authors.

Similarly, AsEVs isolated from primary astrocyte cell cultures that were stimulated with vehicle or corticosterone (to emulate a stress condition) trafficked to the GALT. Interestingly, the membrane gut homing receptor CCR9 is present on AsEVs and mediates their association with the CCR9-endogenous ligand CCL25."

Interestingly, the researchers discovered that signals originating from astrocytes traveled to immune tissues in the rats' gut. Subsequently, they grew astrocytes in their lab and increased the levels of corticosterone within them. This is a hormone that is naturally released in the animals' body when they are stressed.

The team then injected vesicles released by these cells, as well as vesicles released by "non-stressed" astrocytes into rats and observed their gut responses. They found that vesicles derived from "stressed" astrocytes led to greater gut inflammation, while those released by 'non-stressed' astrocytes helped to calm the gut's immune system.

At the histological level, inflammatory parameters (such as lymph vessel diameter or cell number in them), induced by a stress protocol based on movement restriction, increased by treatment with AsEVs from corticosterone-treated astrocytes.

Part 1

Furthermore, while AsEVs from control astrocyte cultures tend to favor an anti-inflammatory profile of the GALT (i.e., increased Treg/Th17 ratio), AsEVs derived from corticosterone-treated astrocytes have an opposite action. Similarly, in vitro experiments with disaggregated mesenteric lymph nodes reveal the immunomodulatory functions of AsEVs from corticosterone-treated astrocytes."

The results of this recent study uncover a new brain-to-gut communication pathway mediated by AsEVs via which stress could worsen the symptoms of IBDs.

Liliana Yantén-Fuentes et al, A novel brain-to-gut communication pathway mediated by astrocyte-derived small extracellular vesicles modulates stress-induced intestinal inflammation, Molecular Psychiatry (2025). DOI: 10.1038/s41380-025-03289-2.

Part 2

Rewriting history using modern technology

DNA from Napoleon's 1812 army identifies pathogens likely responsible for the army's demise during retreat from Russia

It's very exciting to use a technology we have today to detect and diagnose something that was buried for 200 years

In the summer of 1812, French emperor Napoleon Bonaparte led about half a million soldiers to invade the Russian Empire. But by December, only a fraction of the army remained alive. Historical records suggest that starvation, cold, and typhus led to their demise.

In a new study published in Current Biology, a team of microbial paleogenomicists extracted DNA from the soldiers' teeth and found no trace of typhus. Instead, they identified two pathogens known to cause enteric fever and relapsing fever—ailments which likely contributed to the army's downfall.

For centuries, historians have debated the factors that contributed to Napoleon's army's demise. Accounts from doctors and army officers suggested it was likely the result of typhus, an infectious disease that was common among armies of the time.
The discovery of body lice—the main vector of typhus—on the remains of Napoleon's soldiers, and the DNA of Rickettsia prowazekii—the bacterium responsible for typhus—further bolstered this assumption.

With new technology in hand capable of analyzing ancient DNA, researchers set off to reanalyze samples from Napoleon's fallen soldiers to see whether typhoid was indeed the culprit.

The researchers extracted and sequenced DNA from the teeth of 13 soldiers buried in a mass grave in Vilnius, Lithuania, which was along the route of the French army's retreat from Russia. They then removed all environmental contamination to isolate and identify DNA fragments from bacterial pathogens.

Part 1

Instead of pathogens for typhus, the team found traces of Salmonella enterica, a bacterium that causes enteric fever, and Borrelia recurrentis, responsible for relapsing fever, which is also transmitted by body lice.

The researchers did not detect R. prowazekii or Bartonella quintana, the cause of trench fever, which has been identified in previous research on different soldiers from this site. Researchers say this discrepancy could be explained by the usage of different sequencing technologies. Earlier studies relied on polymerase chain reaction, or PCR, a technology that makes many copies of a specific DNA segment from limited starting material.
Ancient DNA gets highly degraded into pieces that are too small for PCR to work. New method now used is able to cast a wider net and capture a greater range of DNA sources based on these very short ancient sequences.

Paratyphoid Fever and Relapsing Fever in 1812 Napoleon's Devastated Army, Current Biology (2025). DOI: 10.1016/j.cub.2025.09.047. www.cell.com/current-biology/f … 0960-9822(25)01247-3

Part 2

How the brain's activity, energy use and blood flow change as people fall asleep

A new study by investigators  has used next-generation imaging technology to discover that when the brain is falling asleep, it shows a coordinated shift in activity.

