Astronomers at the Center for Astrophysics | Harvard & Smithsonian have proposed a new explanation for some of the universe’s most puzzling early galaxies, nicknamed “little red dots.”
In the study, published in The Astrophysical Journal Letters, Authors Fabio Pacucci and Abraham (Avi) Loeb suggest that these galaxies are the result of very slowly spinning dark matter halos, an extremely rare cosmic structure.
These faint, compact objects, discovered in deep space images from the James Webb Space Telescope (JWST), have challenged scientists’ understanding of how galaxies and black holes formed in the early universe.
Their paper, “Cosmic Outliers: Low-Spin Halos Explain the Abundance, Compactness, and Redshift Evolution of the Little Red Dots,” offers a physical explanation for the dots’ distinctive properties.
“Little red dots are very compact and red distant galaxies that were completely undetected before the James Webb Space Telescope,” said Pacucci. “They are arguably the most surprising discovery by JWST to date. Our work shows that these could naturally form in dark matter halos with very low spin.”
A Puzzle in the Early Universe
These galaxies are primarily visible when the Universe was just one billion years old, but likely formed much earlier, Pacucci said, during a time known as the cosmic dawn. Despite being about one-tenth the size of typical galaxies, astronomical observations show them to appear unusually bright. Astronomers believe their striking red color suggests they are shrouded in dust or filled with older stars.

For years, astronomers have debated whether the light we observe from these objects is generated by stars or central supermassive black holes.
“It’s a fundamental mystery,” said Pacucci. “If they contain black holes, those black holes are enormous for such small galaxies. But if they only contain stars, the galaxies are too compact to contain all of them, reaching central stellar densities that are unthinkable.”
Rather than focusing on what powers the luminous dots, Pacucci and Loeb took a different approach: they examined how such objects might form in the first place.
The Low-Spin Cycle
Dark matter halos are the invisible, spinning scaffolding around which galaxies form. In their paper, the authors show that the luminous dots formed in halos that are in the lowest 1% of the spin distribution. In other words, 99% of all halos spin faster than those. These low-spin halos would naturally create extremely compact galaxies. Much like the swings ride at a carnival, the faster the halo spins, the further out the swings stretch, causing the galaxy forming at its center to expand; likewise, a slow spin keeps the swings’ radius smaller.
This hypothesis also explains why luminous dots are relatively rare: they represent just 1% of the abundance of typical galaxies, but are more common than quasars, the extremely bright centers supermassive black holes that shine at the center of some galaxies.

In addition, the theory helps clarify why luminous dots are only observed during a brief 1-billion-year period in the early universe. As the universe evolves, dark matter halos grow larger and gain more angular momentum, making it more difficult to form compact, low-spin galaxies.
“Dark matter halos are characterized by a rotational velocity: some of them spin very slowly, and others spin more rapidly,” Loeb said. “We showed that if you assume the little red dots are typically in the first percentile of the spin distribution of dark matter halos, then you explain all their observational properties.”
Prime Environments for Black Holes
While the paper does not resolve whether little red dots are powered by stars or black holes, it suggests they are prime environments for rapid stellar or black hole growth.
“Low-spin halos tend to concentrate mass in the center, which makes it easier for a black hole to accrete matter or for stars to form rapidly,” said Pacucci.
Some of the dots show broad emission lines in their spectra, which are possible signs of active black holes, but they lack the X-ray emission typically associated with them. Pacucci is leading new programs to understand better the nature of these peculiar astrophysical sources. For example, finding similar nearby galaxies will clarify what they evolve into further out in space.
“Our work is a step toward understanding these mysterious objects,” he said. “They might help us understand how the first black holes formed and co-evolved with galaxies in the early universe.”

