2025-10-08 01:55:14
The ‘fourth pillar’ of brain communication potentially impacts Alzheimer’s and other diseases.
Brain cells are like tiny trees. They have an intricate web of roots that take in signals and a trunk that passes these signals to branches dotted with hubs called synapses, where the messages are shuttled to neighboring neurons.
It’s a very loose analogy. But it may be more accurate than neuroscientists previously thought.
At eye level, trees seem to grow alone, physically separated from other nearby trees. But under the soil, their roots are covered in a fungus with tiny thread-like channels. These weave tree roots into a vast web called the “mycorrhizal network.” Through these physical connections, trees can share water, nutrients, and chemical signals such as hormones—allowing them to communicate in what’s been dubbed a “woodwide web.”
Neurons may have a similar network. A new study imaging mouse and human brains discovered dynamic nanotube tunnels connecting dendrites, the roots of neurons. These wispy structures seemingly spawn from any point on the vast dendritic network and dissolve in minutes or hours.
Scientists don’t yet know exactly what they do. But the nanotubes can transfer electrical signals between neurons, a feat usually only attributed to synapses. They also allow neurons to share proteins, including those related to Alzheimer’s disease.
“The discovery suggests that the current understanding of the brain’s organization may be incomplete, overlooking a hidden layer of connectivity,” wrote Dimitri Budinger and Michael Heneka at the University of Luxembourg, who were not involved in the study.
Nanotubes are common in nature. Bacteria notoriously extend their membranes into tubes to share genetic material with their neighbors. This networking makes it easy to rapidly spread genes that are beneficial to the bugs, including those conferring antibiotic resistance.
Mammalian cells do it too. Around two decades ago, one team noticed fragile, membrane-like tubes spontaneously connecting rat kidney cells in a dish. Although both sides of the nanotube highways are open like a straw, they have surprisingly precise rules on cargo regulation. For example, some allow cells to transport select organelles—relatively self-contained components with specific functions inside cells—but only in one direction. Other cargo, such as proteins floating inside the cell’s watery interior are completely banned.
Scientists later discovered these elusive nanotunnels in a variety of other cell types grown in petri dishes, such as immune cells, cancer cells, and stem cells. The tunnels helped regulate viral infection, the spread of cancer, and organ development. Earlier this year, a group observed nanotubes in living zebrafish embryos. What job the nanotubes do seems to depend on the cell and tissue type, but they share similarities in their structural makeup and transient nature.
Telltale signs also suggest they help the brain stay healthy, at least in a dish. As the toxic proteins involved in Parkinson’s and Alzheimer’s disease accumulate, neurons form nanotubes that reach out to microglia, the brain’s immune cells. Called tunneling nanotubes, or TNTs, the newly built thoroughfares shuttle toxic proteins from neuron to microglia. In exchange, the microglia donate healthy mitochondria to the damaged neurons for an antioxidant boost.
“It was thrilling to observe that microglia play an active role in maintaining neuronal health and supporting neurons in times of need,” study author Hannah Scheiblich, who worked with Heneka on the project, said in a press release at the time.
Scientists are studying TNTs in other brain diseases, such as stroke and brain cancer. But observing them in the brain has been a headache. The tunnels are incredibly thin—a fraction of a human hair—and extremely fragile. Under conventional microscopy they easily get lost in the dense, chaotic tangle of neuronal branches.
In the new study, the team combed through a large collection of electron microscope images of the mouse and human brain. Here they found signs of curious nanotunnels similar to TNTs. But they weren’t identical. For one, the new tubes connected dendrites—the neuron’s roots that take in signals—rather than sprouting from the longer trunk of a neuron. They were also less than one-third the length of TNTs.
The team next imaged wafer-thin living mouse brain slices and cultured human neurons with super-resolution microscopy. Using machine learning, they teased the slender structures apart from the relatively heftier neural branches and observed them.
Similar to TNTs, dendritic nanotubes are made mostly of a structural protein called actin. They’re highly dynamic, springing up and dissolving in a matter of minutes to hours.
The short timespan could impact how neurons work. Our brain cells transmit messages in three main ways. Synapses are the mainstay. These highly sophisticated “hubs” convert electrical signals into chemical messengers to pass on information. Gap junctions offer a rarer but speedier route: They rely solely on electrical signals. The third are like “spaceships” that neurons use to launch a variety of biomaterials to other nearby cells that influence their function.
