The Universe may have already started slowing down

The universe may not be speeding up after all. According to a new study, its expansion could actually be slowing down, challenging one of modern cosmology’s most fundamental ideas.

The findings, published November 6 in Monthly Notices of the Royal Astronomical Society, question the long-accepted belief that a mysterious force known as “dark energy” is pushing galaxies apart at an ever-increasing rate. Instead, researchers found no convincing evidence that the universe is still accelerating.

If confirmed, the results could reshape scientists’ understanding of dark energy, help resolve the long-standing “Hubble tension,” and transform theories about the universe’s past and future.

Evidence for a Cosmic Slowdown

Lead researcher Professor Young-Wook Lee of Yonsei University in South Korea said, “Our study shows that the universe has already entered a phase of decelerated expansion at the present epoch and that dark energy evolves with time much more rapidly than previously thought.

“If these results are confirmed, it would mark a major paradigm shift in cosmology since the discovery of dark energy 27 years ago.”

For nearly three decades, astronomers have believed that the universe’s expansion was accelerating due to dark energy, a mysterious force acting as a kind of “anti-gravity.” This conclusion was originally based on measurements of distant type Ia supernovae, a discovery that earned the 2011 Nobel Prize in Physics.

Rethinking the Universe’s “Standard Candles”

The new research from Yonsei University challenges that foundation. Type Ia supernovae, long considered reliable “standard candles” for measuring cosmic distances, appear to be influenced by the age of the stars that create them.

Even after standardizing their brightness, the team found that supernovae originating from younger stars tend to look fainter, while those from older stars appear brighter. Analyzing data from 300 host galaxies, the researchers confirmed this age effect with an extraordinary level of confidence (99.999%).

This means that part of the dimming once attributed to cosmic acceleration could actually result from stellar population differences rather than universal expansion.

A New Model Emerges

When the team corrected for this age-related bias, the supernova data no longer fit the standard ΛCDM model, which assumes a constant form of dark energy. Instead, it matched more closely with a newer model supported by the Dark Energy Spectroscopic Instrument (DESI) project.

This alternative model draws on baryonic acoustic oscillations (BAO) — essentially ancient sound waves from the Big Bang — and data from the cosmic microwave background (CMB). Both sources suggest that dark energy is not constant but instead weakens and changes over time.

When researchers combined the corrected supernova data with BAO and CMB results, the evidence became overwhelming: the universe does not appear to be accelerating anymore, but has entered a phase of decelerated expansion.

A Universe Already Slowing

Professor Lee explained, “In the DESI project, the key results were obtained by combining uncorrected supernova data with baryonic acoustic oscillations measurements, leading to the conclusion that while the universe will decelerate in the future, it is still accelerating at present.

“By contrast, our analysis — which applies the age-bias correction — shows that the universe has already entered a decelerating phase today. Remarkably, this agrees with what is independently predicted from BAO-only or BAO+CMB analyses, though this fact has received little attention so far.”

Testing the Findings

To strengthen their conclusions, the Yonsei team is performing what they call an “evolution-free test.” This approach examines only supernovae from young, coeval galaxies — those with stars of similar ages — across the entire redshift range. Early results already support the main finding.

“Within the next five years, with the Vera C. Rubin Observatory discovering more than 20,000 new supernova host galaxies, precise age measurements will allow for a far more robust and definitive test of supernova cosmology,” said research professor Chul Chung, a co-lead author of the study, along with PhD candidate Junhyuk Son.

The Vera C. Rubin Observatory and the Future of Cosmology

Located high in the Chilean Andes, the Vera C. Rubin Observatory houses the world’s most powerful digital camera. Having begun scientific operations this year, it is expected to revolutionize our understanding of both the solar system and the broader universe.

After the Big Bang, roughly 13.8 billion years ago, the universe expanded rapidly before gravity slowed it down. Then, around nine billion years after its birth, scientists discovered that expansion had begun speeding up again. This was attributed to dark energy, which is believed to make up about 70 percent of the universe.

Dark Energy’s Mystery Deepens

Despite decades of study, dark energy remains one of science’s most puzzling enigmas. Last year, data from DESI in Tucson, Arizona hinted that the influence of dark energy might have changed over time, an idea now gaining traction with the Yonsei team’s new results.

