As we age, our body loses its ability to clear out zombie-like cells that have stopped dividing, instead dripping out poison and turning other cells rogue. Restoring the ability to remove these “senescent” cells prevented signs of cognitive decline and frailty in older mice, with hints that the same outcomes could occur in people.

“What’s attractive about this study is that it is not trying to kill [senescent] cells directly,” says Derek Gilroy at University College London, who wasn’t involved in the research. “It is repairing the body’s own waste-disposal system that should have removed them in the first place.”

To better understand why this system goes awry, Katrin Andreasson at Stanford University, California, and her colleagues compared mice aged 6 to 8 months (roughly equivalent to people in their 20s) with mice aged 23 to 25 months (equivalent to people in their late 60s or 70s). They found that the older mice had more of these senescent cells in their organs, including the liver and spleen, as well as in their bone marrow.

Specifically, the senescent cells were neutrophils, immune cells that are normally the body’s first line of defence against infection. These would normally be cleared away by macrophages residing in tissue, which remove damaged cells and debris, but this ability declines with age.

Andreasson and her colleagues traced this decline to prostaglandin E2, a signalling molecule that increases with age. They found that higher prostaglandin E2 activity overstimulates a receptor called EP2 on tissue-resident macrophages, which leaves them less able to remove senescent cells.

Free newsletter

Sign up to Health Check

Sign up to newsletter

Next, the team tested whether blocking this overstimulation could improve signs of ageing by genetically modifying the EP2 gene from tissue-resident macrophages in older mice. These animals went on to clear more senescent neutrophils and showed signs of healthier ageing, including lower levels of inflammation, reduced muscle loss, less visceral fat and better mobility, compared with unmodified mice of the same age. They also performed almost as well as young mice in memory tests. “We were very surprised at the magnitude of the effect,” says Andreasson.

The researchers also tested an experimental drug that blocks EP2. When given orally to older mice for two months, this caused similar age-related improvements to those experienced by the genetically modified mice.

A negative attitude towards ageing is making you age faster

We know that a person’s outlook can have a huge effect on their health, and it’s no different when it comes to ageing. Columnist Graham Lawton looks at new evidence of just how powerful our attitude is – and how to use it to age better

“This is a very promising study, but we need to be careful,” says Gilroy. “EP2 is part of a normal signalling system, and blocking it throughout the body could have unwanted effects.” The mice experienced no known side effects, but Gilroy says it may be safer to target EP2 in ageing macrophages specifically.

Finally, the team found similar patterns in human tissue, with liver samples from older people showing higher EP2 activity and more senescent neutrophils. “The human data are supportive, but still correlative,” says Gilroy. “We haven’t yet shown that blocking EP2 can restore neutrophil clearance in aged human tissue.” 

The researchers are now planning to study whether this process affects the onset of conditions such as Alzheimer’s disease.

A man who became paralysed after a diving accident six years ago regained the ability to move and feel pressure in his hands thanks to brain stimulation. Now, researchers have revealed he maintained this ability for months after the stimulation was turned off. This suggests the intervention has caused a rerouting of his neuronal connections through neuroplasticity.

“We turned everything off completely, for many months, and yet he’s maintained these gains,” says Chad Bouton at the Feinstein Institutes for Medical Research in New York. “That’s unheard of.”

Keith Thomas, 48, was paralysed from the chest down in July 2020. He had no sensation or control over his limbs and had significant muscle wasting, says Bouton.

In 2023, Bouton and his colleagues performed a double neural bypass surgery on Thomas, placing five electrodes into his brain in regions associated with arm movements and feeling. They then connected computer cables to these electrodes, so artificial intelligence could interpret his movement intentions. That information was then wired into electronic splints that stimulated his arms, hands and fingers to carry out his intended movements, enabling him to pick up coffee cups and scratch his face.

To recreate the sense of feeling, the team embedded force sensors into 3D-printed wearable devices for Thomas’s hands and fingers, which sent feedback via electrical stimulation into the brain’s sensory areas.

After conducting a series of experiments – which even involved Thomas feeling objects through another person’s hand – Bouton says the team planned to stop the stimulation for about a month, to test for any lingering effects. “Then we had a fire in the building, and it actually forced us to stop stimulation for even longer than we’d planned, for about three months.”