The researchers found that during NREM (non-rapid eye movement) sleep, parts of the brain that handle movement and sensory input stay active and keep using energy, while areas involved in thinking, memory and daydreaming quiet down and use less energy. Their results are published in Nature Communications.

This research helps explain how the brain stays responsive to the outside world even as awareness fades during sleep.

By revealing how brain activity, energy use, and blood flow interact during sleep, these findings, and the imaging tools scientists used to uncover them, offer new insights into the mechanisms of neurological and sleep-related diseases.

The body cycles through two types of sleep several times each night: NREM and REM (rapid eye movement). NREM is the deep, restorative stage of sleep that plays a key role in physical health, brain function and disease prevention. Yet, many of its underlying processes and impacts on long-term health remain poorly understood. Previous studies have suggested that NREM helps clear waste from the brain.

Using a new tri-modal EEG-PET-MRI technique that combines EEG to study brain activity, fMRI to analyze blood flow, and functional PET (fPET)-FDG to monitor glucose metabolic dynamics, researchers examined the brains of 23 healthy adults during brief afternoon sleep sessions.

The researchers found that energy use and metabolism decrease as sleep deepens, while blood flow becomes more dynamic, especially in sensory areas that stay relatively active. At the same time, higher-order cognitive networks quiet down, and cerebrospinal fluid flow increases. Together, these findings support the idea that sleep helps clear waste from the brain while maintaining sensitivity to sensory cues that can trigger awakening.

Simultaneous EEG-PET-MRI identifies temporally coupled and spatially structured brain dynamics across wakefulness and NREM sleep", Nature Communications (2025). DOI: 10.1038/s41467-025-64414-x

Physicists create the smallest pixel in the world 

Smart glasses that display information directly in the field of vision are considered a key technology of the future—but until now, their use has often failed due to cumbersome technology. However, efficient light-emitting pixels are ruled out by classical optics if their size is reduced to the wavelength of the emitted light.

Now, physicists  have taken a decisive step toward luminous miniature displays and, with the help of optical antennas, have created the world's smallest pixel to date.

With the help of a metallic contact that allows current injection into an organic light-emitting diode while simultaneously amplifying and emitting the generated light, they have created a pixel for orange light on an area measuring just 300 by 300 nanometers. This pixel is just as bright as a conventional OLED pixel with normal dimensions of 5 by 5 micrometers.

To put this into perspective, a nanometer is one millionth of a millimeter. This means that a display or projector with a resolution of 1,920 x 1,080 pixels could easily fit onto an area of just one square millimeter. This, for example, enables integration of the display into the arms of a pair of glasses from where the light generated would be projected onto the lenses.

Cheng Zhang et al, Individually addressable nanoscale OLEDs, Science Advances (2025). DOI: 10.1126/sciadv.adz8579

Life's Ingredients Found Frozen Beyond The Milky Way For First Time

For the first time, astronomers have seen life's building blocks in ice beyond the borders of our galaxy.
Among a mix of complex organic molecules trapped in ice circling a newborn star in the Large Magellanic Cloud, researchers found ethanol, acetaldehyde, and methyl formate – compounds that have never before been spotted in ice form outside the Milky Way.
Moreover, another identified compound, acetic acid, has never before been conclusively identified in ice anywhere in space.

The discovery by astrophysicists suggests that the ingredients for the chemistry that gives birth to life are widespread and robust across the cosmos, and not limited to our own galaxy.
Complex organic molecules (COMs) in an astrophysical context are molecules with at least six atoms, at least one of which is carbon. The category includes molecules such as ethanol (CH₃CH₂OH), methyl formate (HCOOCH₃), and acetaldehyde (CH₃CHO), as well as larger molecules such as iso-propyl cyanide ((CH3)2CHCN).

They're important to scientists because they're the chemical precursors to the molecules that build life, such as amino acids, sugars, and nucleobases. Finding them in space, therefore, sheds light on the origins of prebiotic chemistry and where those precursor compounds were likely forged before Earth was even born.

https://iopscience.iop.org/article/10.3847/2041-8213/ae0ccd

Why earthquakes sometimes still occur in tectonically silent regions

Earthquakes in some parts of stable world should not be able to occur even if the subsurface has been exploited for decades. This is because the shallow subsurface behaves in such a way that faults there become stronger as soon as they start moving. At least that is what geology textbooks teach us. And so, in theory, it should not be possible for earthquakes to occur. So why do they still occur in such nominally stable subsurfaces?