With advanced instruments like DESI and the Vera C. Rubin Observatory, astronomers hope to finally uncover what dark energy really is — and how it shapes the fate of the universe.

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Astronomers discover dying stars eating their planets

A new study from astronomers at UCL (University College London) and the University of Warwick suggests that aging stars may be destroying the giant planets orbiting closest to them.

When stars like the Sun exhaust their hydrogen fuel, they begin to cool and expand, transforming into red giants. For our Sun, this dramatic phase is expected to occur in roughly five billion years.

The research, published in the Monthly Notices of the Royal Astronomical Society, analyzed nearly half a million stars that had recently entered this “post-main sequence” stage of evolution.

Searching for Planets Around Evolving Stars

The team identified 130 planets and potential planet candidates (i.e., that still need to be confirmed) orbiting closely around these aging stars, including 33 new candidates never detected before.

They found that such planets were far less common around stars that had expanded and cooled enough to qualify as red giants (i.e., those further along in their post-main sequence evolution). This pattern suggests that many of these planets may already have been destroyed.

Evidence of Planetary Destruction

Lead author Dr. Edward Bryant (Mullard Space Science Laboratory at UCL and the University of Warwick) explained: “This is strong evidence that as stars evolve off their main sequence they can quickly cause planets to spiral into them and be destroyed. This has been the subject of debate and theory for some time but now we can see the impact of this directly and measure it at the level of a large population of stars.

“We expected to see this effect but we were still surprised by just how efficient these stars seem to be at engulfing their close planets.”

According to Dr. Bryant, the destruction occurs through a powerful gravitational struggle known as tidal interaction. As a star grows and expands, these forces intensify. “Just like the Moon pulls on Earth’s oceans to create tides, the planet pulls on the star,” he said. “These interactions slow the planet down and cause its orbit to shrink, making it spiral inwards until it either breaks apart or falls into the star.”

What It Means for the Solar System

Co-author Dr. Vincent Van Eylen (Mullard Space Science Laboratory at UCL) added perspective: “In a few billion years, our own Sun will enlarge and become a red giant. When this happens, will the solar system planets survive? We are finding that in some cases planets do not.

“Earth is certainly safer than the giant planets in our study, which are much closer to their star. But we only looked at the earliest part of the post-main sequence phase, the first one or two million years of it — the stars have a lot more evolution to go.

“Unlike the missing giant planets in our study, Earth itself might survive the Sun’s red giant phase. But life on Earth probably would not.”

To carry out their research, the team used data from NASA’s Transiting Exoplanet Survey Satellite (TESS). They employed an algorithm to identify small, repeated dips in starlight caused by planets passing in front of their stars. Their focus was on giant planets with short orbits (i.e., taking no more than 12 days to circle their star).

Starting with more than 15,000 possible signals, the researchers used rigorous checks to eliminate false positives, ultimately narrowing the list to 130 confirmed or candidate planets. Of these, 48 were already known, 49 were known candidates awaiting confirmation, and 33 were completely new discoveries.

Fewer Planets Around Older Stars

The researchers found that stars further along in their evolution were significantly less likely to host nearby giant planets. The overall occurrence rate was just 0.28%, with younger post-main sequence stars showing a higher rate (0.35%) comparable to main sequence stars. The most evolved stars — those classified as red giants — showed a sharp drop to 0.11%. (For this analysis, the smallest 12 of the 130 identified planets were excluded.)

Using TESS data, astronomers can estimate a planet’s size (radius). To confirm whether these objects are true planets or low-mass stars or brown dwarfs (“failed stars” that never ignited nuclear fusion), their mass must be determined.

This is done by measuring the tiny shifts in the motion of the host star caused by a planet’s gravitational pull. These “stellar wobbles” allow scientists to infer the planet’s mass.

Dr. Bryant added: “Once we have these planets’ masses, that will help us understand exactly what is causing these planets to spiral in and be destroyed.”

The research was supported by the UK Science and Technology Facilities Council (STFC).