The unexpected interruption led to surprising findings: Thomas continued to maintain strength, feeling and function in his hands. “He’s now also controlling individual fingers with even more accuracy, so that’s big,” says Bouton.

In a video interview with New Scientist, Thomas raised his elbows nearly to shoulder level and described feeling “tingling” in his wrist in response to pressure, even when he’s “unplugged from the computer”. “When I first felt it, it was amazing,” he says. “I’m used to it now.”

Sergey Stavisky at the University of California, Davis, says the work suggests that this approach promotes lasting recovery of the nervous system. “The goal is to help the nervous system partially heal so the person can move their own body better,” he says.

Free newsletter

Sign up to Health Check

Sign up to newsletter

“If these improvements persist even when the system is turned off, then the device is doing more than temporarily restoring function,” says Daniel Lu at the University of California, Los Angeles. “It may be helping the nervous system reorganise itself through neuroplasticity.”

This describes the brain’s ability to rewire itself by forming new neural connections, such as after an injury or even in response to a new hobby. “After an injury such as spinal cord injury, those same mechanisms may help restore function by strengthening spared pathways or recruiting alternative circuits, allowing neural signals to travel through networks that were previously too weak to support meaningful movement,” says Lu.

The researchers have observed stronger neural responses in Thomas’s sensory cortex since the intervention.

But this is just a single case report, so it’s unclear how well this approach would work on other people with paralysis from different types of injuries. Charles Greenspon at the University of Chicago says he has spent years working on stimulation to restore touch in people with spinal cord injuries and continues to find that some respond better than others, and some not at all. “And we have no idea why,” he says. “So, the question is: can you replicate it? This is a really ambitious study, but we need to see them replicating their results in more participants before we believe the hype.”

As to Thomas’s future, “at this point now we know nothing’s impossible, or anything’s possible”, says Boulton. “I think it’s possible he will continue to to improve,” he adds.

💬 Artificial intelligence and big data are flooding discovery pipelines with high-potential drug candidates, but this rapid innovation has created a new challenge. Simply put, our capability to design miracle molecules is vastly outstripping our technology to mass-manufacture them safely for the global public. Moving drug making from the scale of lab flasks to commercial bioreactors introduces non-linear biological and engineering shifts that can undermine tasks like purification.

⚡In this New Scientist CoLab podcast, experts from global life sciences leader Cytiva explain the hidden, high-stakes science of purification that is required to close the gap between drug discovery and the pharmacy shelf.

Our guests are:

Henrik Ihre, Distinguished Fellow, Cytiva

Paul Belcher, Business Leader, Cytiva

🎧 Stay tuned to learn about:

➡ The process of taking a drug from theoretical to the shop shelf

➡ How the drug purification works

➡ The human cost when purification goes wrong

➡ The challenges of keeping pace in manufacturing as AI supercharges drug discovery

Chapters:

(00:00) Intro – How drugs go from discovery to reality

(03:49) The purification process

(10:05) Why small scale success doesn’t mean industrial scale success

(13:00) The challenge of the expanding drug pipeline

(21:39) Understanding the molecules that are being purified

(23:20) What is a chromatography resin?

(25:24) Why purification gets more difficult later in the process

(27:15) The human impact when purification goes wrong

(32:59) The future of AI drug discovery

(37:52) Is AI helping with purification?

(40:32) How it feels to be advancing drug discovery

About the sponsor:

Cytiva: ⁠https://www.cytivalifesciences.com/ ⁠

About the podcast:

New Scientist CoLab explores the boundaries of innovation and the intersection of business, science and technology. Hosted by Justin Mullins.

Don’t miss an episode – subscribe now:

⁠https://www.youtube.com/@NewScientistCoLab⁠  

Connect with New Scientist:

Website: ⁠https://www.newscientist.com/⁠ 

Instagram: ⁠https://www.instagram.com/newscientist/⁠ 

The best treatment for multiple sclerosis (MS) might be antivirals that target the Epstein-Barr virus. Pharmaceutical companies are now being called on to develop such drugs after researchers studied the immune responses of people with and without the condition.

“There aren’t good Epstein-Barr virus drugs currently available, but they can be developed,” says Michael Levy at Harvard Medical School. “That might be the most useful specific therapy for MS in the future.”