Geosciences researchers  considered this question. They discovered that as a result of millions of years of inactivity, extra stress can build up on the faults which can result in a single release. This research, recently published in the journal Nature Communications, is vitally important in the search for safe locations for applications such as geothermal energy production and energy storage.

Faults can be found almost everywhere. Faults in the shallow subsurface are usually stable, so we do not expect shock movements to occur along them. Nevertheless, shock movements often do occur in the stable first few kilometers of the subsurface. In such instances, we generally find a correlation with human activities. What exactly explains that paradox of shallow faults, which become stronger with movement, but then suddenly become weak and are subsequently released with a tremor?

Induced earthquakes (those caused by human activities) often take place on inactive faults that have not moved for millions of years. Although these faults do not move, we still observe a very slow growth of the surface that connects them. This sort of 'fault healing' gives rise to additional strength. It is this extra fault strength that can cause an acceleration once a fault has been set in motion. This acceleration is what causes earthquakes to occur in stable subsurfaces, despite textbooks telling us that this ought not to happen there.

As such areas do not have a history of earthquakes, the people living there are more at risk as infrastructure has not been built to withstand earthquakes. "Furthermore, these earthquakes take place at a depth where human activities occur, in other words, no more than several kilometers deep. That is considerably less deep than the majority of natural earthquakes." Therefore, they can be more hazardous and cause more ground shaking.

Interestingly, this potential acceleration, in the form of an earthquake, occurs only once. As soon as that extra fault strength, which has been built up over millions of years, finds a way out, the situation becomes stable again.

As a result, there is no more earthquake activity at that spot. This means that, although the subsurface in such areas will not settle immediately after human operations stop, the strength of the earthquakes—including the maximum expected magnitude—will gradually decrease.

Part 1

If faults do indeed become stronger when they move, then these already broken pieces will quietly slip past each other, and in doing so, act as a barrier. That makes it harder for earthquakes to increase in size. This makes it possible to lower the estimated risk of an earthquake, as this risk is primarily determined by the maximum magnitude of an earthquake.

Meng Li et al, Frictional healing and induced earthquakes on conventionally stable faults, Nature Communications (2025). DOI: 10.1038/s41467-025-63482-3

Part 2

Study links cockroach infestations to higher household allergens and endotoxins

Researchers have shown a link between the size of cockroach home infestations and the levels of both allergens and endotoxins in those homes, with lowering roach infestation numbers through pest control triggering significant declines in the levels of allergens and endotoxins. The study's findings suggest that eliminating cockroach infestations could help improve indoor environmental health by greatly reducing allergens and endotoxins.

Endotoxins are bacterial cellular components that get released when bacteria die. As omnivores that will eat just about anything, cockroaches have a rich and diverse gut microbiome. Previous research has shown that cockroaches shed a lot of endotoxins through their fecal matter, although house pets – and humans – can also shed endotoxins. The researchers in this study found that a large amount of the endotoxins found in household dust was associated with cockroach feces.

Endotoxins are important to human health, as inhalation of these components has been shown to provoke allergic responses. 

The researchers found significant amounts of endotoxins in infested homes, with female cockroaches excreting about twice the amount that males excreted. Female cockroaches eat more than males, so more endotoxins are shed from their fecal matter.  More endotoxins were found in kitchens than in bedrooms, as more cockroaches live in kitchens where they find more food.

When you eliminate cockroaches, you eliminate their allergens. Small decreases in cockroaches don't lower allergen levels because the remaining live cockroaches deposit more allergens. Endotoxins significantly decreased in homes where cockroaches were eliminated. This research shows that the cockroach is the most important depositor of endotoxin in infested homes.

Researchers  also saw that allergens and endotoxins can be airborne. 

There exists the implication that asthma can be worse due to interactions between allergens and endotoxins.

Cockroaches?! Eeek!

I don't have a single cockroach in my home. Because I don't like them, I see to it they don't come inside my home. 

 Madhavi L. Kakumanu et al, Indoor Allergens and Endotoxins in Relation to Cockroach Infestations in Low-Income Urban Homes, Journal of Allergy and Clinical Immunology: Global (2025). DOI: 10.1016/j.jacig.2025.100571

How a coral stiffens its skeleton on demand

Touch the branches of Leptogorgia chilensis, a soft coral found along the Pacific coast from California to Chile, and its flexible arms stiffen. Researchers have discovered the mechanism underlying this astonishing ability, one that could advance fields as varied as medicine, robotics and manufacturing.