A University of Queensland study suggests the antivenom given to people bitten by Eastern Brown Snakes may not be as effective as it could be, prompting a review of hospital cases.
Professor Bryan Fry from UQ’s School of the Environment led a team which assessed the blood-clotting toxins in venoms from every Australian brown snake species.
“We discovered not all brown-snake venoms are the same – meaning that lifesaving antivenom may need an urgent upgrade,” Professor Fry said.
“Some venoms formed a rock-solid clot in blood, while others spun up a rapid but flimsy web of clots that shredded almost instantly.
“Both venoms can kill but they do it in completely different ways.”
The team used a process called thromboelastography, which assesses blood coagulation, and showed Eastern Brown Snakes (Pseudonaja textilis) from southern Australia have a ‘taipan-like’ venom that builds a strong, stable blood clot.
Venom from northern populations of Eastern Brown Snake, as well as all other brown snake species, triggered fragile blood clots, but lightning fast.

“Our data shows the effect on blood of an Eastern Brown Snake bite in northern areas and a bite in southern Australia are chalk and cheese,” Professor Fry said.
“Currently Australia’s brown-snake antivenom is produced using a pool of venom of unstated geographic origin.
“If it doesn’t have both northern and southern Eastern Brown Snake venom, coverage could be patchy and the antivenom efficacy could vary widely.
“Clinical reports have all brown snake bite cases together regardless of species or location so any differences for the southern population versus all other brown snakes could be obscured.
“Our next step is to go back through hundreds of hospital charts to ascertain if there is a difference, which we can do because the southern strong-clot lineage lives where no other brown snake occurs.
“We can re-code every reported bite by geography and tease apart the clotting patterns between the strong and weak clotting types of brown snakes.

“We will also urgently test the available human and veterinary antivenoms to see if the differences in venom biochemistry are mirrored by variations in antivenom efficacy.
“While existing antivenoms have saved lives, with new information we can move to precision toxicology, matching the right antivenom to the right snake, and ultimately, to the right patient.”
Professor Fry’s team is also sequencing the venom genes to pinpoint the mutations responsible for the differences in northern and southern Eastern Brown Snakes.
“We showed the geographic difference in venom effect overlays with a genetic divide within the Eastern Brown Snake,” he said.
“Our research demonstrates how diet steers venom evolution, because the southern populations consume more reptiles than the northern populations which eat more mammals.
“By appreciating both the evolutionary fine-tuning and the clinical outcomes of these venoms we can better tailor our medical responses.”
The research paper has been published in Toxins.

It’s a fact of life: Some people age better than others.
Some ease into their 90s with mind and body intact, while others battle diabetes, Alzheimer’s or mobility issues decades earlier. Some can withstand a bad fall or bout of the flu with ease, while others never leave the hospital again.
New University of Colorado Boulder-led research, published this month in the journal Nature Genetics, sheds light on why that is.
In it, an international team of co-authors identify more than 400 genes associated with accelerated aging across seven different sub-types. The study reveals that different groups of genes underlie different kinds of disordered aging, a.k.a. frailty, ranging from cognitive decline to mobility issues to social isolation.
The findings lend support to what is known as the “geroscience hypothesis” — the idea that to treat the multiple chronic illnesses that come with aging, we must treat aging itself.
“To be able to identify treatments to stop or reverse accelerated biological aging, you need to know what the underlying biology is,” said Isabelle Foote, first author on the paper and a postdoctoral researcher at CU’s Institute for Behavioral Genetics. “This is the largest study yet to use genetics to try to do that.”
Redefining ‘frailty’
The study centers around “frailty,” a catch-all term for the “multisystem physiological decline” that often comes with aging.

More than 40% of U.S. adults over age 65 are considered frail.
Doctors typically assess frailty using a 30- point index that measures things like walking speed, grip strength, number of diagnosed illnesses and amount of social activity. The problem, said Foote, is that two people can get the same high frailty score even though one is cognitively sharp but can’t walk and another is in good physical health but has a poor memory.
This lack of distinction has made it hard for doctors to make recommendations and for scientists to pinpoint the underlying causes of unhealthy aging.
“Aging is not just one thing. There are many ways to be frail,” said Dr. Kenneth Rockwood, a leading expert in frailty, based at Dalhousie University in Nova Scotia, Canada and co-author on the study. “The question then becomes: What genes are involved?”
To find out, the team conducted a “genome-wide association study” analyzing DNA and health information from hundreds of thousands of participants in the UK Biobank and other public datasets to see which genes were associated with 30 frailty symptoms.
They identified 408 genes associated with accelerated aging/frailty, a significant increase from the 37 genes previously identified.