MS is caused by an immune attack on myelin, a fatty sleeve that wraps around nerves. The loss of myelin reduces their ability to transmit signals and can cause a wide range of symptoms, including muscle weakness. Drugs that suppress the immune system can slow the progression of the condition.

There is strong evidence that the Epstein-Barr virus (EBV), which causes mononucleosis, or glandular fever, is also the cause of MS. “I think most MS researchers now would agree that EBV plays a major role in the development of the disease,” says team member Kjetil Bjornevik at the Harvard T.H. Chan School of Public Health.

But exactly how remains a mystery. Almost everyone is infected with EBV during their childhood or teen years. It mainly infects immune cells known as B-cells, where it can remain dormant for the rest of a person’s life. But in some cells, the virus can reactivate.

The big question is why only around 1 in 1000 people develop MS when nearly everyone gets EBV. This suggests there is something different about the immune response to EBV in people who go on to develop MS, says team member Natalia Drosu at Massachusetts General Hospital. “Our question for this study was: in people with MS, what parts of EBV does the immune system respond to? And do those responses look different from people who don’t have MS?”

The team focused on immune cells known as CD4 T-cells, which circulate in the body. Although these aren’t the cells that directly attack myelin, there are multiple lines of evidence suggesting they play a role in MS, says Drosu.

The team found that, in 30 people with MS, most of the CD4 T-cells targeting EBV were specifically targeting viral proteins produced when the virus is actively replicating, rather than the proteins associated with its dormant stage. What’s more, people with MS produced twice as many of these cells, on average, as 30 people without the condition.

Free newsletter

Sign up to Health Check

Sign up to newsletter

The researchers then looked at CD4 T-cells in 60 people with MS before and after they began drug treatments that reduce their number of B-cells. They found these treatments reduced the T-cell response to EBV almost to the levels seen in people without MS.

In addition, the team found low levels of EBV in the saliva of these people before they were treated to reduce their number of B-cells, which shows that the virus was replicating in their bodies. After treatment, viral levels dropped below detectable levels in most people.

The thinking has been that B-cells help drive the harmful immune response in people with MS, says Levy, and this is why drugs that reduce B-cell levels are effective. But the results suggest these drugs also work by eliminating B-cells infected with EBV, he says, thereby reducing the immune response caused by active viral replication. “We’re thinking that depleting B-cells is also depleting the reservoir of the Epstein-Barr virus.”

If so, targeting EBV directly with antivirals might be just as effective as B-cell-depleting drugs, but without the undesirable side effects of treatments that weaken the immune system, such as an increased risk of infections. “I think a lot of patients would prefer a specific drug,” says Bjornevik. “If we can show that an antiviral had a similar effect as the most effective MS drugs, I think there will be a big market for that drug.”

Another approach already being trialled for treating MS is using modified immune cells called CAR T-cells. While existing drugs merely reduce B-cell levels, CAR T-cells can temporarily eliminate them altogether. Dozens of people with MS have gone into remission after CAR-T treatment, says Levy.

Strongest evidence yet that the Epstein-Barr virus causes lupus

Lupus has been linked to the Epstein-Barr virus – which causes glandular fever, or mono – before, but we now have evidence of how it can bring about the autoimmune condition

But EBV might linger in some other cell types and reinfect B-cells as they slowly recover in the years after the CAR T-cell treatment, he says. “Then we would need the antivirals… so we just have to wait and see.” CAR T-cells can also have serious side effects, says Bjornevik, so antivirals could be safer as well.

There are also vaccines against EBV under development. “If people don’t get infected with EBV, their risk of MS would be virtually zero,” says Drosu. “So I think vaccines are [a] very promising strategy to eradicate MS.”

But 1000 people would have to be vaccinated to prevent just one case of MS, Levy points out. However, EBV causes many other problems, including a number of cancers, and has also been linked to other autoimmune conditions, such as lupus and rheumatoid arthritis.  

A monkey with a distinctive mask-like face, found in a remote part of the Democratic Republic of the Congo, has been declared a new species – only the fifth new species of monkey documented from Africa in the past 75 years.

The monkey is known as likweli to local people who hunt it for bushmeat, and it has been given the scientific name Colobus congoensis. It lives in one of the most inaccessible parts of Africa, without paved roads or infrastructure.

