Source: Time, Dominique Mosbergen
Photo: Logan Weaver @LGNWVR

In the 1990s, molecular biologist Cynthia Kenyon made a discovery in a tiny roundworm that transformed our understanding of aging.

She found that a single gene mutation could double the worm’s lifespan, proving that the aging process, previously considered unchangeable, could be modified—at least in some creatures. That opened the door to the notion that drugs and other interventions could potentially slow aging and improve health span, the amount of time spent in good health, in people.

“Back then, people thought that if you studied aging, it was because you probably weren’t a very good scientist,” says Kenyon, who now heads aging research at Calico Life Sciences, the secretive longevity biotech backed by Google’s parent company Alphabet. “People thought I was wasting my time.”

Today, some 30 years since her groundbreaking research was published, many companies including Calico are working to develop treatments that could boost health span. Researchers have been able to extend the health and lifespans of more complex animals like mice, and many scientists think that helping people live healthier for longer is within reach, too.

“Since the days of Ponce de León and the fountain of youth and even before that, it’s always been a dream of people to live forever or at least age in a healthy way,” says Kenyon, a former professor at the University of California, San Francisco. “But now we can actually start from science and not just wishful thinking.”

As part of TIME’s series interviewing longevity leaders and influencers, we spoke to Kenyon about her seminal discovery and her excitement for the future of longevity research and treatments.

This interview has been condensed and edited for clarity.

When did your interest in aging science first take root?

When I was little, I liked animals and nature. I explored the woods and had a lot of pets, and I was interested in what you might call “truth”—understanding myself and the world. I realized that science was a good way to address the truth.

As my career as a scientist progressed, I began to get really interested in aging biology, which wasn’t well understood at the time. All animals appear to age, yet they age at really different rates. Among mammals, whales can live to be hundreds of years old, but other mammals live only a few years. But how does that happen?

My thinking was: the reason different species age at different rates is because they have different genes, and evolution changed those genes from an early precursor. For example, dogs have much shorter lives than we do, and they age much more quickly than we do, but humans and dogs evolved from a common precursor that gave rise to all mammals. What happened that led to these different lifespans? It occurred to me that there had to be genes that control the aging process, and I wanted to understand what those genes were.

Was there a specific project that sparked these questions about aging?

I was working in my laboratory on a type of roundworm called C. elegans. It’s very tiny, about the size of a comma in a sentence, and it ages really quickly and dies within a few weeks. But it’s a complex animal: it has different tissues and muscles, a gut, and a little brain that can do lots of things.

At the time, there were a couple of researchers who were looking for gene changes that affected lifespan in C. elegans. They found a gene change that made worms live longer, but the problem was that it also decreased the worms’ fertility. I thought, “My gosh, I just want to look for these genes myself.” I became really, really, really obsessed with the idea of trying to find gene changes that allowed the worms to live longer.

I also had this idea that maybe there were universal genes that control the rate of aging in all animals—like a thermostat for temperature, except this would be a thermostat for lifespan. Turning it up or down could make animals age faster or slower. I thought that maybe every animal had a little dial like that, but evolution set this dial differently in different species. It was just a hypothesis, and we still don’t know if it’s true or not, but I think aspects of it might be true.

That idea motivated me. It made me think that there could be a great discovery to be made, and I had the tools to do it—I had this little animal, a little worm with a three-week lifespan. So, I could do an experiment, and at the end of three weeks, I could just do another one. I was really, really excited about it.

Were other scientists as enthusiastic as you were?

Nobody would work on it, actually, because they thought this just couldn’t be done. People assumed that there would be all these different genes, so you’d get all these tiny little effects. Everybody had an idea of why it wouldn’t work.

But I was lucky. It turned out to be right that you could find a mechanism [for aging] and get a big change.

We started by looking for long-lived mutant worms and we found one that had a mutation in the gene DAF-2. This gene had previously been identified, and it was known that it played a role in the development of the worm before puberty. It controlled a switch that allowed the animal to grow to an adult or, under stressful conditions, to pause for a while and wait until conditions improved in the environment before growing to become an adult.

What we discovered was that partially disabling DAF-2 caused the worms to live twice as long as normal. They were completely fertile, active, and healthy. They aged more slowly. It was really amazing. It wasn’t a miracle because it was science, but it was like a miracle.

We also found that these long-lived worms needed another gene called DAF-16. Without a functional DAF-16 gene, they aged more quickly. So right away, not only did we find a gene change that could double the worm’s lifespan, but we had a little circuit: this one gene was somehow talking to this other gene, and there was a kind of a program, in a way, for aging.

I always tell young scientists: if you have a good idea and you think it’s possible that it’ll work after thinking really critically about it, always do it—even if everybody else says no.

How did the DAF-2 discovery transform the field of aging research?

This whole area of science had been like a cesspool. Really, no one wanted to work on it. People thought it was a waste of time. But, my God, it then became hot, it became interesting. That was 30 years ago now, but since that time, it’s just become more and more interesting.

There are now all these different ways of extending lifespan and health span in mice. We’ve seen that a version of these genes can make mice live longer and look younger. There are also labs that have shown that clearing senescent cells [damaged cells that stop dividing but don’t die] can improve health span in mice and others that have apparently been able to turn back the clock by using [special proteins known as] Yamanaka factors that can make mice much healthier and youthful. We don’t know yet if that will ever be possible in humans, but people are trying.

Is that what you and your colleagues are working on at Calico?

I won’t go into specifics, but Calico and many other companies are trying to slow down aging in people. Calico is taking more than one approach, which I think is a smart thing to do.

Aging is very tightly linked to age-related diseases, so the idea is, if you could slow down aging, it would give us new ways of treating diseases like Alzheimer’s, heart disease, cancer, and osteoarthritis. It would also be a way of learning more about these pathways in humans.

I’m really excited about the possibility that we could be healthier. I’m not talking about living longer while being sick. Can you imagine going into the nursing home and just staying there twice as long? No one wants that. But my goal in life is to help people to just be healthier when they’re older. And that’s what Calico lets me do. As an academic, I couldn’t be as close to the translational aspect of this—bringing this science to people. That’s why I’m so in heaven right now with my job.

I’m just super excited about the whole field. We’re on the brink of something unbelievable. Or maybe not. We won’t know until we know—and really proving it in humans won’t be easy, but I still think we are part of something that’s really big.

I remember giving a talk about the DAF-2 mutation in the early 1990s at one of these big scientific conferences. It was this huge room, and it was so empty. There were only like 30 people in there, and most of them were people I knew and people who were also working on C. elegans. And I remember standing there and spreading my arms and saying, “This room should be full!” I was so passionate about it.

And now, when I give talks or when other researchers give talks about aging, the room is full—even overflowing sometimes. Just thinking about it, tears are welling up in my eyes. It’s like a dream come true.

Is there anything you’ve changed in your life in the hopes of extending your own health span?

As a matter of fact, yes. At some point, I decided to try giving the long-lived C. elegans some sugar, because other researchers had found that sugar made other animals live shorter lives. And it happened with the worms too. They didn’t live as long—and interestingly, they lived shorter because the same genes that made them live longer were having the opposite effect.

When I got this result, I thought, “Oh no.” At the time, I ate tons of sugar. I was a sugar addict. I remember going to Costco one time and buying a bag of sugar that was so big, it came up almost to my waist.

I decided to follow a low-glycemic diet, and I’ve basically been doing that for 23 years. I do that and I exercise—aerobics and weight-lifting. I don’t take any pills or anything to live longer. The reason I don’t is, I would like a Phase III clinical trial to be done first before I try anything. But the problem here is, those trials cost a ton of money to do. What I would love to see is a kind of World Health Span Organization—like the World Health Organization, but for health span—where lots of governments chip in and we could do clinical trials for a lot of these substances.

I know other people are taking their chances. They are taking things like metformin or rapamycin, but I don’t know—I would say, buyer beware. Until the proper trials are done, I think exercise and the diet that I’m eating right now is about the best I can do for myself. I don’t actually know that they are going to extend my lifespan, but I feel great.

https://time.com/collections/future-of-living

Source: Newsweek, Hannah Millington
Photo: Left shows the brain not treated, right shows the brain treated. (IBEC)

Scientists have achieved a “striking” reversal of Alzheimer’s disease in mice by restoring the normal function of the brain’s vasculature—the network of blood vessels that supplies it with oxygen and nutrients.

Researchers at the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital of Sichuan University (WCHSU), working with partners in the UK, showed this was possible using nanotechnology.