Dendritic nanotubes seem to be a jack of all trades. They transmit electrical signals in the form of calcium, which neurons need to activate. When they artificially raise the amount of calcium in one neuron, neighboring neurons also register a boost. Adding a chemical that destroys the nanotubes partially blocks the effect.
Dendrites are mini-computers on their own, with synapses processing incoming signals in parallel and then shuttling the results to other parts of the cell for more processing. Nanotubes seem to operate independently of synapses. They create a network that could alter the activity of dendrites and allow neurons to share information outside the usual synaptic routes.
“What makes dendritic nanotubes conceptually exciting is that they expand the repertoire of known forms of communication among neurons,” wrote Budinger and Heneka.
Unlike TNTs, dendritic nanotubes are closed at both ends. While scientists are not exactly sure how and why this happens, the quirk could help regulate the transport of proteins—including harmful ones. When the team added human amyloid-beta—a protein involved in Alzheimer’s—to a single mouse neuron in a petri dish, it rapidly spread to other neurons. The transfer was nipped in the bud by destroying the nanotubes.
The wispy tunnels also showed up in a mouse model of Alzheimer’s. Their connectivity increased in the front part of the brain at three months of age—the rough equivalent of young adult in human years—and well before there were any signs of toxic amyloid-beta clumps.
But the effects were nuanced. Computer simulations supported the idea that the nanotubes contribute to amyloid-beta spreading but only at low doses, which could help dilute the toxic burden for a single cell. At high doses, however, the tunnels disintegrate and sequester the clumps inside infected cells, potentially to keep them from spreading further.
These results only scratch the surface. The team is exploring which cargo—specific proteins, RNA molecules, or organelles—are preferentially transported, how their abundance alters during aging and disease, and if they intersect with classic TNTs.
Still, the discovery “underscores that the brain’s connectome, the complete map of all the neural connections in the brain, is more than a wiring diagram of synapses” and should include these transient, nanoscale links that come and go, wrote Budinger and Heneka. They’re the “fourth pillar of intercellular communication.”
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2025-10-07 00:52:18
In a ‘red teaming’ effort led by Microsoft researchers, biosecurity programs struggled to flag AI-generated toxins.
AI is expanding our protein universe. Thanks to generative AI, it’s now possible to design proteins never before seen in nature at breakneck speed. Some are extremely complex; others can tag onto DNA or RNA to change a cell’s function. These proteins could be a boon for drug discovery and help scientists tackle pressing health challenges, such as cancer.
But like any technology, AI-assisted protein design is a double-edged sword.
In a new study led by Microsoft, researchers showed that current biosecurity screening software struggles to detect AI-designed proteins based on toxins and viruses. In collaboration with The International Biosecurity and Biosafety Initiative for Science, a global initiative that tracks safe and responsible synthetic DNA production, and Twist, a biotech company based in South San Francisco, the team used freely available AI tools to generate over 76,000 synthetic DNA sequences based on toxic proteins for evaluation.
Although the programs flagged dangerous proteins with natural origins, they had trouble spotting synthetic sequences. Even after tailored updates, roughly three percent of potentially functional toxins slipped through.
“As AI opens new frontiers in the life sciences, we have a shared responsibility to continually improve and evolve safety measures,” said study author Eric Horvitz, chief scientific officer at Microsoft, in a press release from Twist. “This research highlights the importance of foresight, collaboration, and responsible innovation.”
The rise of AI protein design has been meteoric.
In 2021, Google DeepMind dazzled the scientific community with AlphaFold, an AI model that accurately predicts protein structures. These shapes play a critical role in determining what jobs proteins can do. Meanwhile, David Baker at the University of Washington released RoseTTAFold, which also predicts protein structures, and ProteinMPNN, an algorithm that designs novel proteins from scratch. The two teams received the 2024 Nobel Prize for their work.
The innovation opens a range of potential uses in medicine, environmental surveys, and synthetic biology. To enable other scientists, the teams released their AI models either fully open source or via a semi-restricted system where academic researchers need to apply.
Open access is a boon for scientific discovery. But as these protein-design algorithms become more efficient and accurate, biosecurity experts worry they could fall into the wrong hands—for example, someone bent on designing a new toxin for use as a bioweapon.