“A typical expedition involves multiple modes of transportation: a flight, followed by a motorcycle ride, two days of hiking on foot and finally travel by dugout canoe to reach the monkey’s range,” says Kate Detwiler at Florida Atlantic University.

One of the most intriguing features of likweli is its facial appearance, says Detwiler. The light-coloured skin around the mouth and beneath the nose is unlike that of any other African colobus species, but resembles the facial pattern seen in some Asian colobine monkeys.

Detwiler and her colleagues believe the species’ mask-like face may represent ancestral traits that were present before the African and Asian colobine lineages diverged over 8 million years ago. “If so, likweli may have retained characteristics that were subsequently modified or lost in the other African colobus species,” says Detwiler.

Free newsletter

Sign up to The Earth Edition

Sign up to newsletter

Like other colobus monkeys, likweli also has a distinctive body odour that defies description, she says.

Scientists first became aware of the species in 2008 when a team surveying on the banks of the Lomami river, in what is now Lomami National Park, took a photo that showed only a part of a monkey that had not been seen before, high in the canopy.

Then, in November 2018, another group again spotted the monkey, which is about 1.3 metres long and weighs around 7 kilograms. Between 2018 and 2022, there were 114 recorded observations of the new species, 25 of which were from vocalisations.

In 2021, several monkeys that had been killed by hunters for bushmeat were confiscated and handed over to researchers. Detailed morphological and genetic analysis confirmed they were indeed a wholly separate species. Genetic tests and recordings of their vocalisations also added to the evidence of their uniqueness.

“The genetic analyses revealed that likweli is a deeply divergent lineage that split from its closest known relative, Colobus satanas, approximately 4 to 5 million years ago,” says Detwiler. “That was much older than we expected and provided strong evidence that likweli represents a distinct species.”

Likweli is isolated from C. satanas by more than 1200 kilometres and several major river barriers. Unlike most other members of the genus, which have habitats exceeding 60,000 square kilometres, likweli is only known to exist in 1700 square kilometres of rainforest.

“Hunting is one of the primary threats facing likweli, particularly because the species has such a small known range and appears to occur at low densities,” says Detwiler.

Because of the risk of poaching and the monkey’s small population and home range, the team is proposing that the species should be listed as endangered. “Now that likweli has been recognised as a distinct species, another important step would be to grant it protected status under national law,” says Detwiler. “This would make it illegal to hunt the species, including in the buffer zone surrounding the park.”

When the final of the 2026 men’s football World Cup kicks off in New Jersey this weekend, players can expect temperatures of over 30°C (86°F). Indeed, much of the tournament has been played in challenging conditions – like the high elevation and thin air of Mexico City’s Estadio Azteca – giving pundits plenty to chew over.

But one factor has been less discussed: humidity. High temperatures may be uncomfortable, but it is really the combination of heat and high humidity that can make a football match – indeed, any activity – physiologically unbearable. Humid conditions make it harder for our bodies to benefit from sweating, as the air is already laden with moisture, hampering our ability to cool down.

This impact of humidity is still underappreciated. One way of taking both humidity and heat into account is the wet bulb globe temperature (WBGT), a measure of heat stress used by sports organisations. As New Scientist went to press, the most extreme match of this World Cup (Uruguay vs Cape Verde) had an estimated WBGT of over 33°C (91°F) – a level at which people are advised to suspend all outdoor activity. Most of us simply aren’t prepared for such conditions, as we explore here.

It is really the combination of heat and humidity that can make activities unbearable

Yet, if we understand the dangers of humidity, we can start to grasp the advantages of dry heat. We detail the many ways in which saunas and heat therapy can keep you healthy, from cardiovascular benefits to protection against Alzheimer’s disease. The key is that saunas operate at extremely low humidity, allowing us to sweat comfortably while reaping the benefits of getting decidedly hot.

Saunas aside, we should still be wary of extreme heat. With European heatwaves on the rise, the 2030 men’s football World Cup – to be played across Portugal, Spain and Morocco – is likely to see low humidity but temperatures of up to 40°C (104°F). With no sign of us cutting carbon emissions, the World Cups of the early 21st century may one day be fondly remembered as nice and cool.