“Our study demonstrated remarkable efficacy in achieving rapid Aβ clearance [in Alzheimer’s the main ‘waste’ protein is amyloid-β], restoring healthy function in the blood–brain barrier [known as the BBB] and leading to a striking reversal of Alzheimer’s pathology,” said study author Lorena Ruiz Perez, researcher at the Molecular Bionics group from the IBEC, in a statement.

Typically, nanomedicine relies on nanoparticles as carriers for therapeutic molecules, while this approach uses nanoparticles that act as therapeutic agents in their own right, known as supramolecular drugs.

Instead of targeting neurons or other brain cells, the therapy restores the proper function of the BBB, the “vascular gatekeeper” that regulates the brain’s environment, according to the researchers.

“By restoring this ‘gatekeeper,’ we help the brain rebalance itself and make any other therapy work better,” Giuseppe Battaglia, Catalan Institution for Research and Advanced Studies (ICREA) research professor at IBEC, told Newsweek.

“Today, no treatment reliably reverses Alzheimer’s; at best, some slow aspects of decline. Our results point to a new path: fix the barrier that keeps the brain healthy.”

Battaglia explained a therapy that restores the brain’s own defenses could mean “fewer day-to-day declines, longer periods of independence and better responses to existing medications for families, which could translate into more meaningful time together and a reduced caregiving burden.”

The findings highlight the importance of vascular health and the link between diseases like dementia and Alzheimer’s with a compromised vascular system.

The team demonstrated that targeting a specific mechanism enabled undesirable “waste proteins” produced in the brain to pass through the BBB and be eliminated in the blood flow.

In Alzheimer’s, an accumulation of Aβ affects the normal functioning of the neurons. The brain’s natural clearance system for toxic species like this protein stops working properly.

In the study, the researchers used mouse models genetically programmed to produce larger amounts of Aβ and develop a significant cognitive decline mimicking Alzheimer’s disease.

“Only 1h after the injection [of the supramolecular drugs] we observed a reduction of 50-60 percent in Aβ amount inside the brain,” said study author Junyang Chen, researcher at WCHSU and University College London student.

“Animals show lasting functional recovery months later, suggesting durable benefits, not just a short-term effect,” said Battaglia. “No damage or toxicity [was] observed in animals; they tolerate the therapy well.”

In one experiment, they treated a 12-month-old mouse (equivalent to a 60-year-old human) with the nanoparticles. Analyzing its behaviour and memory after six months, they found the animal, then aged 18 months (comparable to a 90-year-old human), had recovered the behaviour of a healthy mouse.

“We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses. But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What’s remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels,” explained Chen.

By imitating the way natural molecules interact with the LRP1 receptor (which usually acts as a “molecular gatekeeper”), the precision of the supramolecular drugs can bind to Aβ, cross the BBB and initiate the process of removing toxic species from the brain, according to the team, restoring the vasculature’s waste-clearing function.

This offers hope for developing effective clinical interventions to address vascular contributions to Alzheimer’s disease and ultimately improve patient outcomes, according to the team.

More research is needed to see how the findings translate in humans. “This is an innovative early-stage approach with encouraging results in mice. The rapid clearance of amyloid and the behavioural improvements are particularly striking. As with any preclinical study, further testing, including safety studies and validation in larger models, will be critical before considering human trials,” said Francesco Aprile—professor in biological chemistry at Imperial College London, who was not involved in the study—in a statement.

“The BBB serves a similar role for all of us. If we can safely trigger the same recovery of barrier function in people, we expect improved brain housekeeping: steadier nutrient delivery, reduced inflammation and more effective clearance of toxic proteins. That combination could slow disease progression and boost the impact of other treatments,” said Battaglia.

Do you have a tip on a health story that Newsweek should be covering? Do you have a question about Alzheimer’s? Let us know via health@newsweek.com.

Update 10/08/25, 06:17 a.m. ET: This article was updated with additional comments from Francesco Aprile.

Reference
Chen, J., Xiang, P., Duro-Castano, A., Cai, H., Guo, B., Liu, X., Yu, Y., Lui, S., Luo, K., Ke, B., Ruiz Perez, L., Gong, Q., Tian, X., & Battaglia, G. (2025). Rapid amyloid-β clearance and cognitive recovery through multivalent modulation of blood–brain barrier transport. Signal Transduction and Targeted Therapy. https://doi.org/10.1038/s41392-025-02426-1.

https://www.msn.com/en-us/health/other/scientists-achieve-striking-reversal-of-alzheimer-s-in-mice

Source: Life Hacker, Meredith Dietz
Photo: René Ramos/Lifehacker/Jonathan Knowles/Stone, Antagain/iStock via Getty Images; Neurable/Master & Dynamic

What if headphones could read your mind the way a smartwatch reads your wrist?

This week, neurotech startup Neurable launched its MW75 Neuro headphones with a pretty seductive pitch—one that I’m not quite buying.

Just slip on this pair of headphones, and you’ll gain unprecedented access to your brain’s inner workings. Track your focus. Measure your mental fatigue. Quantify your cognitive performance. It’s supposed to be the quantified-self movement’s next frontier—moving from steps and heart rates to the most intimate data source of all: your brainwaves.

If you ask me, a pair of headphones that can read your mind sounds either too good to be true, or too creepy to be good. Neurable doesn’t plan to stop at headphones, and they aren’t the only company making a name in the space. Glasses, helmets, what have you—the next wave of wearable devices are targeting the brain. Whether you find it tempting or find it terrifying, the real question: Is this technology even real? Can “brain tracking” headphones actually measure anything meaningful, or are people paying $499 for an elaborate placebo wrapped in EEG sensors?

Unsurprisingly, the answers are a little wrinkly.

What are brain wearables in theory?

The concept behind brain wearables is this: Using electroencephalography (EEG) sensors embedded in headphone ear cups, devices like Neurable’s MW75 Neuro claim to track electrical signals from your brain, translating them into actionable insights about your mental state. The headphones promise to tell you when you’re losing focus, when you need a break, and even provide a “cognitive snapshot” of your brain health over time.

For the wellness-obsessed, it’s pretty much catnip. Where fitness trackers gave us visibility into our physical states, brain wearables promise to illuminate the black box of our mental performance. In theory, you could optimize not just your workout routine, but your work-work routine, catching burnout before it catches you.

The problem, according to experts across technology law and neuroscience, is that we’re nowhere near ready for this technology to become mainstream—neither from a regulatory standpoint nor a scientific one. Let’s start with the science.

How does the science of brain wearables hold up?

Before getting into the fairly obvious privacy nightmare, there’s a fundamental question about whether these devices can actually deliver on their promises.

José M. Muñoz, an associate at The Centre for Neurotechnology and Law in the United Kingdom and the International Center for Neuroscience and Ethics in Spain, is blunt in his assessment: “For years, there has been an ongoing debate regarding the effectiveness, accuracy, and challenges of direct-to-consumer neurotechnologies such as this new device from Neurable,” he explains. “Although it is true that the algorithms analyzing brain data collected via EEG are steadily improving, this remains a neurotechnology that is still insufficiently accurate outside of a medical or clinical setting.”

The problems are both technical and practical. EEG data quality is extremely sensitive to electrode placement—sometimes within a range of millimeters. When users place these sensors themselves, without medical supervision, their reliability plummets. Moreover, the most accurate EEG studies use far more electrodes than the handful embedded in a pair of headphones.

“In sum, you may be wearing these headphones and believing they are helping to improve your mental health, physical performance, or attention,” Muñoz says. “But what you are really improving are the manufacturer’s algorithms, while handing over your brain data in exchange for very little.”

In other words, it’s the tech tale old as time: You’re not the customer being served by this technology. You’re the data source training it.

Dr. Annu Navani offers a more measured perspective. She acknowledges that brain wearables have “significant limitations, including being currently expensive, less clinically validated, and less convenient or comfortable than wrist-worn trackers.” The metrics they provide are also harder to translate into practical guidance—most people intuitively understand what to do with their step count, but what action should you take when your “cognitive load score” hits 73?

Rather than replacing traditional fitness trackers, Navani believes brain wearables will likely “complement rather than replace conventional devices, targeting a niche of users interested in cognitive and neuro-performance insights.” Traditional wearables, she points out, still provide reliable, validated data for basic health metrics that users can easily understand and apply.

Who is really reading your mind here?

Think about it (and hey, maybe relish in the fact that no headphones are successfully reading those thoughts): Your brainwave data is arguably the most intimate biometric information you possess. We’re talking about a window into your mental and emotional states. So what happens when you willingly give up this data with no meaningful oversight?