Thankfully, there’s a major security checkpoint. Proteins are built from instructions written in DNA. Making a designer protein involves sending its genetic blueprint to a commercial provider to synthetize the gene. Although in-house DNA production is possible, it requires expensive equipment and rigorous molecular biology practices. Ordering online is far easier.
Providers are aware of the dangers. Most run new orders through biosecurity screening software that compares them to a large database of “controlled” DNA sequences. Any suspicious sequence is flagged for human validation.
And these tools are evolving as protein synthesis technology grows more agile. For example, each molecule in a protein can be coded by multiple DNA sequences called codons. Swapping codons—even though the genetic instructions make the same protein—confused early versions of the software and escaped detection.
The programs can be patched like any other software. But AI-designed proteins complicate things. Prompted with a sequence encoding a toxin, these models can rapidly churn out thousands of similar sequences. Some of these may escape detection if they’re radically different than the original, even if they generate a similar protein. Others could also fly under the radar if they’re too similar to genetic sequences labeled safe in the database.
The new study tested biosecurity screening software vulnerabilities with “red teaming.” This method was originally used to probe computer systems and networks for vulnerabilities. Now it’s used to stress-test generative AI systems too. For chatbots, for example, the test would start with a prompt intentionally designed to trigger responses the AI was explicitly trained not to return, like generating hate speech, hallucinating facts, or providing harmful information.
A similar strategy could reveal undesirable outputs in AI models for biology. Back in 2023, the team noticed that widely available AI protein design tools could reformulate a dangerous protein into thousands of synthetic variants. They call this a “zero-day” vulnerability, a cybersecurity term for previously unknown security holes in either software or hardware. They immediately shared the results with the International Gene Synthesis Consortium, a group of gene synthesis companies focused on improving biosecurity through screening, and multiple government and regulatory agencies, but kept the details confidential.
The team worked cautiously in the new study. They chose 72 dangerous proteins and designed over 76,000 variants using three openly available AI tools that anyone can download. For biosecurity reasons, each protein was given an alias, but most were toxins or parts of viruses. “We believe that directly linking protein identities to results could constitute an information hazard,” wrote the team.
To be clear, none of the AI-designed proteins were actually made in a lab. However, the team used a protein prediction tool to gauge the chances each synthetic version would work.
The sequences were then sent to four undisclosed biosecurity software developers. Each screening program worked differently. Some used artificial neural networks. Others tapped into older AI models. But all sought to match new DNA sequences with sequences already known to be dangerous.
The programs excelled at catching natural toxic proteins, but they struggled to flag synthetic DNA sequences that could lead to dangerous alternatives. After sharing results with the biosecurity providers, some patched their algorithms. One decided to completely rebuild their software, while another chose to maintain their existing system.
There’s a reason. It’s difficult to draw the line between dangerous proteins and ones that could potentially become toxic but have a normal biological use or that aren’t dangerous to people. For example, one protein flagged as concerning was a section of a toxin that doesn’t harm humans.
AI-based protein design “can populate the grey areas between clear positives and negatives,” wrote the team.
Most of the updated software saw a boost in performance in a second stress test. Here, the team fed the algorithm chopped up versions of dangerous genes to confuse the AI.
Although ordering a full synthetic DNA sequence is the easiest way to make a protein, it’s also possible to shuffle the sequences around to get past detection software. Once synthesized and delivered, it’s relatively easy to reorganize the DNA chunks into the correct sequence. Upgraded versions of multiple screening programs were better at flagging these Frankenstein DNA chunks.
With great power comes great responsibility. To the authors, the point of the study was to anticipate the risks of AI-designed proteins and envision ways to counter them.
The game of cat-and-mouse continues. As AI dreams up increasingly novel proteins with similar functions but made from widely different DNA sequences, current biosecurity systems will likely struggle to catch up. One way to strengthen the system might be to fight AI with AI, using the technologies that power AI-based protein design to also raise alarm bells, wrote the team.
“This project shows what’s possible when expertise from science, policy, and ethics comes together,” said Horvitz in a press conference.
The post Dangerous AI-Designed Proteins Could Evade Today’s Biosecurity Software appeared first on SingularityHub.