In a paper in Proceedings of the National Academy of Sciences,

they describe how the coral's skeleton—made of millions of mineral particles suspended in a gelatinous matrix—compacts itself to ward off danger.

When stimulated, the coral's tissues expel water, shrinking the gel and squeezing the particles closer together until they jam in place.

Physicists have long studied this phenomenon, known as "granular jamming," by manipulating grainy substances like sand and coffee grounds, but this marks the first time granular jamming based on hard particles has been observed in a living organism.

They're basically made of chalk- calcium carbonate, the same cheap and plentiful white powder that forms eggshells, sticks of chalk, marble, limestone and pearls. What gives their skeletons interesting properties is how the calcium carbonate is structured and organized.

While marine biologists recognized long ago that soft corals like L. chilensis have skeletons containing granular particles, the grains' shapes had primarily been used to classify different species.

Li, Ling, Mineralized sclerites in the gorgonian coral Leptogorgia chilensis as a natural jamming system, Proceedings of the National Academy of Sciences (2025). DOI: 10.1073/pnas.2504541122. doi.org/10.1073/pnas.2504541122

Humanity rises as wildlife recedes: Two studies show the extent of human domination over nature

Wolves roaming the Mongolian steppes cover more than 7,000 kilometers a year. The Arctic tern flies from pole to pole in its annual migration. Compared to these long-distance travelers of land, sea and sky, humans might seem like the ultimate couch potatoes. But a new study shows otherwise.

In a paper published recently in Nature Ecology & Evolution,  researchers report that the total movement of humans is 40 times greater than that of all wild land mammals, birds and arthropods combined. Since the Industrial Revolution some 170 years ago, human movement has skyrocketed, while animal movement in nature has dwindled to levels that could endanger ecosystems.

Life, by its very nature, is always in motion, shaping both the natural world and human society. Yet until now, no comparison has been made among different species as to the magnitude of their overall movement. Birds, for example, cross vast distances but their overall body mass is tiny. By contrast, deep-sea fish may travel only short distances, but their combined biomass is enormous—about a thousand times greater than that of all birds.

Researchers  have now quantified and compared the movement of different species, shedding light on the power dynamics between humans and the rest of the animal kingdom.

The index they created, called the biomass movement metric, is calculated by multiplying the total biomass of a species—that is, the combined mass of all its members—by the total distance that species travels in a year. Calculating this metric globally made it possible, for the first time, to quantify global movement across animal species—and then compare it to that of humankind.

Part 1

The researchers broke down human movement by mode of transportation. They found that about 65% of human biomass movement is by car or motorbike, 10% by airplane, 5% by train and 20% by foot or on a bicycle. Remarkably, the biomass movement of humans walking is six times greater than that of all wild land mammals, birds and arthropods combined.

On average, each person travels about 30 kilometers a day by various means—slightly more than wild birds. By comparison, wild land mammals (excluding bats) travel only about 4 kilometers a day. In the air, human biomass movement by airplane is ten times greater than that of all flying wildlife.

We often marvel at the power of nature compared to how small we are. But in practice, even the great migrations we see in Africa in nature documentaries—some of the largest land migrations on Earth—barely compare to the human biomass movement associated with people gathering from around the world for a single World Cup tournament.
Animals spend a large portion of their energy on movement, and measuring their biomass movement enabled the scientists to compare the energetic cost of transport across species. Scientists found, for example, that a single airline burns as much energy as all wild birds combined. It may be hard to grasp just how much humankind affects nature, but the biomass movement metric does provide a quantitative measure that reveals the true balance of power on Earth.
This power balance is dramatically changing. Humanity continues to develop and expand while nature is in decline. Most biomass movement occurs in the oceans, but even those vast habitats are severely affected by human activity now.
Since the Industrial Revolution, human biomass movement has soared by 4,000%, while that of marine animals has dropped by about 60%.
Today we know that animal movement is critical for ecosystems to function properly and that ecosystems must remain connected to one another to survive. The global decline in animal movement is a warning sign to us all, say the researchers.

Yuval Rosenberg et al, Human biomass movement exceeds the biomass movement of all land animals combined, Nature Ecology & Evolution (2025). DOI: 10.1038/s41559-025-02863-9

Lior Greenspoon et al, The global biomass of mammals since 1850, Nature Communications (2025). DOI: 10.1038/s41467-025-63888-z

Part 2

Chimpanzees in Uganda use flying insects to tend their wounds, study reveals

Animals respond to injury in many ways. So far, evidence for animals tending wounds with biologically active materials is rare. Yet, a recent study of an orangutan treating a wound with a medicinal plant provides a promising lead.