“I hope brain wearables are not the future of fitness tracking, or any industry, at least certainly not yet and not any time soon,” says Star Kashman, a technology attorney and founding partner of a cyber law firm. “We are still somehow facing a complete lack of federal regulation in the U.S. when it comes to biometric data, data privacy law, and minimal to no cybersecurity standards for these devices, and no protective regulations for users.”

The implications are stark: “What happens when a ‘brain wearable’ is hacked?” Kashman asks. The lack of regulation means users have little recourse and limited knowledge about how their neural data is being stored, used, or potentially sold.

Regulation aside, individual consumers do still have their own privacy concerns. The sort of consumer ready to spend hundreds of dollars on headphones might just be the same type of person who is uncomfortable with constant surveillance. “Unless someone is so obsessed with optimizing their fitness journey that they ignore the serious risks present, I just do not see this becoming the norm anytime soon,” Kashman notes. Just look at Meta’s push for smart glasses. The tech has got to be good and ready before consumers are going to drop hundreds of dollars and risk their most private bodily information.

The bottom line

So, simply put, at the time of this publication, asked with my own private brain waves: Are brain wearables the future of fitness tracking? Almost certainly not in the way their manufacturers hope. The technology is too immature, the regulatory landscape too barren, and consumer wariness too high for these devices to start popping up like Fitbits tomorrow.

I’d say what we’re witnessing instead is the familiar pattern of the wellness industry: a genuine technological development (EEG monitoring does work in controlled settings!) being prematurely commercialized and marketed with promises that totally outstrip the reality. The result is an expensive product that may provide some users with interesting data, but likely offers more placebo than breakthrough.

For now, brain wearables occupy an awkward position: too invasive for casual users, too unproven for serious applications, and too unregulated to trust. They may have a future, but it’s not this one—not until the science catches up to the marketing, and the law catches up to both.

Until then, your regular fitness tracker measuring your heart rate and steps? That’s probably telling you more useful information about your health than any headphones reading your brainwaves ever could.

https://lifehacker.com/health/are-brain-wearables-the-future-of-fitness-tracking

Source: Smithsonian Magazine, Olivia Ferrari
Photo: A microscopic view of a sea lamprey’s reconnected spinal cord shows how it healed after being cut. (Daniel Cojanu, Under Current Productions)

The sea lamprey looks like it’s from another planet, but this ancient creature has a surprising amount in common with humans

Key takeaways: Sea lampreys and research

Sea lampreys have large neurons and synapses, making them ideal for neuroscience research.

Scientists study the creatures to learn more about how we might recover from spinal cord injuries.

With a suction-cup mouth and over 100 teeth, the sea lamprey has earned the nickname “vampire fish” and comparisons to sea monsters. Sea lampreys are one of the world’s most ancient fish species, killing prey by latching their suction-cup mouth onto a fish’s skin and rasping away the fish’s flesh with a rough tongue to feed on blood and bodily fluids.

Sea lampreys sound like something from a horror movie, but the creatures have been crucial to almost two centuries of neuroscience research. Neuroscientists study sea lamprey spinal cells, which the animals can regenerate if their spinal cord is damaged, as a model to understand the human nervous system, spinal cord injuries and neurological disease. The evolution of human brains and nervous systems is also closely tied to these alien-like creatures.

Neurologists and zoologists began studying lampreys in the 1830s, examining their nerve cells to understand how the spinal cord works. Lamprey research took off after 1959, when biologists first described lampreys’ ability to regenerate spinal cord neurons and eventually swim after spinal damage.

Sea lampreys are ideal for neuroscientists to work with because the animals have large nerve cells and synapses, making observation easier than in other species. “The synapses are so big that you can see them, and you can record from them and access them very easily,” says Jennifer Morgan, neuroscientist at the University of Chicago’s Marine Biological Laboratory. The creatures also have a similar molecular and genetic toolkit to humans, she says, which can make it simpler to translate research from lampreys to humans and find tools that work in both species.

Lampreys thrive in different types of water, all over the globe. “[Lampreys] have been found on every continent except for Antarctica,” says Morgan, whose lab uses sea lampreys for research. “So, they’re very hearty animals and super easy to maintain.”

The sea lamprey (Petromyzon marinus) filter feeds as a larva but becomes parasitic once it reaches adulthood, latching onto fish and feeding on their blood. They can feed on trout, salmon and other large, commercially important fish, and one sea lamprey can destroy up to 40 pounds of fish per year.

Much of the supply of sea lampreys for research comes from the Great Lakes, where lampreys wreak havoc on the fishing industry. Although the species is native to the Atlantic Ocean, improvements in the late 1800s and early 1900s to canals connecting Lake Ontario and Lake Erie to the ocean enabled lampreys to bypass Niagara Falls, which had previously been a natural barrier. From there, lampreys invaded the lakes, where they have no natural predators. By the 1960s, lampreys had devastated trout fisheries in the region and a control program began to weed them out using pesticides.

Sea lampreys’ invasion of the Great Lakes has actually boosted their use in research. Over the last century, the Great Lakes Fishery Commission has directed considerable amounts of research funding toward lampreys, to study their life cycle and how to eradicate them. This put more lampreys in labs, resulting in studies on other aspects of their anatomy and evolution.

Collectors catch wild lampreys in the Great Lakes, says Morgan, and send them to the lab in coolers.

“Great Lakes fisheries harvested these lampreys, and they wanted scientists to understand them more,” says Robb Krumlauf, developmental biologist and scientific director emeritus at the Stowers Institute for Medical Research, who also researches lampreys sent from the Great Lakes. “They had a natural supply that they could give to those who are interested in the research.”

Although lampreys look like they’re from another planet, they have more in common with us than it might seem. Lampreys branched off from other vertebrates about 500 million years ago, so they have some of the oldest traits in the lineage: they’re at the base of the vertebrate branch of the evolutionary tree. Because of this, studying lampreys’ genomes can clarify important evolutionary steps in the lineage—like when vertebrates developed jaws, or arms and legs.

Sea lampreys survived multiple mass extinction events, including the asteroid 66 million years ago that wiped out roughly 80 percent of life on Earth. “It’s a chance to have a glimpse of the past. It’s sort of like a living fossil,” says Krumlauf.

Krumlauf studies how sea lamprey evolution and human evolution are related through how our faces and heads develop. The brain region that shapes facial and cranial features is similar across vertebrates, from lampreys to chickens to mice to zebrafish, even though all these animals’ heads look quite different.

“There’s a common toolkit,” says Krumlauf. “If you have building materials, and they’re all the same, you can build a garden shed or you can build a mansion––what’s different is the way the blueprint is put together.”

Studying lampreys shows how these blueprints evolved in the earliest vertebrates, says Krumlauf. His research links facial and head development in the animals to the development of craniofacial abnormalities in humans.

The evolutionary history of lampreys and other vertebrates also helps scientists like Yi-Rong Peng, ophthalmologist and neurobiologist at UCLA, illuminate the evolution of vision.

Peng’s research has found lamprey retinal cells are similar to those of other vertebrates, such as mice, chickens and zebrafish. Such a finding suggests retinal vision, like humans have, evolved early in the vertebrate lineage. Studying the overlaps between animal retinas gives a window into how vertebrates saw the world 500 million years ago. And understanding how the retina first formed in humans can help Peng’s research team study retinal cell degeneration that leads to blindness.

Morgan’s lab studies how sea lampreys regenerate spinal cords, and its work could lead to advances that help humans recover from spinal damage. When researchers cut a sea lamprey’s spinal cord, it becomes paralyzed but can regenerate nerve connections. The process does not have to be perfect to work, adds Purdue University science historian Kathryn Maxson Jones. Lampreys’ original neuron connections don’t reform in the same way, but cells grow in flexible ways to compensate for damage––biology can take different routes to achieve the goal of a spinal cord that works again. And the large size of lampreys’ cells and synapses enable the research team to closely examine the whole process.

Sea lampreys are also crucial to Morgan’s research on Parkinson’s disease. A specific protein’s accumulation in the brain is linked to the progression of the disease, so injecting that protein into lamprey synapses allows the researchers to observe how it affects the nervous system.

This gives insight into how the disease progresses in the human nervous system and how exactly neurons can recover. Scientists observe how damaged lamprey neurons regenerate and how many synaptic connections are restored, guiding how to target treatment in human brains.