2025-10-04 22:00:00
OpenAI’s New Video App Is Jaw-Dropping (for Better and Worse)Mike Isaac and Eli Tan | The New York Times ($)
“After we spent less than a day with the app, what became clear to us was that Sora had gone beyond being an AI-video generation app. Instead, it is, in effect, a social network in disguise; a clone of TikTok down to its user interface, algorithmic video suggestions, and ability to follow and interact with friends.”
Us Jobs Market Yet to Be Seriously Disrupted by AI, Finds Yale StudyDan Milmo | The Guardian
“Analysis by Yale University’s Budget Lab found there had been no ‘discernible disruption’ since ChatGPT’s release in November 2022. Researchers said its conclusion was not surprising because historical trends pointed to technological upheaval in workforces taking place over decades rather than months or years.”
Scientists Made Human Eggs From Skin Cells and Used Them to Form EmbryosEmily Mullin | Wired ($)
“In a controversial step that raises the possibility of a new kind of infertility treatment, scientists report that they have produced functional human eggs in the lab that were able to be fertilized with sperm. The proof-of-concept study, published today in the journal Nature Communications, involves using human skin cells to generate eggs, some of which were capable of producing early-stage embryos.”
Gavin Newsom Signs First-In-Nation AI Safety LawChase DiFeliciantonio | Politico
“California Gov. Gavin Newsom signed a first-in-the-nation law on Monday that will force major AI companies to reveal their safety protocols—marking the end of a lobbying battle with big tech companies like ChatGPT maker OpenAI and Meta and setting the groundwork for a potential national standard.”
This Startup Wants to Put Its Brain-Computer Interface in the Apple Vision ProEmily Mullin | Wired ($)
“The Santa Barbara, California, company is testing both a software component (an augmented reality BCI app) and a hardware add-on (a custom headband that can read brain signals) with the Vision Pro. The trial will include up to 10 participants in the US with speech impairments due to paralysis from spinal cord injury, stroke, traumatic brain injury, or amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig’s disease.”
Meet the Arc Spacecraft: It Aims to Deliver Cargo Anywhere in the World in an HourEric Berger | Ars Technica
“‘The nominal mission for us is pre-positioning Arcs on orbit, and having them stay up there for up to five years, able to be called upon and then autonomously go and land wherever and whenever they’re needed, being able to bring their cargo or effects to the desired location in under an hour,’ said Justin Fiaschetti, co-founder and chief executive of Inversion, in an interview with Ars before the event.”
Physicists Smash Record With Magnetic Field 700,000 Times Stronger Than Earth’sGayoung Lee | Gizmodo
“Under the right conditions, superconducting magnets allow electricity to flow essentially undisturbed, producing intense magnetic fields for a variety of uses, including nuclear fusion experiments. Naturally, a larger magnetic field gives scientists more room to explore—something that may soon be available to physicists in China, thanks to the creation of a record-setting superconducting magnet.”
Debt Is Fueling the Next Wave of the AI BoomAsa Fitch | The Wall Street Journal ($)
“In the initial years of the AI boom, comparisons to the dot-com bubble didn’t make much sense. Three years in, growing levels of debt are making them ring a little truer. …While big tech companies are still at AI’s forefront and are in solid financial shape, a crop of more highly leveraged companies is ushering in an era that could change the complexion of the boom.”
New AI Research Claims to Be Getting Closer to Modeling Human BrainReed Albergotti | Semafor
“[AI startup] Pathway also says it has found a way to constantly update the connections between artificial neurons—what’s known in neuroscience as Hebbian learning. So, while the core part of Pathway’s model will stay fixed, like a traditional LLM, another part of it will change as you interact with it, allowing it to continuously learn.”
The Alien Intelligence in Your PocketWebb Wright | The Atlantic ($)
“The more effective AI becomes in its use of natural language, the more seductive the pull will be to believe that it’s living and feeling, just like us. ‘Before this technology—which has arisen in the last microsecond of our evolutionary history—if something spoke to us that fluidly, of course it would be conscious,’ Anil Seth, a leading consciousness researcher at the University of Sussex, told me. ‘Of course it would have real emotions.'”