Chimpanzees, for example, are known to lick their wounds and sometimes press leaves onto them, but these behaviors are still only partly understood. We still do not know how often these actions occur, whether they are deliberate, or how inventive chimpanzees can be when responding to wounds.

Recent field observations in Uganda, east Africa, are now revealing intriguing insights into how these animals cope with wounds.

In  research published in Scientific Reports, based in Kibale National Park, Uganda, chimpanzees have been seen applying insects to their own open wounds on five occasions, and in one case to another individual.

Behaviors like insect application show that chimpanzees are not passive when wounded. They experiment with their environment, sometimes alone and occasionally with others. While we should not jump too quickly to call this "medicine," it does show that they are capable of responding to wounds in inventive and sometimes cooperative ways.

Each new insight reveals more about chimpanzees, offering glimpses into the shared evolutionary roots of our own responses to injury and caregiving instincts.

In all observed cases, the sequence of actions seemed deliberate. A chimpanzee caught an unidentified flying insect, immobilized it between lips or fingers, and pressed it directly onto an open wound. The same insect was sometimes reapplied several times, occasionally after being held briefly in the mouth, before being discarded. Other chimpanzees occasionally watched the process closely, seemingly with curiosity. Part1

Most often the behavior was directed at the chimpanzee's own open wound. However, in one rare instance, an adolescent female applied an insect to her brother's wound. A study on the same community has shown that chimpanzees also dab the wounds of unrelated members with leaves, prompting the question of whether insect application of these chimpanzees, too, might extend beyond family members. Acts of care, whether directed towards family or others, can reveal the early foundations of empathy and cooperation.

 Kayla Kolff et al, Insect applications to open wounds by chimpanzees in the wild: first insights from East African chimpanzees, Scientific Reports (2025). DOI: 10.1038/s41598-025-16582-5

Part2

Exploring mechanisms behind attachment issues

Stoicism says attachment is not good. But  overcoming biochemistry is extremely difficult. Especially when you are young. 

And then not giving enough care also makes people detached. 

Children can sometimes develop health, behavioral, and attachment issues that persist when their needs are not met by their caregiver. Now from eNeuro, researchers explored whether mouse pups also experience these issues from early life adversity.

Their discoveries provide an opportunity for researchers to explore the mechanisms of health and behavioral deficits from early life adversity.

When the researchers limited bedding for making nests, this impaired maternal care and increased stress hormone signaling in pups after just one week. Offspring also experienced long-term stunted growth trajectories.

Behaviorally, while some attachment behaviors remained unchanged, many were affected: Pups vocalized less when they were separated from their mothers after one week, did not approach their mothers after about two weeks, and had anxiety-like behavior by week three.

Giving credit where credit is due, work in rats relates an increased stress response from impaired maternal care to attachment deficits. But this work was only done in one age group. Researchers used thorough, 24/7 videotape footage of moms and their pups to show how impaired maternal care leads to attachment deficits at different timepoints.

This isn't a linear relationship. It seems that there is a threshold for how bad maternal care must be to disrupt the offspring's behavior. This supports an existing hypothesis that you don't have to be a perfect parent, you just need to provide adequate care.

Erratic Maternal Care Induces Avoidant-Like Attachment Deficits in a Mouse Model of Early Life Adversity, eNeuro (2025). DOI: 10.1523/ENEURO.0249-25.202

Rapid tooth loss linked to higher risk of death in older people

In older adults, tooth loss may be linked to serious health risks. A team of  researchers analyzed data from 8,073 older participants and found that people who lost their teeth more quickly had a higher risk of dying, regardless of how many teeth they started with.

The researchers emphasize the need to closely monitor the progression of tooth loss among older adults, as it is an important indicator of broader physiological decline.

Modifiable habits like regular brushing, avoiding smoking, and routine dental checkups play a key role in how quickly teeth are lost. Studies show that consistent oral care can lower mortality rates among older adults with missing teeth. Making oral health a stronger focus of public health efforts could be an easy way to improve overall well-being, suggests the study published in BMC Geriatrics.

Old age or not, oral health is a major problem in humans across the globe. In 2022, the World Health Organization released a "Global Oral Health Status Report," which showed that almost half of the world's population (~3.5 billion people) has some form of dental disease. It highlighted tooth loss as one of the most common problems.