Some genes, they found, were strongly linked to certain subtypes of unhealthy aging, including: “disability”; “poor cognition”; “metabolic problems”; “multiple diseases”; “generally unhealthy lifestyle”; and “limited social support.”
For instance, the SP1 gene, associated with immune function and Alzheimer’s disease was strongly associated with the broad “poor cognition” subtype, whereas the FTO gene, a gene known to be associated with obesity, seemed to underly several different categories of unhealthy aging.
“What this paper does is not only identify sub-facets of disordered aging but also demonstrate that there is very different biology underlying them,” said senior author Andrew Grotzinger, assistant professor of psychology and neuroscience at CU Boulder. “The tangible next step is to figure out how to treat this underlying biology.”
An anti-aging pill?
In the near term, the authors suggest that clinical measurements of frailty — which often shows up long before specific diseases — be expanded to include the six subtypes.
That way, someone diagnosed as cognitively frail could be guided toward therapies to prevent dementia, while someone frail in the metabolic domain might take steps to prevent diabetes or heart disease.
Foote envisions a day when people could get a “polygenic risk score” offering more detailed insight into what kind of unhealthy aging they are prone to.
But the holy grail, she says, would be to identify the molecular pathways that drive aging itself and develop therapies to put the brakes on.
Is a single anti-aging pill on the horizon?
Not likely.
But could there one day be a pill to treat a package of age-related metabolic issues, and another to address numerous cognitive issues?
It’s a tantalizing idea, said Grotzinger.
“This paper suggests that it’s probably not going to be a single magic pill to address all the diseases that come with aging, but maybe it doesn’t need to be hundreds anymore.”

11 hours agoShareSaveMichael BuchananSocial Affairs CorrespondentShareSaveBBCFamilies calling for an inquiry into maternity care in East Sussex say they feel “ignored, exhausted and dismissed” after meeting the chair of a national review.The group met with Baroness Amos on Wednesday, claiming she was poorly briefed and that no progress was made.The families, who all lost babies under the University Hospitals Sussex NHS Trust, have been campaigning for 18 months for an inquiry and insist that senior midwife Donna Ockenden is appointed to lead it.The Department of Health and Social Care (DHSC) said Baroness Amos would work closely with families to “uncover the truth”.In June, Health Secretary Wes Streeting announced a rapid review into maternity services in England and last week appointed Baroness Amos, a former senior diplomat, to lead it. Streeting said he wanted the work to be completed by December and that up to 10 local areas would have their maternity services examined as part of the investigation.Nine families in Sussex, who say medical errors led to their babies’ deaths, were promised a review by Streeting and the group thought the meeting with Baroness Amos would progress the case.But they said the chair told them that she was not aware of the history or expectations of the families, and that she did not have the power to decide who would lead it.’Deeply dispiriting'”We have spoken to Wes Streeting directly and to the Department of Health & Social Care again and again about the toll these meetings take on us,” the families said in a statement.”To set aside an hour of our time for a meeting where appropriate preparation had not taken place was deeply dispiriting, and to feel we have still not made progress on our review, despite many months of presenting a clear case for one, drafting the terms of reference and securing the support of Donna Ockenden, is infuriating.”Ms Ockenden is currently leading a review of maternity care in Nottingham having previously examined services at the Shrewsbury and Telford NHS trust.PA MediaShortly before the meeting, the families were told that Kathryn Whitehill, a former inspector with the Care Quality Commission, had been appointed as an investigator on the review, causing anger among several families who had suffered poor maternity care.”Bereaved parents had been promised they would be consulted on any appointments and have consistently fed back to the government that this investigation cannot be undertaken by anyone working for the regulators responsible for holding trusts accountable for maternity safety,” the statement from the families added.”These organisations are part of the system that has continued to deliver unsafe maternity care, and as such should be part of the focus of the investigation rather than leading it.”The appointment of Ms Whitehill “raises serious doubts about whether the review can be independent or trusted”, the statement added.The DHSC said she had been seconded due to her professional skills, expertise and experience and that she has not been permanently appointed to the review.The concerns of the group come in the wake of criticism of the rapid review last week from a wider group of families.The Maternity Safety Alliance, which represents families from areas which have experienced poor maternity care, said Streeting’s inquiry was “doomed to fail” before it has begun due to the behaviour of the Department of Health and NHS England.Some other families have however expressed a willingness to work with Baroness Amos.A DHSC spokesperson said: “The Secretary of State has been working closely with harmed and bereaved families throughout this process to ensure they are at the heart of decision making.”Families asked for fresh eyes, independence, and compassion. Baroness Amos has been appointed because her of outstanding record of leadership and driving change – nationally and internationally. “She will work closely with families to appoint her expert panel and finalise terms of reference to uncover the truth, confront problems and drive the improvements needed so every woman and baby receives safe, high-quality care.”More on this storyRelated internet links