Morgan’s research team hopes to move from understanding nervous system damage in lampreys and humans to how to fix it.

When you cut your finger and the area becomes numb, that’s because of damage to the nerve endings in the finger, which is part of your peripheral nervous system, explains Morgan. But you do eventually get feeling back, because humans can regenerate cells in the peripheral nervous system––just not in our central nervous system.

But lampreys can. “When lampreys regenerate the spinal cord and recover function, they are using a lot of the same changes in gene expression that occur during regeneration of the peripheral nervous system in mammals,” says Morgan.

“Why we can’t do that in our spinal cord is a big question. But I think learning from the adaptations of these animals, that can do these really neat feats of nature like regeneration, will tell you something about the recipe that needs to happen, the conditions that need to be met,” adds Morgan.

And the parallels between lampreys’ brain features and ours make crucial research possible when studying human brains isn’t an option. “It often points us in the direction of things we would’ve never looked at in humans,” says Krumlauf.

https://www.smithsonianmag.com/science-nature/this-invasive-vampire-fish-is-helping-researchers-understand-the-human-nervous-system-in-jaw-dropping-ways

Source: Studyfinds.org
Photo: Conceptual image of a man walking on the street with his smartphone being charged by his hoodie. (AI-generated image created by StudyFinds)

In a nutshell

Scientists finally cracked the code on making fabric that can generate electricity from body heat by creating a special polymer coating for silk that stays stable for over a year—previously, similar materials would degrade within days when exposed to air.

This isn’t just lab-perfect technology—the coated silk yarn can survive through seven rounds in the washing machine while still keeping most of its electrical properties, and it can stretch quite a bit without breaking.

While we’re not charging smartphones with our t-shirts just yet (the power output is still very low), this breakthrough could realistically power small sensors embedded in clothing, like health monitors that wouldn’t need battery changes or charging.

Forget to bring your charger with you on vacation? What if your clothing could generate electricity from the heat your body naturally produces? This futuristic concept is now approaching reality thanks to scientists at Chalmers University of Technology in Sweden and Linköping University.

Researchers say the remarkable new textile technology converts body heat into electricity through thermoelectric effects, potentially powering wearable devices from your clothing. The innovation, described in an Advanced Science paper, centers on a newly developed polymer called poly(benzodifurandione), or PBFDO, which serves as a coating for ordinary silk yarn.

“The polymers that we use are bendable, lightweight and are easy to use in both liquid and solid form. They are also non-toxic,” says study first author Mariavittoria Craighero, a doctoral student at the Department of Chemistry and Chemical Engineering at Chalmers, in a statement.

Unlike previous attempts at creating thermoelectric textiles, this breakthrough addresses a critical barrier that has long hampered progress: the lack of air-stable n-type polymers. These materials are characterized by their ability to move negative charges and are essential counterparts to the more common p-type polymers in creating efficient thermoelectric devices.

“We found the missing piece of the puzzle to make an optimal thread – a type of polymer that had recently been discovered. It has outstanding performance stability in contact with air, while at the same time having a very good ability to conduct electricity. By using polymers, we don’t need any rare earth metals, which are common in electronics,” explains Craighero.

How Thermoelectric Textiles Work

Thermoelectric generators work by converting temperature differences into electrical energy. When one side of a thermoelectric material is warmer than the other, electrons move from the hot side to the cold side, generating an electrical current. The human body continuously generates heat, creating natural temperature gradients between the skin and the surrounding environment.

For efficient thermoelectric generation, both p-type (positive) and n-type (negative) materials must work together. While p-type materials have been well-established in previous research, creating stable n-type materials has been a persistent challenge. Most n-type organic materials degrade rapidly when exposed to oxygen in the air, often becoming ineffective within days.

What makes this development particularly exciting is the remarkable stability of PBFDO-coated silk. Unlike similar materials that degrade within days when exposed to air, these new thermoelectric yarns maintain their performance for over 14 months under normal conditions without any protective coating. The researchers project a half-life of 3.2 years for these materials – an unprecedented achievement for this type of organic conductor.

Beyond electrical performance, the mechanical properties of the PBFDO-coated silk are equally impressive. The coated yarn can stretch up to 14% before breaking and, more importantly for everyday use, it can withstand machine washing.

“After seven washes, the thread retained two-thirds of its conducting properties. This is a very good result, although it needs to be improved significantly before it becomes commercially interesting,” states Craighero.

The material also demonstrates remarkable temperature resilience. During testing, the researchers found that PBFDO remains flexible even when cooled with liquid nitrogen to extremely low temperatures. This exceptional mechanical stability allows the material to withstand various environmental conditions and physical stresses that would be encountered in real-world use.

The Future of Daily Wear?

To showcase the technology’s potential, the research team created two different thermoelectric textile devices: a thermoelectric button and a larger textile generator with multiple thermoelectric legs.

The thermoelectric button demonstrated an output of about 6 millivolts at a temperature difference of 30 degrees Celsius. Meanwhile, the larger textile generator achieved an open-circuit voltage of 17 millivolts at a temperature difference of 70 degrees Celsius.

With a voltage converter, this could help power ultra-low-energy devices, such as certain types of sensors. However, the current power output—0.67 microWatts at a 70-degree temperature difference—is far below what would be required for USB charging of standard electronics.

While these power outputs mark a major step forward in thermoelectric textiles, it’s important to note that the temperature differences used in lab tests—up to 70 degrees Celsius—are significantly higher than what would typically be experienced in everyday clothing. This means real-world performance may be lower than laboratory results suggest.

Potential Uses in Healthcare and Wearable Tech

Despite current limitations in power output, the technology shows particular promise for healthcare applications. Small sensors that monitor vital signs like heart rate, body temperature, or movement patterns could potentially operate using this technology, eliminating the need for battery changes or recharging.

For patients with chronic conditions requiring continuous monitoring, self-powered sensors embedded in clothing could provide valuable data without the hassle of managing battery life. Similarly, fitness enthusiasts could benefit from wearables that never need charging, seamlessly tracking performance metrics during activities.

Beyond health monitoring, the technology could eventually support other low-power functions in smart clothing, such as environmental sensing, location tracking, or simple LED indicators. As power conversion efficiency improves, applications could expand to include more power-hungry features.

The Challenges Ahead

Currently, the production process is time-intensive and not suitable for commercial manufacturing, with the demonstrated fabric requiring four days of manual needlework to produce.

“We have now shown that it is possible to produce conductive organic materials that can meet the functions and properties that these textiles require. This is an important step forward. There are fantastic opportunities in thermoelectric textiles and this research can be of great benefit to society,” says Christian Müller, Professor at the Department of Chemistry and Chemical Engineering at Chalmers University of Technology and research leader of the study.

One key challenge identified through computer simulations is the electrical contact resistance between components. Reducing this resistance could potentially increase power output by three times or more. The researchers also investigated how factors like thermoelectric leg length and thread count affect performance, providing valuable insights for future designs.

Interest in these types of conducting polymers has grown significantly in recent years. They have a chemical structure that allows them to conduct electricity similar to silicon while maintaining the physical properties of plastic materials, making them flexible. Research on conducting polymers is ongoing in many areas such as solar cells, Internet of Things devices, augmented reality, robotics, and various types of portable electronics.

Looking Forward

What’s clear is that there is a viable pathway toward practical thermoelectric textiles that can function reliably in everyday conditions. By addressing both the electrical and mechanical requirements for textile integration, this work bridges the gap between laboratory demonstrations and potential real-world applications.

The development of these polymers also aligns with sustainability goals by eliminating the need for rare earth metals commonly used in electronics. With further refinement and scaling of the manufacturing process, this technology could eventually lead to clothing that powers our devices using nothing but our body heat.

For widespread adoption, researchers will need to develop automated production methods that can efficiently coat and assemble the thermoelectric textiles at scale. Additionally, improving power output while maintaining stability remains a critical goal for future research.

Methodology

The researchers coated ordinary silk thread with PBFDO polymer by dipping it into a specially formulated ink and drying it multiple times. They constructed two test devices: a button sewn onto wool fabric and a larger generator with 16 thermoelectric legs sewn through felt wool. Performance was measured by placing these devices between surfaces of different temperatures and recording the electricity generated.

Results

The PBFDO-coated silk achieved impressive stability, maintaining conductivity for over 14 months in normal conditions with a projected half-life of 3.2 years. It withstood stretching up to 14% and survived seven machine washings while retaining two-thirds of its conductivity. The larger textile generator produced 0.67 microwatts at a 70K temperature difference, while computer simulations suggested that optimizing electrical contacts could significantly boost performance.