While losing teeth with age is often inevitable, its impact can be far-reaching. It not only affects quality of life by making it harder to chew and enjoy food, but has also been linked to higher death rates—not just overall mortality, but from specific causes like heart disease, lung cancer, and pneumonia.

Part 1

Over 3.5 years, the team studied 8,073 older adults aged 73 to 91. They tracked how quickly participants lost teeth over time, measuring this as the average number of teeth lost per year. Based on the tooth loss pattern, the participants were divided into four groups: stable (no teeth lost per year), slow loss (more than zero but less than two teeth lost per year), moderate loss (two to under four teeth lost per year), and rapid loss (4 or more teeth lost per year).

The data were then entered into a Cox regression analysis—a statistical method that accounts for the relative risk of an event—to determine whether faster tooth loss was associated with a higher mortality risk. They found that those with rapid tooth loss had a 33% higher risk of death compared to those who lost none. Also, with each tooth lost per year, the risk increases by 4%.

The researchers note that further investigation into the mechanisms underlying this relationship is needed to develop effective interventions. Until then, raising awareness of the hidden health risks of rapid tooth loss among both health care professionals and the public could go a long way toward encouraging habit modification.

Linjia Duan et al, Tooth loss progression and mortality among older adults: results from the Chinese longitudinal healthy longevity survey (CLHLS), BMC Geriatrics (2025). DOI: 10.1186/s12877-025-06419-1

Part 2

Fat breakdown in skin cells restarts hair growth in mice

Researchers  report that adipocyte lipolysis activates epithelial hair follicle stem cells and drives hair regeneration via monounsaturated fatty acid signaling.

Healthy hair follicles are still present in balding men, but they are often miniaturized, producing thinner, weaker hairs that eventually stop producing. For a while, even though the follicles stop growing visible hair, previous studies show they still contain stem cells and could, theoretically, be reactivated.

Skin is a lipid-rich organ where fatty tissue cushions, insulates, and secretes endocrine factors. Previous studies have linked inflammation after minor injury to hair regrowth and have described crosstalk between dermal white adipose tissue and hair follicle stem cells with both stem cell activation and dormancy. Specific roles for adipocytes in regeneration remained unclear.

In the study, "Adipocyte lipolysis activates epithelial stem cells for hair regeneration through fatty acid metabolic signaling," published in Cell Metabolism, researchers employed mouse models of skin injury to determine whether inflammation-triggered adipocyte lipolysis promotes hair regrowth and to define the downstream metabolic pathway in epithelial hair follicle stem cells.

Mouse experiments were conducted using topical sodium dodecyl sulfate (SDS) irritation and controlled dermal laser injury, with female mice used predominantly. Mice were shaved on postnatal day 49 to synchronize with the start of the second telogen phase, when hair follicles are naturally resting and hair doesn't normally regrow for about six weeks.

Investigators applied 7.5% SDS to induce contact dermatitis, tracked timing of epidermal and follicular responses by histology, EdU labeling, lipid testing and immunostaining, and profiled transcripts with bulk and spatial transcriptomics.
Skin irritation produced rapid skin redness and scaling at the surface, outer skin thickened and immune cells flooded in. Several days later, growth of new hair was observed.
Part1

Dermal white fat beneath the skin shifted into lipolysis. Lipid droplets in adipocytes shrank, staining showed less stored fat, phosphorylated PLIN1 increased, triglycerides fell, and free fatty acids rose. Blocking the rate-limiting lipase ATGL with a drug or by genetic deletion prevented lipolysis and halted hair regeneration. A deeper thermal injury model showed the same dependence on adipocyte lipolysis.

Measurements of norepinephrine and chemical sympathectomy indicated no required role for sympathetic nerves.

Inflammatory signals in the skin rose after irritation. Single knockouts of tumor necrosis factor-alpha (TNFα) and Interleukin-1 (IL-1), cytokines required for activating the innate immune response, did not stop lipolysis or hair regrowth. Broad anti-inflammatory steroid treatment to dampen cytokine induction blocked adipocyte lipolysis, and prevented hair renewal.

Macrophages emerged as key drivers. Transcriptomic analyses pointed to macrophage signatures, with spatial data showing infiltration into dermal fat.

Depleting macrophages with clodronate liposomes reduced serum amyloid A3 (SAA3) induction, suppressed lipolysis, and stopped hair regrowth, while neutrophil depletion and loss of adaptive immunity did not block regrowth.