Should We Intervene in Evolution? The Ethics of ‘Editing’ NatureDavid Farrier | Aeon
“It wasn’t our intention that humanity would become the planet’s greatest evolutionary force; yet the fact that we are confronts us with an urgent and difficult question. Some animals, plants and insects can adapt but, for many, the pace of change is too great. Should we try to save them by deliberately intervening in their evolution?”
The Quest to Sequence the Genomes of EverythingGlenn Zorpette | IEEE Spectrum
“The road map calls for more than 1.65 million genome sequences between 2030 and 2035 at a cost of $1,900 per genome. If they can pull it off, the entire project will have cost roughly $4.7 billion—considerably less in real terms than what it cost to do just the human genome 22 years ago.”
Can Today’s AI Video Models Accurately Model How the Real World Works?Kyle Orland | Ars Technica
“Over the last few months, many AI boosters have been increasingly interested in generative video models and their seeming ability to show at least limited emergent knowledge of the physical properties of the real world. That kind of learning could underpin a robust version of a so-called ‘world model’ that would represent a major breakthrough in generative AI’s actual operant real-world capabilities.”
Is Space Becoming Too Dangerous for Satellites?Margo Anderson | IEEE Spectrum
“Whether the object is a defunct satellite or a stray hunk of glass from a solar panel that shattered long ago, every item circling Earth is also a potential projectile. And nearly all of this junk, traveling at least eight times as fast as a rifle bullet, can be damaging in a collision.”
The post This Week’s Awesome Tech Stories From Around the Web (Through October 4) appeared first on SingularityHub.
2025-10-03 22:00:00
Scientists hope to make atomic qubits compatible with the existing architecture of standard silicon chips.
Quantum entanglement—once dismissed by Albert Einstein as “spooky action at a distance”—has long captured the public imagination and puzzled even seasoned scientists.
But for today’s quantum practitioners, the reality is rather more mundane: Entanglement is a kind of connection between particles that is the quintessential feature of quantum computers.
Though these devices are still in their infancy, entanglement is what will allow them to do things classical computers cannot, such as better simulating natural quantum systems like molecules, pharmaceuticals, or catalysts.
In new research published recently in Science, my colleagues and I have demonstrated quantum entanglement between two atomic nuclei separated by about 20 nanometers.
This may not seem like much. But the method we used is a practical and conceptual breakthrough that may help to build quantum computers using one of the most precise and reliable systems for storing quantum information.
The challenge facing quantum computer engineers is to balance two opposing needs.
The fragile computing elements must be shielded from external interference and noise. But at the same time, there must be a way to interact with them to carry out meaningful computations.
This is why there are so many different types of hardware still in the race to be the first operating quantum computer.
Some types are very good for performing fast operations, but suffer from noise. Others are well-shielded from noise, but difficult to operate and scale up.
My team has been working on a platform that—until recently—could be placed in the second camp. We have implanted phosphorus atoms in silicon chips, and used the spin of the atoms’ cores to encode quantum information.
To build a useful quantum computer, we will need to work with lots of atomic nuclei at the same time. But until now, the only way to work with multiple atomic nuclei was to place them very close together inside a solid, where they could be surrounded by a single electron.
We usually think of an electron being far smaller than the nucleus of an atom. However, quantum physics tells us it can “spread out” in space, so it can interact with multiple atomic nuclei at the same time.
Even so, the range over which a single electron can spread is quite limited. Moreover, adding more nuclei to the same electron makes it very challenging to control each nucleus individually.
We could say that, until now, nuclei were like people placed in soundproof rooms. They can talk to each other as long as they are all in the same room, and the conversations are really clear.
But they can’t hear anything from the outside, and there’s only so many people who can fit inside the room. Therefore, this mode of conversation can’t be scaled up.
In our new work, it’s as if we gave people telephones to communicate to other rooms. Each room is still nice and quiet on the inside, but now we can have conversations between many more people, even if they are far away.
The “telephones” are electrons. By their ability to spread out in space, two electrons can “touch” each other at quite some distance.
And if each electron is directly coupled to an atomic nucleus, the nuclei can communicate via the interaction between the electrons.
We used the electron channel to create quantum entanglement between the nuclei by means of a method called the “geometric gate,” which we used a few years ago to carry out high-precision quantum operations with atoms in silicon.
Now—for the first time in silicon—we showed this method can scale up beyond pairs of nuclei that are attached to the same electron.