38 minutes agoShareSaveCatrin Nye and Adam EleyBBC NewsShareSaveGetty ImagesBaby food manufacturers must cut levels of salt and sugar in their products and stop promoting snacks for babies under the age of one, the government has said.The new guidance would also restrict the use of marketing claims that suggest health benefits without scientific evidence.Firms that do not make their products healthier within 18 months may face action.It comes four months after a BBC Panorama investigation found top-brand baby food pouches lacked key nutrients and parents were often being misled by marketing.Manufacturers told the BBC they were committed to providing high quality and nutritious foods, and marketing and labelling them in a responsible way.There has been significant growth in the baby food and drink market in recent years. Food in pouches makes up more than a third of this market and there’s been a rise in sales of snacks like fruit and vegetable-based straws, puffs and wafers.”Companies are dressing these products up as being healthy, when actually they’re much like a crisp or a sweetie. They’re putting profit before health,” says former chief nutritionist to the government, Dr Alison Tedstone. “I hope an ethical business will stand back and think about the health of our children.”In June, NHS advice was updated to tell parents they should not rely on baby food pouches as everyday meals, with experts believing they can cause health problems for children if used as their main source of nutrition.These new government guidelines now turn to manufacturers – telling them to improve their products and ranges. This has been a key demand of health campaigners who say it is companies that need to improve, so not all the pressure is on parents.Family photoKristal, a mum of two from Leeds, has used commercial baby food to feed her son Austin, who is now two.”Like most parents I take my children’s health and nutrition very seriously,” she told the BBC.”[But] for far too long there have been misleading marketing messages about the nutritional value of baby food and implied ‘healthiness’ of some of the infant snack foods”.Companies have previously been able to market products to babies as young as four months old, even though government guidelines state that solid foods should not be given to babies under six months.Firms have also marketed snacks to infants under 12 months, when NHS guidance for parents says children under one do not need snacks.The new guidelines say both of these practices should now be phased out, which could have significant ramifications for manufacturers.Under the guidelines, sugar levels will be restricted in finger foods, snacks, desserts and non-refrigerated yoghurts, but there is no maximum level of sugar permitted in fruit pouches. This is despite many such products containing more sugar in a single pouch than a one-year-old should have in a day.Companies have also been told to restrict the use of marketing claims on their products which are not based on scientific evidence. Experts argue these claims often make products appear healthier than they really are, and sometimes even appear a better choice than homemade food.Some leading baby food pouches carry labels such as “just good stuff” or “packed with goodness”, despite BBC Panorama finding some products to be low in key nutrients and very high in sugar.But there is concern the guidelines are not clear on what is and isn’t permissible. Dr Vicky Sibson, a public health nutritionist and director of the charity First Steps Nutrition Trust, describes them as “open to exploitation” by companies.A version of these guidelines was first drafted five years ago by Public Health England for the then-Conservative government.However, the guidelines were never published as prime ministers changed and new priorities came in during the Covid-19 pandemic.Dr Alison Tedstone led the team that wrote those guidelines and told the BBC she hopes “this is the line in the sand”.The guidelines are voluntary, and the government hopes they will be followed.But none of the companies approached by the BBC responded when asked if they would adhere to the guidelines in full.A public relations firm representing Ella’s Kitchen, a market leader, disputed whether some of its products fell under the guidelines relating to the advertising of snacks.It told the BBC their carrot and parsnip melty puffs and tomato and basil melty sticks – advertised clearly as snacks on supermarket websites, and in the ”snacks and finger foods“ section on their own website – were actually intended to be used as part of a meal or ”picky plate”.Dr Vicky Sibson called the Ella’s Kitchen response “disingenuous”, adding that parents regularly use such products as snacks. She said puffs and melty sticks were wholly inappropriate for use within main meals as infants need food that is high in nutrients.Dr Tedstone said she heard such arguments time and time again from baby food companies and that it was “inevitable” some companies would not adhere to the guidelines.The government says “additional or alternative measures” will be considered if businesses fail to implement these guidelines by February 2027.Campaigners hope this would take the form of improved mandatory legislation. The government declined to specify if this was an option.The guidelines apply in England only, but it’s expected that manufacturers will sell any updated ranges or products across the UK.The British Specialist Nutrition Association (BSNA), an industry body that represents the biggest baby food companies including Ella’s Kitchen, Organix, Kiddilicious and Hipp Organic, told the BBC its members “have carried out significant improvements to recipes in recent years, including reducing sugar and increasing vegetable content, and continually review on-pack information”.”We will continue to work towards the published guidelines,” it added. “Baby foods can play an important role alongside home-prepared meals and offer options for parents on-the-go.”Heinz and Kiddilicious did not respond to the BBC. Organix and Ella’s Kitchen did not provide their own statements, referring us to the BSNA.Piccolo said they “remain committed to evolving with the guidance to best serve families”.Charlotte Stirling-Reed, a baby weaning expert and author, told the BBC that she hoped brands adhered “for the future health of children”.She added that families should not feel guilty for having used the products.”This is about making changes to the food products that are available for young children, not about shaming us as parents.”Do you have more information about this story?You can reach Catrin Nye by email at catrin.nye@bbc.co.uk, or her Instagram account.