Limitations

Power output remains low, suitable only for very low-power devices. Lab testing used temperature differences (up to 70K) much higher than typical real-world conditions, meaning actual performance would likely be lower. Production is currently time-intensive, requiring four days of manual work for a single demonstration piece. While stability is impressive compared to other similar materials, some degradation still occurs over time, particularly after washing.

Discussion and Takeaways

This research represents a breakthrough in creating stable n-type materials for thermoelectric textiles, potentially enabling practical applications in wearable technology. The work provides valuable insights for optimizing future designs, particularly regarding electrical contact resistance. By eliminating the need for rare earth metals, these organic materials also support sustainability goals. While commercial products are still years away, this development represents a significant step toward self-powered electronic textiles.

Funding and Disclosures

The research was supported by the European Union’s Horizon 2020 program (Marie Skłodowska-Curie grant), the Knut and Alice Wallenberg Foundation, the European Research Council, the Swedish Research Council, and Linköping University. Author Simone Fabiano is disclosed as a co-founder and chief scientific officer of n-ink, a company with potential interests in the technology.

Publication Information

Published in Advanced Science (2024) as “Poly(benzodifurandione) Coated Silk Yarn for Thermoelectric Textiles” by researchers from Chalmers University of Technology, Linköping University, and Chung-Ang University. Available as an open-access paper under Creative Commons Attribution License.

https://studyfinds.org/your-clothes-could-soon-charge-your-phone-new-thermoelectric-yarn

Source: Time, Alice Park
Photo: David Sinclair is peering at nerve cells chemically reprogrammed to slow the aging process. (Tony Luong for TIME)

Later this year, a handful of people with a rare eye condition will receive a novel injection that is designed to quite literally turn back time.

Nonarteritic anterior ischemic optic neuropathy—known as NAION—can cause sudden blindness when blood flow to the optic nerve is blocked. It’s not clear what causes the condition, although diabetes, high blood pressure, and smoking are known to be risk factors. Some early evidence also suggests GLP-1-based weight-loss drugs such as Wegovy, Ozempic, Mounjaro, and Zepbound might also make patients twice as prone to the condition compared with those not taking the medications. Whatever its cause, there are no treatments for NAION. And if it strikes one eye, there is a good chance it will also affect the other, leading to complete blindness.

Scientists hope to change that with what is potentially much more than an eye treatment. The injection will test a new gene therapy that, instead of targeting specific genetic mutations that cause NAION, attempts to return certain optic-nerve cells to their pre-NAION state. It would be the equivalent of pressing a biological rewind button that takes the affected cells back to a younger condition—one in which they haven’t yet been struck by NAION or any other disease.

To some scientists, this sounds wildly ambitious. To others, extremely unlikely. Either way, it is just the kind of big—and controversial—swing that is emblematic of the growing field of science devoted to untangling and reversing what is a central fact of life: aging.

The particular therapy behind the NAION treatment is based on the work of David Sinclair, a professor of genetics at Harvard Medical School and director of the Paul F. Glenn Center for Biology of Aging Research. He has spent decades trying to understand the wear-and-tear processes that age our cells and is convinced that many conditions that plague us—from joint issues to metabolic processes that break down as we get older—could be avoided and even reversed.

“The real stroke of brilliance is the notion that you make the cell younger, and then it would be more resilient to injury,” says Dr. Joseph Rizzo, professor of ophthalmology at Harvard Medical School and Mass Eye and Ear, who is leading the study. “To me, that was the winning concept.”

Rizzo’s team will give the treatment to three volunteers, all of whom have NAION in one eye. Each will receive an injection of three genes designed to reprogram the targeted optic-nerve cells.

If successful, the treatment could potentially be used for more common age-related eye conditions like glaucoma—and even other chronic diseases like dementia, arthritis, and heart disease. And it is only one of a growing suite of potential treatments designed to address aging, as scientists race to reverse time at a cellular level.

Some, including Dr. Valter Longo at the University of Southern California, support the idea of periodic fasting regimens to stress cells into a more resilient, younger state, while others, like Dr. James Kirkland from Cedars-Sinai Medical Center, are developing drugs to remove older cells that refuse to die but damage healthy cells around them, contributing to age-related conditions.

Their ultimate goal? To uncover something that has long fascinated humanity: the key to defeating—or at least slowing—old age.

Even if it works, the NAION study would only be a first step on the road to fulfilling that fantasy. The genetic and molecular science making the trial possible has advanced by leaps in recent decades—but it remains a good way off from delivering a pill or injections to erase the damage we inflict on our bodies by just living. Stress, exposure to pollution, drinking, and hours on the couch—there’s no easy way to undo it all. But that’s not hindering the search for a quick fix. Everywhere you look there is evidence of a voracious interest in clearing away the layers of daily life and somehow rediscovering the elusive fountain of youth—whether by popping anti-aging supplements touted on social media (even David Beckham sells one) or adopting some of the often extreme treatments depicted in billionaire Bryan Johnson’s Netflix documentary, Don’t Die.

This public frenzy has unlocked a flood of investment from venture capitalists—funding for longevity startups is up by 75% over the past year, according to CB Insights—and pharmaceutical companies. The opportunity for them, if they can create new drugs or pioneer techniques to slow or reverse aging, is potentially colossal. “Every single person on the planet is aging,” says Dr. Mehmood Khan, CEO of the aging philanthropy Hevolution, which is based in Saudi Arabia (one of the largest funders of aging research in the world). “This affects every organism. It’s personal.”

But longevity scientists working today temper this enthusiasm with a sobering reality. Their focus is not on immortality, or even adding a few more years to people’s lives. It’s ensuring that they spend those final years in as healthy a condition as possible.

They are in the business of increasing health span, not lifespan. “We are not focused on trying to work on longevity,” says Kirkland, director of the Center for Advanced Gerotherapeutics at Cedars-Sinai. But it could be a welcome side effect. “Hopefully we live to 100 or something like that, completely functional, and just not wake up one morning.” The goal is to extend the number of years (however many they may end up being) during which people can live independently, actively, and without being encumbered by serious disease.

That’s not just a matter of semantics; improving health span would have substantial economic and societal benefits. Researchers estimate that increasing health span by just one year in the U.S. would lead to a $38 trillion boost in the economy due to increased productivity from a larger, more vital workforce and savings in health care costs in treating age-related diseases. Reframing longevity in these terms is catalyzing a renewed interest in researching aging.

“Everybody recognizes that at this point of increasing prosperity and increasing life expectancy all around the world, the burden of caring for older adults suffering from chronic diseases has emerged as one of the most pressing global challenges of our times,” says Dr. Shalender Bhasin, professor of medicine at Harvard University and director of the Claude D. Pepper Older Americans Independence Center at Brigham and Women’s Hospital.

By 2030, the cost of chronic diseases like diabetes and heart disease, measured in lost productivity and health care expenditures, is expected to reach $47 trillion worldwide. “We have an historic opportunity and imperative for governments, companies, academic, and regulatory agencies to work together to modify the life trajectory,” he says. “Extending health span will be even more important than extending lifespan.”

For decades, antiaging strategies have largely been confined to the beauty and supplement industries, where the promises were grand but the evidence scarce. Science took longer to wade into the field, held back by the assumption that aging was inevitable. It wasn’t until the 1930s, when scientists first demonstrated that rats that ate drastically less tended to live longer, that scientific efforts to crack the aging conundrum attracted more scientists’ attention. But dramatically cutting calories isn’t practical for most people. So researchers shifted instead to restoring specific organs or tissues—but those efforts weren’t guided by a deep understanding of how cells and tissues age.

Advances in genetics and molecular biology, including critical discoveries about stem cells and how they develop to become different cells in the body, began deconstructing the black box that had cloaked aging for so long. There are currently dozens of studies testing whether certain compounds can slow down the many cellular signs of aging, like the DNA damage and oxidative stress you collect from too much time in the sun or exposure to pollution or toxic chemicals in the environment. Damage is also caused by tobacco and poor diets, not exercising, and diseases like obesity and Type 2 diabetes. Some of the studies are exploring how the diabetes drug metformin, for example, might help slow down (and therefore preserve) the metabolic system. Researchers are also exploring ways in which the microbes that live in our guts and skin contribute to the balance between health and disease, and whether specific types of so-called microbiomes are more or less linked to health span.