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Scientists find hidden brain source that fuels dementia

Scientists at Weill Cornell Medicine have identified a surprising culprit that may contribute to dementia: free radicals generated in a particular region of brain support cells known as astrocytes. The study, published Nov. 4 in Nature Metabolism, found that blocking this specific site reduced inflammation and protected neurons. The results point toward a promising new strategy for treating neurodegenerative diseases such as frontotemporal dementia and Alzheimer’s disease.

“I’m really excited about the translational potential of this work,” said Dr. Anna Orr, the Nan and Stephen Swid Associate Professor of Frontotemporal Dementia Research in the Feil Family Brain and Mind Research Institute and member of the Appel Alzheimer’s Disease Research Institute at Weill Cornell, who co-led the study. “We can now target specific mechanisms and go after the exact sites that are relevant for disease.”

How Mitochondria and Free Radicals Affect the Brain

The research focused on mitochondria, the cell’s energy-producing structures that convert food into usable energy. In the process, mitochondria release reactive oxygen species (ROS) — molecules commonly known as free radicals. At normal levels, ROS help regulate essential cell functions, but excessive or poorly timed production can damage cells.

“Decades of research implicate mitochondrial ROS in neurodegenerative diseases,” said Dr. Adam Orr, an assistant professor of research in neuroscience in the Feil Family Brain and Mind Research Institute at Weill Cornell, who co-led the work.

Because of this connection, scientists have long tested antioxidants as a potential way to neutralize ROS and slow neurodegeneration. However, these clinical trials have largely failed. “That lack of success might be related to the inability of antioxidants to block ROS at their source and do so selectively without altering cell metabolism,” Dr. Adam Orr explained.

A New Way to Stop Harmful Free Radicals

As a postdoctoral researcher, Dr. Orr developed a drug discovery platform designed to find molecules that specifically suppress ROS at individual mitochondrial sites while leaving normal functions intact. Through this approach, the team identified a group of compounds called S3QELs (“sequels”), which showed potential to block harmful ROS activity.

The researchers focused on Complex III, a mitochondrial site known for producing ROS that can leak into the rest of the cell, potentially causing damage. To their surprise, the excess ROS did not originate from neurons, but from astrocytes — non-neuronal cells that provide structural and metabolic support to neurons.

“When we added S3QELs, we found significant neuronal protection but only in the presence of astrocytes,” said Daniel Barnett, a graduate student in the Orr lab and the study’s lead author. “This suggested that ROS coming from Complex III caused at least some of the neuronal pathology.”

Further experiments showed that when astrocytes were exposed to disease-related factors such as inflammatory molecules or proteins linked to dementia (including amyloid-beta), their mitochondrial ROS production increased dramatically. Treatment with S3QELs suppressed much of this rise, while blocking other ROS sources did not have the same effect.

Barnett discovered that ROS oxidized certain immune and metabolic proteins involved in neurological disease, altering the activity of thousands of genes tied to inflammation and dementia.

“The precision of these mechanisms had not been previously appreciated, especially not in brain cells,” said Dr. Anna Orr. “This suggests a very nuanced process in which specific triggers induce ROS from specific mitochondrial sites to affect specific targets.”

Promising Results in Animal Models

When the team administered the S3QEL compound to mice engineered to model frontotemporal dementia, they observed reduced astrocyte activation, lower levels of inflammatory gene expression, and a decrease in a tau modification linked to dementia. Remarkably, these effects appeared even when treatment began after symptoms had already started.

Extended treatment improved lifespan, was well tolerated, and produced no significant side effects. Dr. Anna Orr attributes this to the compound’s highly targeted action.

The team plans to continue developing the S3QEL compounds in collaboration with medicinal chemist Dr. Subhash Sinha, professor of research in neuroscience in the Brain and Mind Research Institute and member of the Appel Alzheimer’s Disease Research Institute at Weill Cornell.

They also intend to investigate how disease-associated genes influence ROS production and whether certain genetic variants that raise or lower dementia risk might do so by altering mitochondrial ROS activity.

Changing How Scientists Think About Free Radicals

“The study has really changed our thinking about free radicals and opened up many new avenues of investigation,” said Dr. Adam Orr. The potential of these findings to open new research approaches to inflammation and neurodegeneration is highlighted in the journal.