Researchers at the Icahn School of Medicine at Mount Sinai have found that prenatal exposure to acetaminophen may increase the risk of neurodevelopmental disorders, including autism spectrum disorder and attention-deficit/hyperactivity disorder (ADHD), in children. The study, published on August 14 in BMC Environmental Health, is the first to apply the rigorous Navigation Guide methodology to systematically evaluate the rigor and quality of the scientific literature.
Acetaminophen (often sold under the brand name Tylenol®, and known as paracetamol outside the United States and Canada) is the most commonly used over-the-counter pain and fever medication during pregnancy and is used by more than half of pregnant women worldwide. Until now, acetaminophen has been considered the safest option for managing headache, fever, and other pain. Analysis by the Mount Sinai-led team of 46 studies incorporating data from more than 100,000 participants across multiple countries challenges this perception and underscores the need for both caution and further study.
The Navigation Guide Systematic Review methodology is a gold-standard framework for synthesizing and evaluating environmental health data. This approach allows researchers to assess and rate each study’s risk of bias, such as selective reporting of the outcomes or incomplete data, as well as the strength of the evidence and the quality of the studies individually and collectively.
“Our findings show that higher-quality studies are more likely to show a link between prenatal acetaminophen exposure and increased risks of autism and ADHD,” said Diddier Prada, MD, PhD, Assistant Professor of Population Health Science and Policy, and Environmental Medicine and Climate Science, at the Icahn School of Medicine at Mount Sinai. “Given the widespread use of this medication, even a small increase in risk could have major public health implications.”
The paper also explores biological mechanisms that could explain the association between acetaminophen use and these disorders. Acetaminophen is known to cross the placental barrier and may trigger oxidative stress, disrupt hormones, and cause epigenetic changes that interfere with fetal brain development.
While the study does not show that acetaminophen directly causes neurodevelopmental disorders, the research team’s findings strengthen the evidence for a connection and raise concerns about current clinical practices.
The researchers call for cautious, time-limited use of acetaminophen during pregnancy under medical supervision; updated clinical guidelines to better balance the benefits and risks; and further research to confirm these findings and identify safer alternatives for managing pain and fever in expectant mothers.