In our experiment, the phosphorus nuclei were separated by 20 nanometers. If this seems like still a small distance, it is: There are fewer than 40 silicon atoms between the two phosphorus ones.
But this is also the scale at which everyday silicon transistors are fabricated. Creating quantum entanglement on the 20-nanometer scale means we can integrate our long-lived, well-shielded nuclear spin qubits into the existing architecture of standard silicon chips like the ones in our phones and computers.
In the future, we envisage pushing the entanglement distance even further, because the electrons can be physically moved, or squeezed into more elongated shapes.
Our latest breakthrough means that the progress in electron-based quantum devices can be applied to the construction of quantum computers that use long-lived nuclear spins to perform reliable computations.
This article is republished from The Conversation under a Creative Commons license. Read the original article.
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2025-10-03 04:46:20
She won the genetic lottery, but a healthy lifestyle also contributed to her extreme lifespan.
Maria Branyas Morera lived a simple life in a small town in Catalonia, Spain. She loved quality time with family and friends, playing with dogs, reading books, and tending to her garden. She played the piano well into her 110s. And before she died last year at 117, she was the oldest documented person alive.
Her extreme longevity caught the attention of Manel Esteller, a geneticist at the University of Barcelona with a keen interest in longevity. Although Branyas was only one person, her genes, metabolism, and other molecular markers could a shine light on healthy longevity for the rest of us.
Over several years, Esteller and colleagues collected samples of blood, saliva, urine, and stool for a deep dive into her unique biology. Although at the beginning of the study Branyas lived at home with her two daughters—both in their 90s and healthy—she eventually moved into an assisted living home.
Her biology painted a surprising picture of the factors contributing to health in old age. On the one hand, her telomeres—the protective end caps on chromosomes—were exceedingly short, as expected for someone her age. Telomere shortening is usually associated with damaged DNA and a higher risk of cancer. Yet Branyas never had cancer.
Compared to other elderly woman living in the area, Branyas had very low levels of chronic inflammation, which tends to creep up and wreak havoc as we age. And her gut microbiome—a regulator of general health heavily influenced by diet—resembled that of people much younger.
The authors caution that Branyas’s results are for only one exceptional person, and we’d need larger population-sized studies before interpreting them for the general public. In addition, her lifestyle choices likely played a large role in her longevity.
“Our genes are the cards in a poker game. But how we play them is what really matters,” Esteller told Nature.
Aging is an intricate mix of nature and nurture, and it’s notoriously difficult to tease them apart. Studies in worms, flies, and mice have unearthed hallmarks of aging in a web of genes, metabolic signals, stem cell health, inflammation, and epigenetics (which genes are switched on or off).
How these diverse biological signals interact and ultimately contribute to the aging process is still mostly mysterious. But supercentenarians—people over 110 years old—offer clues. This select group doesn’t just live longer, its members are also healthier and often spared from age-related diseases like diabetes, cancer, dementia, and heart problems.
Is the fountain of youth hiding in their biology?
People who live past 100 are rare. A previous study transformed centenarian blood cells into stem cells. Scientists used these to model the aging process at a cellular level and investigate the genetics and other factors underlying centenarian health and lifespan.
Supercentenarians are even rarer. Only one in five million people live past 110 in industrialized nations, making them an especially valuable source of scientific study. When asked if she’d like to contribute, Branyas answered “please study me”—a last wish before she passed away.
Branyas was born in San Francisco but moved to Spain when she was eight. She was very outgoing and maintained a Mediterranean diet full of seafood, olive oil, and vegetables. She walked nearly everywhere and mostly refrained from smoking and heavy drinking.
Her long life wasn’t free of tragedy. She buried her son when he was 52 and watched extended family members pass from common age-related diseases: Alzheimer’s, cancer, kidney failure, and heart disease. Still, Branyas made new friends and maintained a sharp mind as the clock ticked.
The first look into her biology left scientists scratching their heads. Like other elderly people, Branyas had multiple hallmarks of aging. Her telomeres were exceedingly short, suggesting they were less able to protect her DNA as her cells divided. She also had clumps of mutated blood cells linked to vascular diseases and blood cancer. Some of her immune cells—those producing antibodies—showed typical signs of aging. These protective cells often go rogue in the twilight years and attack normal tissue, contributing to chronic inflammation that damages organs.