Authors conclude that a macrophage-to-adipocyte-to-stem cell axis converts injury signals into localized metabolic communication that activates epithelial hair follicle stem cells. Topical monounsaturated fatty acids promoted hair growth in mice, suggesting therapeutic potential for hair loss.

Validation with human skin was not tested and the suggested mechanistic linchpin found is SAA3-dependent lipolysis in mice, whereas human skin mainly uses SAA1/2.

Kang-Yu Tai et al, Adipocyte lipolysis activates epithelial stem cells for hair regeneration through fatty acid metabolic signaling, Cell Metabolism (2025). DOI: 10.1016/j.cmet.2025.09.012

Part 2

Caught on camera: Rats snatching bats from the sky 

For the first time, brown rats have been filmed actively hunting bats, snatching some from the air and capturing others on the ground. The rodents were caught on camera at bat hibernation sites in northern Germany. According to a paper published in the journal Global Ecology and Conservation, researchers think this predation could be significant enough to threaten local bat populations.

This study is the first to systematically document brown rats hunting in urban Europe. Scientists set up infrared and thermal imaging cameras to monitor bats at two hibernation sites in the towns of Segeberg and Lüneburg-Kalkberg. Observations were made during peak bat activity over several months between 2020 and 2024.

The cameras revealed two distinct hunting strategies. Some rats stood upright, using their tails for balance as they grabbed the bats while they were flying. Others attacked them when they were resting on the ground. At the Segeberg site, the team recorded 13 confirmed kills over five weeks and found a cache of 52 bat carcasses. Similar remains and evidence of bat predation were also discovered at the Lüneburg-Kalkberg site.

The number of kills may not sound large, but the researchers calculated that even a small rat colony could kill up to 7% of the roughly 30,000 bats at the Segeberg site in a single winter. The attacks also occurred at a time when the bats were most vulnerable—during swarming and hibernation—meaning even limited predation could threaten the long-term survival of the population.

The study highlights the importance of bat conservation strategies. The flying mammals help control insect populations and support healthy ecosystems by pollinating plants and dispersing seeds. But protecting bats is not only good for the environment; it also benefits human health, as the researchers point out.

Florian Gloza-Rausch et al, Active predation by brown rats (Rattus norvegicus) on bats at urban mass hibernacula in Northern Germany: Conservation and one health implications, Global Ecology and Conservation (2025). DOI: 10.1016/j.gecco.2025.e03894

Sinking Indian megacities pose 'alarming' building damage risks

Sinking land is quietly destabilizing urban infrastructure in India's largest cities, putting thousands of buildings and millions of people at risk, according to Virginia Tech scientists.

Groundwater overuse is a critical driver of the problem, say the researchers in their paper published in Nature Sustainability.

When cities pump more water from aquifers than nature can replenish, the ground quite literally sinks. This study shows that this overexploitation of groundwater is directly linked to structural weakening in urban areas.

Using satellite radar data from 2015–23, the research team assessed differential ground sinking, or subsidence, in New Delhi, Mumbai, Chennai, Kolkata, and Bengaluru, covering more than 13 million buildings and home to nearly 80 million people.
Results revealed that 878 square kilometers of urban land, or about 339 square miles, is sinking, with nearly 1.9 million people exposed to subsidence rates greater than 4 millimeters per year.
The study estimates that 2,406 buildings in New Delhi, Mumbai, and Chennai are already at high risk of structural damage. If current subsidence trends continue, over 23,000 buildings could face a very high risk within the next 50 years.

Land subsidence compounds the threats from flooding and earthquakes. When the ground beneath a city sinks unevenly, it weakens foundations, damages utility lines, and amplifies structural vulnerability.

The silent strain we see today could lead to tomorrow's disasters if cities do not adapt their infrastructure and groundwater management policies, say the researchers.

The study demonstrates the value of cutting-edge satellite techniques in preventing tragedy.

The findings extend beyond India, warning that subsidence-driven building damage is an emerging global urban challenge. As more cities depend on stressed aquifers and expand rapidly, subsidence will continue to erode infrastructure resilience worldwide.

 Building damage risk in sinking Indian megacities, Nature Sustainability (2025). DOI: 10.1038/s41893-025-01663-0.

How harmful bacteria know where to cluster and cause infection

The bacterium known as Pseudomonas aeruginosa is an unwelcome visitor in the human body. Serious infections can result when a bunch of these bugs settle together on a surface to form a biofilm—a community of microbes like the slime on spoiled food, but in this case residing inside a person.