“Pregnant women should not stop taking medication without consulting their doctors,” Dr. Prada emphasized. “Untreated pain or fever can also harm the baby. Our study highlights the importance of discussing the safest approach with health care providers and considering non-drug options whenever possible.”
With diagnoses of autism and ADHD increasing worldwide, these findings have significant implications for public health policy, clinical guidelines, and patient education. The study also highlights the urgent need for pharmaceutical innovation to provide safer alternatives for pregnant women.
The study was conducted in collaboration with the University of California, Los Angeles; University of Massachusetts Lowell; and Harvard T.H. Chan School of Public Health.
Funding for this study was provided by the National Cancer Institute (U54CA267776), the National Institute of Environmental Health Sciences (R35ES031688), and the National Institute on Aging (U01AG088684).

An international team of scientists, co-led by researchers at the University of Florida and Trinity College Dublin, has cracked a decades-old mystery in human biology: how our bodies absorb a micronutrient that we rely on for everything from healthy brain function to cancer defense.
Queuosine – pronounced “cue-o-scene” – is a vitamin-like micronutrient that we can’t make ourselves but can only get from food and our gut bacteria. It’s vital to our health, yet its importance went unnoticed for decades.
Now, in a study published this week in the Proceedings of the National Academy of Sciences, researchers have discovered the gene that allows queuosine to enter the cells, a discovery that opens the door for potential therapies to be created to leverage the micronutrient’s role in cancer suppression, memory and how the brain learns new information.
“For over 30 years, scientists have suspected that there had to be a transporter for this nutrient, but no one could find it,” said Valérie de Crécy-Lagard, a UF/IFAS microbiology and cell science distinguished professor and department associate chair, as well as one of the study’s principal investigators. “We’ve been hunting for it for a long time. This discovery opens up a whole new chapter in understanding how the microbiome and our diet can influence the translation of our genes.”
The study was funded by various nations’ health entities, including the National Institutes of Health , Research Ireland (formerly Science Foundation Ireland), and Health and Social Care in Northern Ireland.
Queuosine modifies the molecules that help make proteins, called transfer RNA, which is essential in decoding your body’s DNA.
“It’s like a nutrient that fine-tunes how your body reads your genes,” she said. “The idea that this small compound, which people have barely heard of, plays such an important role, is fascinating.”
The gene that allows access to the cell has also been shrouded in medical mystery. The identification of the long-sought gene, SLC35F2, lays the groundwork for future studies that could lead to new medications, given that the gene has previously been studied regarding how viruses and cancer drugs get into cells, but scientists didn’t know what the gene did in a healthy body until now, de Crécy-Lagard said.

“We have known for a long time that queuosine influences critical processes like brain health, metabolic regulation, cancer and even responses to stress, but until now we haven’t known how it is salvaged from the gut and distributed to the billions of human cells that take it in,” said Vincent Kelly, professor in Trinity College Dublin’s School of Biochemistry and Immunology, and joint senior author of the article.
Queuosine is a microscopic molecule first discovered in the 1970s, but for years its role in human health flew under the radar until recently, and researchers from across the world involved in this study hope others take notice about this micronutrient’s role in the body’s bigger health picture.
The research united experts from UF, San Diego State University, the Ohio State University and partner institutions in Ireland and Northern Ireland.
“We don’t think we could have cracked it without the full team,” de Crécy-Lagard said. “It’s a perfect example of what international collaboration can achieve.”