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German nurse gets life in jail after murdering 10 to reduce workload

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ADHD services shutting door to new NHS patients as demand soars, BBC finds

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BMA rejects fresh offer to end doctor strikes

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LED mask ads banned over acne and rosacea claims

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A 480-million-year-old parasite still infects oysters today

A surprising new study has revealed that a parasite still troubling modern oysters first began infecting shell-dwelling sea creatures hundreds of millions of years before the dinosaurs vanished.

Researchers reporting in iScience used high-resolution 3D imaging to examine 480-million-year-old fossil shells from Morocco, a site famous for its exceptionally preserved marine life. The scans uncovered a pattern of unusual markings etched both on the surfaces of the shells and inside them.

“The marks weren’t random scratches,” explained Karma Nanglu, a paleobiologist at UC Riverside and lead author of the study. “We saw seven or eight of these perfect question mark shapes on each shell fossil. That’s a pattern.”

Javier Ortega-Hernandez, a Harvard evolutionary biologist and co-author, recalled the team’s initial confusion. “It took us a while to figure out the mystery behind these peculiar-looking traces. It was as if they were taunting us with their question mark-like shape,” he said. “But as often happens, we came across the answer while deep in obscure literature before our eureka moment.”

Ancient Worms Behind the Mystery Marks

After comparing the markings with modern examples, the scientists concluded that they were made by a soft-bodied marine bristle worm belonging to a group known as spionids. These worms, still common today, bore into the shells of mussels and oysters but typically don’t kill their hosts outright.

“They parasitize the shells of bivalves like oysters, not the flesh of the animals themselves,” said Nanglu. “But damaging their shells may increase oyster death rates.”

The fossils studied came from early relatives of modern clams that lived during the Ordovician Period, a time of rapid ecological expansion when marine life became increasingly mobile, predatory, and parasitic. “This is a time when ocean ecosystems got more intense,” Nanglu said. “You see the rise of mobility, predation, and, clearly, parasitism.”

A Half-Billion-Year Parasitic Lineage

The researchers considered other explanations for the distinctive marks, such as self-inflicted shell growth patterns or traces from unrelated organisms. However, the evidence most strongly matched spionid activity.

“There’s one image in particular, from a study of modern worms, that shows exactly the same shape inside a shell,” Nanglu said. “That was the smoking gun.”

The finding offered more than just an identification — it provided a rare evolutionary insight. “This group of worms hasn’t changed its lifestyle in nearly half a billion years,” said Nanglu. “We tend to think of evolution as constant change, but here’s an example of a behavior that worked so well, it stayed the same through multiple mass extinction events.”

Peering Inside Fossils with High-Tech Scans

To reveal the interior structures of the shells, the team used a technique similar to medical CT imaging, called micro-CT scanning. This high-resolution method allowed them to visualize internal burrows and hidden shells embedded within the rock layers, which were stacked like a layered cake.

“We never would’ve seen this without the scanner,” Nanglu said.

The Parasite’s Ancient Life Cycle

The worm’s life cycle helped confirm its identity. The researchers determined that it likely began as a larva that attached itself to a shell, dissolved a small spot to secure its position, and then tunneled deeper as it grew — creating the recognizable question mark shape.

No other known species leaves this precise trace. “”If it’s not a spionid, then it’s something we’ve never seen before,” Nanglu said. “But it would have to have evolved the same behavior, in the same place, in the same way.”

A Survivor Across Deep Time

Remarkably, the same burrowing behavior continues in today’s oceans. Although spionid worms do not consume their hosts directly, the damage they inflict on oyster shells still increases mortality rates in modern fisheries.

“This parasite didn’t just survive the cutthroat Ordovician period, it thrived,” Nanglu said. “It’s still interfering with the oysters we want to eat, just as it did hundreds of millions of years ago.”

Fossil Time Capsules of Ancient Life

The Moroccan fossil site where these discoveries were made is celebrated for capturing behavior frozen in time. Other fossils there have preserved scenes of animals interacting, such as creatures feeding on the remains of squid-like ancestors.

“You’re lucky to get any record of an animal from that long ago,” Nanglu said. “But to see evidence of two animals interacting? That’s gold.”