The grouped-up bacteria attack the lungs of patients with cystic fibrosis and conditions that require the use of ventilators, such as severe COVID-19. Worse still, the World Health Organization lists Pseudomonas among the antibiotic-resistant bacteria presenting the biggest threat to human health.

Now, however, new findings by researchers reveal just how Pseudomonas goes from exploring a surface to committing to it and building a community—a key finding that can help pave the way to understanding how to tackle these types of infections.

The new study revealed how Pseudomonas detects and binds to specific sugars left behind by others from its species that arrived earlier. The cell senses these sugar trails using proteins on its body, and then identifies the sugars using hairlike appendages called pili. These pili are normally used to crawl along a surface, but in this case double as mechanical sensors that test the strength of the sugar bonds.

All of this information is translated into chemical signals inside the cell that guide the operation of other bacterial machinery, such as the controlled secretion of more sugars to make biofilms.

Reported in the journal Nature Microbiology, the results may inform applications in human health and industry. For Pseudomonas, the findings could lead to better approaches for undermining the dangerous bugs' ability to resist drug treatments.

William C. Schmidt et al, Pseudomonas aeruginosa senses exopolysaccharide trails using type IV pili and adhesins during biofilm formation, Nature Microbiology (2025). DOI: 10.1038/s41564-025-02087-4

How Plantago asiatica plants communicate with each other to respond to salt stress

Plants exchange adaptive information, helping them to adjust to environmental challenges. Salt stress in plants, caused by soil salinity, often results in water loss. Plants often cope with this situation by closing the stomatal aperture.

In a study appearing in Plant Signaling & Behavior, the scientists wanted to understand how Plantago asiatica plants utilize both above- and below-ground communication to differentially respond to salt stress cues perceived from neighbors with variable genetic identities.
Interplant cueing or communication is a fascinating method through which neighboring plants exchange adaptive information. Plants can send and receive information through both aboveground and belowground pathways: via the shoot system (involving stems and leaves) and the root system, respectively.
Communication usually relies on volatile organic compounds aboveground and fungal networks in the soil of the root system. This exchange of information helps plants to respond quickly to certain stress situations and enhance their resistance by activating adaptive mechanisms.
Plants exchange information regarding altered nutrient availability, impending competition, neighbor proximity, drought stress, and salt stress. Plant stomata refer to microscopic pores on leaf surfaces that control gas exchange and transpiration. Closure of stomata due to salt stress was previously recorded as a stress response in many plants.
Some studies also reported that unstressed plants show this adaptive mechanism, which is a result of communication with stressed plants.

Plantago asiatica plants communicate salt stress signals through both aboveground and belowground pathways, the new study shows. Aboveground cues induce stomatal closure in neighboring plants regardless of genetic relatedness, while belowground signaling is more effective among genetically similar individuals, suggesting root-mediated communication depends on genetic background.

Kai Ito et al, Integrated above- and below-ground interplant cueing of salt stress, Plant Signaling & Behavior (2025). DOI: 10.1080/15592324.2025.2542560

Scientists find flatworm can grow two heads and flip its body axis

The microscopic flatworm (Stenostomum brevipharyngium) is one of nature's weirder creatures. Chop off its head, and it'll grow one back. Cut it in half, and it'll become two separate healthy worms. And now scientists have discovered an even stranger trick. These unsegmented, soft-bodied invertebrates can grow two heads, a normal one and a backward-facing one, in the middle of their bodies where their tail should be. This developmental error lets the worms permanently reverse their head-to-tail body axis without any noticeable harmful effects.

Scientists have long known how to create double-headed flatworms by applying electrical currents. But this is the first time the two-headed variety has been observed occurring naturally and spontaneously. 

To rule out a permanent genetic cause of the error, the researchers monitored the offspring of the double-headed worms and found that they were all normal. This proves that their axis reversal was due to developmental flexibility rather than genetic mutations.

These findings suggest that whole body regeneration based on pluripotent stem cells provides a flexible developmental framework in which even a reversal of the A-P axis of the adult bilaterian body can be accommodated.

While a genetic mutation has been excluded, the cause of the unusual two-headed creature has yet to be determined. It could be an environmental trigger or even a random developmental error. It's also unknown whether this occurs in the real world. The scientists observed this in the lab, and so we'll have to wait for other research to see if it is a trick the flatworms use in the wild.

Katarzyna Tratkiewicz et al, Spontaneous ectopic head formation enables reversal of the body axis polarity in microscopic flatworms, Proceedings of the Royal Society B: Biological Sciences (2025). DOI: 10.1098/rspb.2025.1941