Today’s NASA/ESA Hubble Space Telescope Picture of the Week offers a closeup of a nearby spiral galaxy. The subject is NGC 2835, which lies 35 million light-years away in the constellation Hydra (The Water Snake).
A previous Hubble image of this galaxy was released in 2020, and the NASA/ESA/CSA James Webb Space Telescope turned its gaze toward NGC 2835 in recent years as well. Do you see anything different between today’s image of NGC 2835 and the previously released versions? Overall, NGC 2835 looks quite similar in all of these images, with spiral arms dotted with young blue stars sweeping around an oval-shaped center, where older stars reside.
This image differs from previously released images because it incorporates new data from Hubble that captures a specific wavelength of red light called H-alpha. The regions that are bright in H-alpha emission can be seen along NGC 2835’s spiral arms, where dozens of bright pink nebulae appear like flowers in bloom. Astronomers are interested in H-alpha light because it signals the presence of several different types of nebulae that arise during different stages of a star’s life. Newborn massive stars create nebulae called H II regions that are particularly brilliant sources of H-alpha light, while dying stars can leave behind supernova remnants or planetary nebulae that can also be identified by their H-alpha emission.
By using Hubble’s sensitive instruments to survey 19 nearby galaxies, researchers aim to identify more than 50,000 nebulae. These observations will help to explain how stars affect their birth neighborhoods through intense starlight and winds.

Aging is particularly harsh on the hippocampus — the brain region responsible for learning and memory.
Now, researchers at UC San Francisco have identified a protein that’s at the center of this decline.
They looked at how the genes and proteins in the hippocampus changed over time in mice and found just one that differed between old and young animals. It’s called FTL1.
Old mice had more FTL1, as well as fewer connections between brain cells in the hippocampus and diminished cognitive abilities.
When the researchers artificially increased FTL1 levels in young mice, their brains and behavior began to resemble that of old mice.
In experiments in petri dishes, nerve cells engineered to make lots of FTL1 grew simple, one-armed neurites — rather than the branching neurites that normal cells create.
But once the scientists reduced the amount of FTL1 in the hippocampus of the old mice, they regained their youth. They had more connections between nerve cells, and the mice did better on memory tests.

“It is truly a reversal of impairments,” said Saul Villeda, PhD, associate director of the UCSF Bakar Aging Research Institute and senior author of the paper, which appears in Nature Aging on Aug. 19. “It’s much more than merely delaying or preventing symptoms.”
In old mice, FTL1 also slowed down metabolism in the cells of the hippocampus. But treating the cells with a compound that stimulates metabolism prevented these effects.
Villeda is optimistic the work could lead to therapies that block the effects of FTL1 in the brain.
“We’re seeing more opportunities to alleviate the worst consequences of old age,” he said. “It’s a hopeful time to be working on the biology of aging.”
Authors: Other UCSF authors are Laura Remesal, PhD, Juliana Sucharov-Costa, Karishma J.B. Pratt, PhD, Gregor Bieri, PhD, Amber Philp, PhD, Mason Phan, Turan Aghayev, MD, PhD, Charles W. White III, PhD, Elizabeth G. Wheatley, PhD, Brandon R. Desousa, Isha H. Jian, Jason C. Maynard, PhD, and Alma L. Burlingame, PhD. For all authors see the paper.
Funding: This work was funded in part by the Simons Foundation, Bakar Family Foundation, National Science Foundation, Hillblom Foundation, Bakar Aging Research Institute, Marc and Lynne Benioff, and the National Institutes of Health (AG081038, AG067740, AG062357, P30 DK063720). For all funding see the paper.