Kirkland focuses on yet another area: senescent cells, or cells that have stopped dividing and are on their way to dying, and the destructive signals they send as they expire. He’s developing drugs called senolytics that target these signals, which could minimize some of the damage that we all recognize as aging. Senescence is one of the fundamental processes of aging, Kirkland says, and each of these “can impact literally hundreds of conditions.”

Positive results from such studies could potentially lead to medicines that may help chip away at the time people spend in poor health. No such products have emerged yet, but promising results from animal studies suggest that it may be possible for certain tissues and organs.

Sinclair, for one, believes that there is a more unified, efficient way to confront aging. The NAION trial is among the first to test his idea that aging is the end product of years of assaults on our genes brought on simply by living, as well as certain lifestyle habits. The net effect on our genes—which scientists call epigenetics, or the way genes are turned on or off within particular cells—is what is aging our cells, he thinks, so to address it, we should start treating aging like a disease. With that approach, he believes we can figure out how to erase the epigenetic changes that build up over time, and give our cells their youth back.

“Time does not go away,” says Sinclair. “We’ll still age.” But the challenge is to control the rate at which that happens as much as possible, so older age starts to look drastically different than it does today—without the extreme frailty, loss of muscle and bone strength, and deterioration of mental and metabolic processes that currently contribute to chronic conditions.

Sinclair caused a stir in 2023 when he claimed to have reprogrammed old cells in mice that he had epigenetically aged, and found that their muscle and kidney cells were acting young again. (Not everyone in the scientific community agreed that he had effectively aged, then rejuvenated, the mice.) He used a technique for which the Japanese stem-cell scientist Shinya Yamanaka had won a Nobel Prize. Yamanaka discovered a set of four genes that could, when delivered by an inactivated virus using gene therapy, revert adult cells to their embryonic forms, so that they could theoretically develop into any of the body’s hundreds of different cells. Before being treated with three of these genes, the mice in which Sinclair accelerated aging were grayer, frailer, and suffering from a number of age-related diseases, compared with normal mice. Once the aged mice received the reprogramming therapy, however, the genes in their muscle and kidney cells began working like those in young mice.

“We saw reversal of gene-expression patterns back to a more youthful state,” Sinclair says. He used the same process to reverse age-related blindness in mice as well. Currently, his lab is testing a chemical cocktail that mimics the gene therapy but doesn’t require injections. It’s still early, but so far, older mice fed the cocktail for four weeks have less frailty and younger-looking coats.

The way he explains it, as mice age (and humans, he believes), the “information” that cells accumulate over time starts to become biological noise. It’s similar to being among the first to arrive at a cocktail party—it’s relatively quiet, you can see who’s there, and probably eavesdrop on a conversation or two. As more people join, the noise level rises, and the sum of everyone’s conversations becomes a cacophony. Similarly, as cells age, their epigenetic blueprint bears the legacy of what they’ve endured. Those effects don’t necessarily alter their genome, but they do change the way genes are activated and suppressed, and how well cells can repair themselves. Sinclair theorizes that cells accumulate these changes over time, and the burden of these alterations ultimately causes them to falter or function abnormally—a sign of aging.

Sinclair calls it the “information theory of aging” and is dedicating the remainder of his career to proving it. But he and his research have their critics, who question whether Sinclair truly rejuvenated the cells since he didn’t show the animals’ muscles or organs actually functioned like younger versions even if their gene activity was changed, without signs of aging. Not to mention the obvious question: What does any of this mean for people?

Part of the controversy centers on the fact that the aging field is still trying to establish the standards by which it defines and ultimately measures success. “Where we are right now is that we’ve got three or four leading classes of interventions that people think may be worth exploring in larger human studies,” says Bhasin. They include senolytics, as well as metabolic drugs like metformin and compounds that boost nicotinamide adenine dinucleotide (NAD), a molecule critical to how cells use energy. But “there is very vigorous debate over what will be the primary end point for the clinical trials of these candidate drugs, and how we define the success or efficacy of the drug.”

Ideally, Bhasin says, what researchers should measure aren’t changes in a specific health metric, such as blood sugar or blood pressure, but a broader range of chronic disease incidence that better captures the overall ability of older people to thrive. “If we can show that the onset of these age-related diseases, which is a quantifiable indicator, or their incidence, is reduced, then that would be very strong evidence of health-span extension,” he says. But such studies would be expensive and require long periods of follow-up, which have hindered the field.

Sinclair, however, remains convinced that his approach does slow aging, and stands by the metrics he used. “Two hundred thousand people die each day from age-related diseases, and I’m not going to wait 15 years,” he says.

Sinclair has long been a lightning rod of controversy in the field because of that defiance—among other things. Depending on whom you ask in the scientific community, he is either a pioneering scientist pushing the limits of our understanding of aging, or a snake-oil salesman. He has a tendency to make grandiose claims about what science can do to slow aging. (The title of his best-selling 2019 book is Lifespan: Why We Age—and Why We Don’t Have To.) He recently resigned from a professional group of aging researchers that he had helped to create after tension arose when he was quoted in a press release claiming that a company he had created had reversed aging in dogs. (Sinclair blames the sloppily written press release and has reworded the statement.) “I probably agree with 80% of what David says about the importance of the field and what it could be, and with the excitement and enthusiasm about the future and discoveries being made,” says Matt Kaeberlein, co-director of the University of Washington Nathan Shock Center of Excellence in the Basic Biology of Aging. “But in my personal opinion, he often gets ahead of his skis and sometimes says things that are not true.”

It doesn’t help that Sinclair is also a serial entrepreneur, which some believe creates a conflict of interest between pursuing commercial interests and objective scientific principles. None of the companies he has helped to create, based largely on work from his lab, has led to a commercial product to slow aging, and some have shuttered before conducting critical studies. That includes his first venture, which GSK bought in 2008, to develop his finding that the red-wine compound resveratrol helped yeast and worms live longer. GSK dropped the project, but Sinclair stands by his findings. What others see as failures, he describes as perhaps before their time.

He and others are now focused on studying the effects of NAD, a jack-of-all-metabolic-trades enzyme involved in determining how well the cell functions.

“You could call them the crown jewels of metabolism,” says Charles Brenner, professor of diabetes and cancer metabolism at City of Hope, of the NAD co-enzymes. “But while the crown jewels of any country in Europe are inside a safe inside of a vault inside of a castle patrolled by armed guards, the crown jewels of our metabolism are exposed to the elements of metabolic stress. When we go outside, get a sunburn, or live life in an oxygenated environment, we generate DNA damage and reactive oxygen species that attack the NAD system.”

The more the NAD system is perturbed, the less able it is to perform its critical functions in regulating a cell’s energy, among other things. Some scientists, including Sinclair, believe that boosting the body’s stores with a NAD supplement is a promising way to slow aging. And Sinclair has created a company, Metro International Biotech, that is manufacturing a precursor molecule that the body turns into NAD; human testing began in March. “Every-one who’s been dosed is doing fine so far,” he says.

Brenner—one of Sinclair’s critics—takes NR (nicotinamide riboside), a precursor that the body turns into NAD, that he discovered in 2004. But he says it’s not because he thinks it will help him live longer or age more slowly. “I don’t make any extravagant claim that NR is a longevity drug,” he says. “The idea of NAD boosting, in my opinion, is to essentially equip people to have higher resiliency in the face of conditions like metabolic stress.”

Brenner believes it’s nearly impossible to truly do a trial that tests NAD boosting’s role in extending life, since too many factors contribute to aging, lifespan, and health span. “There is no way to do that trial, and people who think they can, using biomarkers, are probably fooling themselves,” he says.

That’s not stopping researchers from trying. Bhasin is currently recruiting healthy, fit people to test NMN, another precursor that the body converts to NAD, with a version made by Metro International Biotech. Everyone will be put under physical stress with an intensive exercise regimen and randomly assigned to take the pills or a placebo. They’ll then undergo physical and psychological tests: running on a treadmill, having their respiratory function and muscle tone checked, and having their cognitive skills evaluated. The study will shed light on how boosting NAD affects people under physical stress, which is one of the factors that can indirectly contribute to cell aging.

More research—and replication of results—is needed before any of this will help us all live to 100. But “we are now living in an era where we have the tools to accelerate [the] pace of research,” says Khan. “There is a recognition that with early intervention, we can change the trajectory of health span.”

https://time.com/7266835/aging-longevity-health-span-science

Source: Extreme Tech, Adrianna Nine
Photo: NASA

If the tool can identify microbial fossils here on Earth, it might be able to do the same on the Red Planet.