Yet Branyas wasn’t plagued by any of these age-related killers.
She maintained a cardiovascular and metabolic profile akin to people decades younger. She had little chronic inflammation, and her immune system battled pathogens when needed. At 113, she became the oldest person to survive and recover from Covid-19 in Spain.
These results hint that the markers of aging aren’t necessarily associated with age-related diseases—they could just be signs we’re getting old.
The distinction isn’t academic.
Hallmarks of aging are used in biological “aging clocks” and are being developed into potential early diagnostics for age-related disorders. The decoupling of markers to diseases here “shows that extremely advanced age and poor health are not intrinsically linked,” wrote the team.
Branyas’s unique genetics offer clues to her resilience.
Mitochondria produce energy in our cells, and they falter as we age. These cellular power plants have their own genes. Branyas’s had several rare genetic variants that kept them humming along. They also mopped up dangerous molecules that increase with age and damage cell structures. Her mitochondria were healthier than women decades younger.
She also had an astonishing library of gene variants that protect against autoimmune diseases, cancer, infections, and metabolic disorders like diabetes. For example, some rare variants involved in lipid metabolism kept her blood vessels clear of fatty buildup.
Her blood work was exceptional for her age. She had low levels of bad cholesterol—this contributes to blockage, heart attacks, and stroke—and high levels of good cholesterol. She also carried protective gene variants linked to the brain.
These “could potentially be contributing to the preservation of cognitive function in extreme old age,” wrote the team.
But genes are only part of the story. Other factors include diet, exercise, environment, upbringing, and mental health. Some of these factors are reflected in your gut microbiome. Researchers have begun mapping bacterial strains to metabolic and brain health.
Branyas had high levels of Bifidobacterium, a type of beneficial bacteria that’s common in yogurt and other fermented dairy products—which she ate three times a day. The bacteria are known for their anti-inflammatory properties and protection of the gut barrier. Levels of Bifidobacterium typically drop with age, and older people who maintain higher levels tend to have healthier immune systems.
Before you go on a yogurt shopping spree, the team stresses no single factor contributed to Branyas’s long life.
Dr. Mary Armanios at Johns Hopkins School of Medicine, who was not involved in the study, agrees. “The genetics of longevity are notoriously confusing,” she told The New York Times. While bad genetics can limit lifespan, “I am not sure good genetics are sufficient to overcome socioeconomic limitations.”
The team is now digging further into Branyas’s biology to see how other hallmarks of aging—such as senescence, or the build-up of toxic “zombie” cells—interact with the other factors.
The post This Spanish Woman Lived to 117. Here’s a Deep Dive Into Her Genetics and Habits. appeared first on SingularityHub.
2025-09-30 23:33:15
In a small trial, a gene therapy injected into the brain slowed the disease by 75 percent over three years.
Huntington’s disease is extremely cruel. Symptoms start with random, uncontrollable twitches of the hand. Over time the disease eats aways at memory, thought, and reason. Mood swings and personality changes strip away your identity. Eventually, it leads to an early death.
Worse, unlike other diseases that gradually destroy brain function, such as Alzheimer’s disease, Huntington’s can be diagnosed with a simple genetic test. The disease is inherited through a mutated gene. People with a family history often struggle to decide if they want to get tested. If the results are positive, there are no treatments, and their fates are set.
A new therapy may now kneecap Huntington’s before symptoms take over. Preliminary results from a small group of patients found a single injection of microRNA, a type of gene therapy, into affected brain regions slowed the disease’s progression by 75 percent over three years. The patients had far better motor control, attention span, and processing speed compared to an untreated control group who had similar baseline symptoms.
The drug is being developed by the Dutch gene therapy company uniQure, which summarized the findings in a press release this month. The data hasn’t been published in a preprint article or a scientific journal nor scrutinized by other experts. With only 29 patients involved, it’s hard to generalize the benefits and safety profile for the roughly 75,000 people with Huntington’s in the US, Europe, and UK.
But the findings offer a beacon of hope. Previous attempts at a cure “have shown some small signals if you squint…but there has not been anything close to this,” Steven Finkbeiner at the Gladstone Institutes in California, who was not involved in the study, told the New York Times. And because Huntington’s can be caught early on, the treatment—if further proven effective in a larger population—could begin to ward off symptoms at an earlier age.