When you visit a doctor, you expect them to listen. But in today’s fast-paced health care system, real listening — the kind that makes you feel seen, heard and understood — can be the first thing to go.
A new article, co-authored by Dr. Leonard Berry of Texas A&M University’s Mays Business School, argues that listening isn’t just a nice gesture, it’s a powerful tool that can improve your care and even help heal the health care system itself.
Berry and colleagues at the Institute for Healthcare Improvement in Boston and Henry Ford Health Detroit published their findings in Mayo Clinic Proceedings.
The Case Of The Norwegian Nurse
The team identified what it calls “values-driven listening.” It’s about more than asking questions, it’s about asking the right questions, being present and showing genuine curiosity and compassion.
“Listening is the gateway to healing,” Berry said. “It’s how we connect, understand and ultimately serve better.”
One story in the article shows just how transformative listening can be. A nurse in a Norwegian nursing home asked a patient, “What would make a good day for you?”
The patient responded: “I want to wear my blue shirt.”

“Why the blue one?” the nurse asked.
“That was my wife’s favorite shirt,” the patient said. “She died two years ago today, and I want to honor her.”
The patient shared memories of his wife with the nurse, and afterward, he asked for a wheelchair so that he could tell other patients about her; it was the first time he’d ever asked to interact with other people at the facility.
“That’s not a medical breakthrough,” Berry said, “it’s a human one.”
Six Listening Strategies
The authors outline six types of listening that contribute to better care:
Listening That Is Proximate Being physically present matters. Your provider can learn far more from a quiet moment in the exam room than from a rushed message or chart note. When they’re close, focused and curious, you’re more likely to open up, and that kind of trust is essential for making decisions together about your care. Be sure your provider spends this focused time with you.

Listening That Is Curious Your provider’s curiosity can be just as important as their expertise. When they ask open-ended questions and pay attention to your words, body language and emotions, it creates space for honest conversation. That’s often when key details emerge informing the plan of care. “What are your concerns about the plan of care we’ve discussed?” creates a path for open dialogue in a way that “Do you have any questions?” does not.
Listening That Earns And Enables Trust Trust starts when you feel safe to speak candidly, and that happens when your provider listens without judgment, gives you their full attention and treats your input as essential. At Henry Ford Health, some doctors are using AI-powered tools to handle notetaking during appointments, so they can focus entirely on the conversation.
Listening Aided By Design The design of a clinic or hospital can affect how well you’re heard. Small, crowded spaces make private conversations harder, but simple changes — like your provider sitting down during a visit — can make you feel more cared for and listened to. Some health systems, like Southcentral Foundation in Alaska, have created “talking rooms” that feel less clinical and more personal, showing that listening isn’t just a skill, it’s something built into the space itself.
Listening That Empowers Listening should lead to action, and that includes listening to the people who care for you. When frontline staff are asked what’s wasting time or making care harder, they often have smart, simple fixes. At Hawaii Pacific Health, a program called “Getting Rid of Stupid Stuff” led to hundreds of suggestions, including one that saved nurses 1,700 hours a month by removing a pointless documentation rule. When staff are empowered to speak up, care becomes more efficient, less frustrating and better for everyone.
Listening That Fosters Resilience Caring for others is demanding, and when health care workers are supported, they’re better able to support you. Simple acts like sharing meals and stories with colleagues can help reduce burnout and build emotional strength in those who are caring for you. Some hospitals schedule time for these peer connections, creating space for reflection and support. Ask your provider how their health care system supports its workers.
Listening Is Kindness
Berry and his co-authors write that deep listening benefits all parties: clinician-to patient; clinician-to-clinician; leader-to-clinical and non-clinical staff. It’s a cultural shift that starts with values. “Do you care enough to listen?” they ask.
For patients, this means you should feel empowered to speak up and expect to be heard.
“Your experiences, concerns and insights are not just helpful, they’re essential,” Berry said. “And when your care team listens with empathy and curiosity, it leads to better decisions, stronger relationships and more personalized care.
“Kindness is not a luxury in health care, it’s a necessity. And true listening is one of its most powerful expressions.”