Planetary scientists in Algeria and Switzerland have developed a scientific instrument that could help hunt for signs of life on Mars. Used to locate microbial fossils in gypsum deposits here on Earth, their prototype is expected to be a valuable addition to missions to find the first proof of extraterrestrial life on the Red Planet.

The instrument, called a laser ablation ionization mass spectrometer, delivers rapid, femtosecond-long dual pulses of light to a target, such as sediment. Every pulse ablates, or burns, a thin layer of the material. Not only does this allow scientists to gradually reveal what’s underneath the material’s surface, but what’s vaporized is ionized and analyzed based on its mass-to-charge ratio. The resulting data tells scientists which elements and isotopes are hidden within the material.

Laser ablation mass spectrometry (LIMS) is a fairly new technology, having only attracted attention from planetary scientists over the last decade or so. This particular LIMS instrument, developed by the University of Bern, was built specifically for spaceflight in the hope that it might someday seek out life—or signs of it, at least—on Mars. To make sure it worked, though, the team first had to test it on a Mars analog here on Earth.

They chose the Mediterranean’s famous gypsum formations, which formed 6 million years ago during a sharp increase in salinity dubbed the Messinian Salinity Crisis. Gypsum deposits form quickly, making them an excellent medium for fossils—the fossils form before an organism can decompose. Gypsum is also known to exist in abundance on the surface of Mars, making the Mediterranean an ideal Martian analog.

Testing their LIMS instrument on gypsum samples from Algeria’s Sidi Boutbal quarry, the researchers could distinguish between natural rock features and microbial fossils. They also identified dolomite, a dry mineral that can only collect in acidic environments when a prokaryote—a nucleus-free cell—increases its environment’s alkalinity. On Earth, this means bacteria likely existed within the gypsum.

If LIMS finds itself on a future Mars mission, it could analyze the planet’s rusty sediment deposits for similar signs of life, as well as microbial fossils themselves. This analysis would be particularly valuable along the Red Planet’s shorelines, where water might have allowed life to thrive billions of years ago.

https://www.extremetech.com/science/new-scientific-instrument-could-help-search-for-life-on-mars

Source: ExtremeTech, Adrianna Nine
Photo: Artist’s rendering of a Mars lander that could retrieve Perseverance’s samples and send them to Earth. (NASA/ESA/JPL-Caltech/GSFC/MSFC)

The agency is starting down two different paths toward the samples’ return, but only one will bring the red rocks home.

NASA kicked off the new year with a major announcement: It’s officially tackling the issue of bringing Mars samples to Earth. Though the agency’s Perseverance rover started collecting Martian regolith four years ago, the Mars Sample Return program’s rising costs have made it difficult for officials to land on a specific transportation plan. Now, after investigating a handful of alternate return strategies, the agency has selected two to pursue this year. But only the winning strategy will bring the red rocks home.

In a media briefing on Tuesday, NASA Administrator Bill Nelson and Science Mission Directorate leader Nicky Fox explained that NASA’s original sample return plan had been nixed the year prior. The initial plan would have involved a Mars lander to which Perseverance could have passed the baton, allowing a rocket within the lander to depart from Mars and hop on over to the Moon, where the samples would be retrieved. But according to Nelson, that strategy would have brought the Mars Sample Return program’s total cost to $11 billion, and the samples wouldn’t have made it to Earth until 2040.

“That was just simply unacceptable,” Nelson said during the briefing.

Instead, NASA pieced together a Mars Sample Return Strategic Review team, which would field studies focused on various return methods from across the aerospace industry. The team investigated or rejected strategies based on their ability to reduce risk, cost, and the mission’s timeline. In the end, it chose two methods to begin pursuing in 2025.

The first method involves NASA’s existing “sky crane” architecture, which it successfully used to land Curiosity in 2012 and Perseverance in 2021. This approach uses a large heat shield and parachute for the spacecraft’s initial descent, then slows it down with retrorockets before gently placing the spacecraft on the planet’s surface with a strong cable. Theoretically, the sky crane approach could allow NASA to land a spacecraft on Mars, snag Perseverance’s samples, and return directly to Earth—a far simpler, and therefore cheaper, alternative to NASA’s original plan.

NASA’s second plan is to leverage existing commercial partners, such as SpaceX or Blue Origin, who could devise their own retrieval methodologies. This approach would bring the samples to Earth as early as 2035 and land the Mars Sample Return program’s total cost between $5.8 and $7.1 billion. Nelson said NASA is currently exploring a number of these avenues, but did not specify what the actual return might look like.

For both of these paths, success means bringing home 30 of Perseverance’s 43 cigar-sized titanium sample tubes. And while NASA is now investigating the viability of both plans, only one will have the honor of retrieving the samples. The agency expects to make a final decision in the second half of 2026; the timing of the samples’ return will then depend on how efficiently Congress can fund the mission.

“The samples that we have been collecting on Mars are very carefully selected to provide groundbreaking opportunities for research,” Fox said during the briefing. “Bringing them back will revolutionize our understanding of the planet Mars and indeed our place in the solar system.”

https://www.extremetech.com/science/nasa-is-one-step-closer-to-bringing-mars-samples-to-earth

Source: ExtremeTech, Adrianna Nine
Photo: Wladimir Bulgar/Science Photo Library via Getty Images

The model is the first of its kind to use multiple types of imaging and language-based data to assess a cancer patient’s health.

Stanford Medicine has developed an artificial intelligence model that can accurately predict cancer patients’ prognoses and responses to treatment. The first of its kind to leverage multiple types of imaging and language-based data, the model has already shown promise with several forms of cancer, including lung cancer, gastroesophageal cancer, and melanoma.

Over the last few years, researchers have created a range of experimental AI models that examine imaging data for tiny signs of cancer that doctors and radiologists might easily miss. Early tests show that these models are highly effective. Sybil, a model developed by MIT and the Massachusetts General Cancer Center, can predict patients’ one-year lung cancer development with an 86% to 94% accuracy rate, while Harvard Medical School’s pancreatic cancer prediction model can map a patient’s three-year prognosis with 88% accuracy. Another MIT model even spots signs of the riskiest forms of breast cancer to shield patients from overtreatment.

Impressive as these models are, they share in common one essential shortcoming: They’re only capable of analyzing one form of data at a given time. Each model looks at MRI scans or CT scans or X-ray images or microscopy slides, then identifies areas of concern within that dataset. Even Microsoft’s multi-diagnostic AI model, which accepts a whopping nine forms of imaging data, must examine those types of imaging separately.

Stanford Medicine’s model, MUSK (short for multimodal transformer with unified mask modeling), looks at several types of data at once. In a paper for Nature, the researchers write that MUSK was trained on 50 million pathology images and 1 billion “text tokens” from more than 11,500 patients. Although the images depict different forms of cancer across X-rays, microscopy, and CT and MRI scans, the text tokens represent language-based medical data—exam notes, communications between specialists, and so on—associated with various cancer diagnoses.

MUSK’s ability to analyze multiple types of data simultaneously mimics how doctors assess a person’s imaging results and health records. It also allows MUSK to assist doctors in predicting prognoses, not making diagnoses, the latter of which most medical AI models are focused on.

Across the 16 major types of cancer on which MUSK was trained, the model is capable of accurately predicting a patient’s disease-specific survival 75% of the time, according to a Stanford Medicine release. That’s an 11% improvement over doctors’ average accuracy rate, which hovers around 64%. MUSK has also correctly identified which non-small cell lung cancer patients would benefit from immunotherapy 77% of the time (beating doctors’ 61% accuracy rate) and predicted which melanoma patients were most likely to relapse within 5 years of initial treatment with 83% accuracy.

“The biggest unmet clinical need is for models that physicians can use to guide patient treatment,” said senior study author and radiation oncologist Ruijiang Li. “Does this patient need this drug? Or should we instead focus on another type of therapy? If we can use artificial intelligence to assess hundreds or thousands of bits of many types of data, including tissue imaging, as well as patient demographics, medical history, past treatments, and laboratory tests gathered from clinical notes, we can much more accurately determine who might benefit.”

https://www.extremetech.com/science/stanford-medicines-ai-model-accurately-predicts-cancer-prognoses-treatment

Source: Los Angeles Times, Teresa Watanabe
Photo: High school girls from around the nation wait in line to ask questions of scientist Katie Bouman during the annual Women in STEM program at Caltech in Pasadena. (Ringo Chiu/For The Times)

The auditorium was packed with hundreds of high school girls from across the nation fangirling a YouTube idol they dream to emulate.