All of us have the Huntington’s gene, or HTT. While its exact role in cells is debatable, the gene acts as a central communicator across multiple cellular “phone lines.” It coordinates a large assembly of molecules to turn genes in brain cells on or off and is critical for early development, neuron survival, and maintaining the brain’s overall health.
In Huntington’s disease, however, HTT goes awry. Our genes are made of four molecules represented by the letters A, T, C, and G. Triplets of these letters often dictate the sequence, structure, and function of proteins, the workhorses of our cells. In the disease, one triplet, CAG, repeats like a broken record, resulting in mutated huntingtin proteins that increasingly build up inside the brain throughout a person’s life and gradually wreak havoc.
Although in the beginning brain cells can adapt, their defenses eventually stumble, and symptoms appear. In the US, this usually happens between 30 and 55 years of age.
Families with Huntington’s face a terrible dilemma. If one parent has the disease, each of their children has a 50 percent chance of inheriting it. If they don’t, their offspring are safe. Knowing the diagnosis can help with family and life planning—but it comes at a hefty emotional cost.
How the mutated huntingtin protein destroys brain cells isn’t yet clear, but most scientists agree that clearing it—or preventing it from forming in the first place—could protect the brain.
The protein is massive and made up of multiple fragments. One treatment idea uses small protein “jammers” to prevent an especially toxic form of huntingtin from weaving into large, dangerous aggregates. Another directly targets the CAG repeats with a classic but powerful form of gene therapy. But after initially promising results, a trial was halted due to a high risk of side effects and low chance symptoms would improve. Gene editing strategies, such as CRISPR, that cut out the mutated sequences are gaining steam, but they’re very early stage.
The new therapy developed by uniQUre taps into microRNA. These molecules don’t code for proteins, but they can stop a gene from making one. Like DNA, RNA can also form a double strand if its sequences match. Cells identify double-stranded RNA as alien and destroy it—potentially stopping a toxic protein from forming. The company’s new drug contains two components: A benign viral carrier and a custom genetic sequence that, once inside the cell, produces microRNA tailored to inhibit mutant protein production.
The drug, called AMT-130, doesn’t integrate into or directly edit a patient’s genome, which lowers the risk of disrupting healthy genes or triggering cancer. Although the viral carrier is eventually wiped away by the immune system, the genetic code could last for years, making the drug a potential long-term treatment.
The team injected either a low or high dose of AMT-130 into the brains of volunteers with Huntington’s using an established and highly precise surgical technique. They targeted the striatum, a nub tucked deep inside the brain that’s critical for movement and decision-making and one of the first regions ravaged by the disease. As a control group, they found hundreds of patients of similar age and disease severity, according to an investor presentation (PDF) from the company.
The results were promising. When given the highest dose, 12 people with early stages of the disease experienced, on average, a 75 percent slower decline than those without treatment, as measured using multiple standard Huntington’s assessments.
Roughly 88 percent of treated patients showed marked improvement in their attention, memory, and information processing speed based on one test. Their control over random muscle movements got better, and they were able to perform daily activities with less struggle. A brain protein often associated with symptom severity dropped to levels seen before the trial began. In contrast, those treated with a low dose of the drug had more modest and mixed results.
Multiple people experienced side effects related to the brain surgery. Headaches were the most common complaint. Some experienced brain swelling a few days after the surgery. But overall, the treatment seemed safe.
“The majority of drug-related serious adverse events occurred within the first weeks post treatment and fully resolved with steroids or palliative case,” the company noted in their presentation.
There’s reason to be skeptical. Huntington’s is a life-long disease, and it’s unknown how long the benefits of the single shot last beyond three years. It’s likely multiple shots would be needed throughout a patient’s lifespan, and future studies would have to test the additive effects. The drug slashes levels of both the mutated and normal versions of the huntingtin protein—drugs in the past have as well—which could potentially produce side effects.
New patients are now being enrolled for the trial, and the company hopes to submit an application for FDA approval by late 2026.
“This result changes everything,” Ed Wild, a leader of the project at the UCL Huntington’s Disease Center trial site, said in the press release. “On the basis of these results it seems likely AMT-130 will be the first licensed treatment to slow Huntington’s disease, which is truly world-changing stuff.”
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