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A shapeshifting protein explains rabies’ deadly power

  • Viruses are masters of efficiency, able to take over our cells and control vital processes using only a handful of genes.
  • For years, scientists have wondered how something so small could do so much.
  • Researchers have now uncovered the answer — a discovery that could reshape our understanding of how viruses work and lead to new ways to fight them.

Breakthrough Reveals How Viruses Outsmart Human Cells

A team of Australian scientists has uncovered how certain viruses manage to seize control of human cells, a finding that could lead to the next generation of antivirals and vaccines.

The research, led by Monash University and the University of Melbourne and published in Nature Communications, explains how the rabies virus can manipulate a wide range of cellular activities despite producing only a few proteins.

Scientists believe this same mechanism could also be at work in other deadly pathogens, including Nipah and Ebola viruses. If so, the discovery could pave the way for new treatments that block these viral strategies.

How Viruses Do So Much With So Little

Co-senior author Associate Professor Greg Moseley, head of the Monash Biomedicine Discovery Institute’s (BDI) Viral Pathogenesis Laboratory, described the remarkable efficiency of viruses.

“Viruses such as rabies can be incredibly lethal because they take control of many aspects of life inside the cells they infect,” Associate Professor Moseley said. “They hijack the machinery that makes proteins, disrupt the ‘postal service’ that sends messages between different parts of the cell, and disable the defenses that normally protect us from infection.”

He explained that scientists have long puzzled over how viruses with such limited genetic material could be so powerful. “Rabies virus, for example, has the genetic material to make only five proteins, compared with about 20,000 in a human cell,” he said.

The Key: A Shape-Shifting Viral Protein

Co-first author Dr. Stephen Rawlinson, a research fellow in the Moseley Lab, said the team’s work offers a long-sought answer.

“Our study provides an answer,” he said. “We discovered that one of rabies virus’s key proteins, called P protein, gains a remarkable range of functions through its ability to change shape and to bind to RNA.”

“RNA is the same molecule used in new-generation RNA vaccines, but it plays essential roles inside our cells, carrying genetic messages, coordinating immune responses, and helping make the building blocks of life.”

Taking Over the Cell’s Inner World

Co-senior author Professor Paul Gooley, who leads the University of Melbourne’s Gooley Laboratory, said the viral P protein’s ability to interact with RNA allows it to shift between different physical ‘phases’ within a cell.

“This allows it to infiltrate many of the cell’s liquid-like compartments, take control of vital processes, and turn the cell into a highly efficient virus factory,” Professor Gooley said.

Although this research focused on rabies, he noted that similar tactics may be used by other deadly viruses, including Nipah and Ebola. “Understanding this new mechanism opens exciting possibilities for developing antivirals or vaccines that block this remarkable adaptability,” he added.

Rethinking How Viral Proteins Work

Dr. Rawlinson said the findings challenge how scientists have traditionally viewed multifunctional viral proteins. “Until now, these proteins were often viewed like trains made up of several carriages, with each carriage (or module) responsible for a specific task,” he said.

“According to this view, shorter versions of a protein should simply lose functions as carriages are removed. However, this simple model could not explain why some shorter viral proteins actually gain new abilities. We found that multifunctionality can also arise from the way the ‘carriages’ interact and fold together to create different overall shapes, as well as forming new abilities such as binding to RNA.”

A New Perspective on Viral Adaptability

Associate Professor Moseley said that the ability of the P protein to bind RNA allows it to move between different physical ‘phases’ inside the cell.

“In doing so, it can access and manipulate many of the cell’s own liquid-like compartments that control key processes, such as immune defense and protein production,” he said. “By revealing this new mechanism, our study provides a fresh way of thinking about how viruses use their limited genetic material to create proteins that are flexible, adaptable, and able to take control of complex cellular systems.”

This study involved Monash University, the University of Melbourne, the Australian Nuclear Science and Technology Organisation (Australian Synchrotron), Peter Doherty Institute for Infection and Immunity, Commonwealth Scientific and Industrial Research Organisation (CSIRO), the Australian Centre for Disease Preparedness (ACDP), and Deakin University.

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