There before them stood Katie Bouman, an associate professor of computing and mathematical sciences, electrical engineering and astronomy at Caltech in Pasadena, showing off images of a dark hole ringed by a fire-colored halo. In 2022, Bouman co-led a team of more than 300 researchers from 80 institutions to capture the world’s first image of the supermassive black hole at the center of the Milky Way galaxy.

Bouman’s lecture, part of the Caltech Women in STEM program, had a deeper motive: It showcased a leading woman scientist to help girls envision themselves attending one of the world’s preeminent institutions of science and engineering — fields still dominated by men. And the efforts in this hard-fought, strategic campaign are paying off.

In a milestone breakthrough, more than half of Caltech’s incoming undergraduate class in the fall will be women for the first time in its 133-year history. The class of 113 women and 109 men comes 50 years after Caltech graduated its first class of undergraduate women, who were admitted in 1970.

“What this means for young women is that we are a place that can be representative of them and their experiences … where they can grow and thrive and excel and become really impressive, extraordinary scientists and engineers and go on to make a difference in this really research-heavy profession,” said Ashley Pallie, dean of admissions.

Gloria L. Blackwell, chief executive of the American Assn. of University Women, lauded Caltech’s achievement as crucial progress in reducing the substantial gap of women in science, technology, engineering and math. Although women hold about 60% of degrees in biological sciences, they represent only about 18% in computer science and 20% in engineering, Blackwell said.

Research has shown that boys are not better at math and science than girls, but a persistent message in society says otherwise — and especially discourages Latinas and Black girls from pursuing the fields because they face discrimination and have less access to role models, resources and opportunities, the AAUW says.

Caltech isn’t the first educational institution to reach gender parity in STEM. Harvey Mudd College, a small private institution in Claremont, was an early leader in diversity — a key goal of former President Maria Klawe, a computer scientist and mathematician who stepped down last year after a 17-year tenure. The college enrolled more women than men in 2010 for the first time in its history and in 2014 graduated more women than men in engineering. Today, women make up 52.8% of majors in computer science, 50.5% in engineering and 68.2% in mathematical and computational biology.

At UC Berkeley, another powerful producer of STEM graduates, nearly half of students majoring in those fields identify as women or nonbinary, but the field they enter varies significantly. They make up more than two-thirds of students in biological and biomedical sciences, but about one-third in engineering, computer and informational sciences, and mathematics and statistics.

The long quest for gender parity

For Caltech, a campus of 2,400 undergraduate and graduate students with 47 Nobel awards and more than 50 research centers, the road to gender parity has been long. Women were not admitted until 1970 amid rising demands for gender equality and two years before Congress passed Title IX of the Higher Education Act, which prohibits discrimination on the basis of sex in any educational program receiving federal funds.

Louise Kirkbride was one of 32 members of that inaugural class. A Philadelphia teen and National Merit finalist scouted by Caltech, Kirkbride wanted to attend the institute so badly that she left home for Pasadena without her parents’ permission or support. Institute officials picked her up at LAX, gave her a full scholarship and helped her become an independent minor, Kirkbride said.

“In my mind, Caltech was the hardest school to get into in the world and that made it just kind of irresistible,” said Kirkbride, who went on to found two venture-capital-based startups and currently serves as a Caltech trustee.

On her first day, she said, some male students held up a sign, “Welcome, Kotex,” referring to a tampon brand. She put up with a student who carefully explained “why it had to be true that [women] were admitted as affirmative action” based on the purportedly natural gender distribution of intelligence. One professor said to her class that admitting women would end Caltech’s excellence, and another told her that “you’re a waste of an education.”

But the kindness and support of another professor, Carver Mead, helped her find a home at Caltech. She was so inspired by him that she followed his path and became an electrical engineer.

Mead, now 90 and still engaged in research as a professor emeritus of engineering and applied science, said he has always supported women scientists. “I’ve always had women in my research group, and they’re more collaborative and often provide a lot of leadership in a very quiet way, and it just really changes things,” he said.

During the faculty meeting to debate the issue in 1967, Mead said, many of the “old farts” complained that women would feel outnumbered and would just get married and have children and that “we could have educated somebody who was going to do … science.” He left the meeting and called an MIT woman graduate he knew. She told him she had had no problems being a minority at the Cambridge, Mass., campus. Mead returned, told his colleagues about his “data point” and, as scientists persuaded by evidence, they voted to let women in.

By the time Bouman reached Caltech in 2019 as a faculty member, much had changed. Growing up in Indiana, she was always encouraged to pursue her talent in science and math by her father, a professor of electrical and computer engineering and biomedical engineering at Purdue University. But as an undergraduate at the University of Michigan, she was just one of a handful of women in the electrical engineering department and sometimes felt like an impostor.

“That starts to get in your head a little bit, but if you don’t search for it, then you can kind of just plow forward and not let it worry you,” Bouman, 35, said. “I really tried to put blinders on.”

She graduated summa cum laude from Michigan, earned her doctoral degree at MIT, where she first started her work on black hole imaging in 2013, then became a postdoctoral fellow at Harvard. There, in 2019, she helped develop the code to capture the world’s first image of a black hole and unexpectedly became the face of the international project when a photo of her amazement hit social media. U.S. Rep. Nancy Pelosi (D-San Francisco) hailed her as “an inspiration to all Americans and especially to young women and girls” with STEM dreams. Children sent her their drawings of black holes. One girl even dressed up as her for Halloween.

Bouman said she never intended to be a role model but recognizes the importance of girls seeing women in the sciences. After her lecture, one girl went up to her, asked to take a selfie and told her, “You’re my dream scientist!”

Leah Cevallos, a West Sacramento high school senior, said the science journals she reads “for fun” are dominated by men, so seeing Bouman centered in the black hole breakthrough was inspiring.

“The more you give people the opportunity to see themselves in a place like Caltech, the more we know we’ll find fantastic people who can make great contributions to science and technology and engineering,” said Michelle Effros, who was the first woman faculty member hired into Caltech’s electrical engineering department in 1994.

Pallie, the admissions dean, said she has more than doubled the size of the Women in STEM program to 500 girls and extended it to two days, so potential students and their families can get a deeper sense of Caltech — especially the lab tours to “let the science speak for itself.”

She also revamped the institute’s messaging to say upfront that Caltech is fearsomely difficult, but also a unique and exciting place for the right person. Applications have skyrocketed from 8,000 before the pandemic to 14,000 today. The admission rate has fallen to 3.14%, and the share of students accepting admission offers has increased to 64%.

Pallie said there is still work to do.

“You can’t just be a one-hit wonder,” Pallie said. “Our major goal is to sustain and continue it so this is just part of the DNA of Caltech, that we just are a place where young women see themselves and they know that they can really thrive.”

More work ahead

But even as more women study science, technology, engineering and math, they remain significantly underrepresented in the related workforce. Women hold about 45% of STEM degrees but make up only 28% of the workforce in those fields, said Blackwell of the American Assn. of University Women. Many women face unwelcoming “masculine cultures,” she said, and some experience gender discrimination and opt to leave the field.

But during Caltech’s Women in STEM day, it was all dreams of cutting-edge research and new scientific discoveries.

Miranda Li, a senior at Sierra Canyon High School in Chatsworth, is passionate about astrophysics and astronomy, relieves stress by doing complex math problems and is writing a play about physics. Her tour of a lab that measures gravitational waves was “really cool,” cementing Caltech as one of her top college choices.

Veronika Voss is a member of this year’s milestone class of majority women. She grew up in a rural Minnesota town amid fields of corn and soy. Her tiny high school — graduating class, 68 students — had no Advanced Placement courses and limited offerings of advanced math and science, so she studied on her own with old textbooks and online resources, such as Khan Academy. She gained hands-on experiences with electronics fixing her family’s electrified chicken fence, the engine in her tractor lawnmower and is training as a helicopter mechanic.

To Voss, taking apart engines and figuring out the problem is like solving complicated math equations — both bring her joy.

And so does Caltech, she said. She learned about the institute as a child fascinated by space who followed the work of the Jet Propulsion Laboratory, which Caltech founded and manages. Then she was invited to attend the Women in STEM program. The experience sealed the deal for her to attend Caltech.

“I came to campus and it was like 500 women; I was like, oh my gosh, it is a real place and there’s so many women who are here and they’re all insanely passionate about the same things that I’m very passionate about,” Voss said.

https://www.latimes.com/california/story/2024-08-27/caltech-long-male-bastion-to-enroll-majority-women-for-first-time