A severe outbreak of invasive meningococcal disease, which can cause meningitis and sepsis, in Kent in the UK earlier this year was driven by a bacterial strain that took genes from harmless microbes. This helped the resulting bacteria evade the immune system and obtain iron from blood, boosting their growth.

鈥淲hat was really unusual about the outbreak is quite how explosive it was,鈥� says at Queen Mary University of London, who wasn鈥檛 involved in the discovery. 鈥淸The bacterium] clearly gained a set of genetic changes that made it better at hiding from the immune system and better at harvesting nutrients. That made it a really super powerful bug.鈥�

In March, 21 people 鈥� mostly university or high school students 鈥� are known to have become infected with a strain of Neisseria meningitidis group B at a nightclub in Canterbury, Kent. N. meningitidis usually spreads via close and prolonged contact with saliva from an infected person via things like kissing and sharing drinks or vapes.

N. meningitidis lives harmlessly in the nose and throat of without causing any health problems, but genetic changes can allow it to become more invasive and enter the bloodstream, leading to invasive meningococcal disease (IMD). This can result in sepsis, a life-threatening immune reaction to bacteria, or meningitis, where bacteria infect the thin lining surrounding the brain and spinal cord, causing inflammation.

All the IMD infections in Kent occurred within about a week. Those infected were treated in hospital, with nine requiring intensive care. 鈥淭he incredibly rapid nature of the outbreak was unprecedented [for the UK],鈥� says Wall. 鈥淯sually these [outbreaks] roll over two or three weeks and there鈥檚 one or two cases that end up in hospital.鈥�

To understand this, at the University of Oxford and his colleagues sequenced the entire genome of live N. meningitidis in blood samples taken from six of those infected, including the two people who died.

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These bacterial genomes were almost identical, suggesting the outbreak started from one person. Next, the team compared one of these genomes with 48,000 others from Neisseria strains collected during prior outbreaks or from people without known health problems.

This revealed that the Kent strain had acquired several genes from a harmless strain of N. meningitidis and another bacterium called Neisseria cinerea that lives harmlessly in . Bacteria constantly exchange genetic material via a process called horizontal transfer, which can involve them forming tiny tunnels between each other, through which they transfer copies of genes.

Some of the genes acquired by the Kent strain enhanced its uptake of iron from blood, which it needs to survive and replicate. Others reduced the amount of sugar that was coating a tail-like structure, called the pilus, on the bacterium. This enabled bacteria to clump together and evade destruction by immune cells, such as neutrophils. 鈥淣eutrophils will try and come and eat an individual [bacterium], but they can鈥檛 eat a clump, it鈥檚 too big,鈥� says Wall.

鈥淭here was this catalogue of changes that made this organism really transmissible, but also really invasive,鈥� says Maiden. This meant that several people became very ill and were then less able to transmit the infection to the public. 鈥淚f you鈥檙e ill, you鈥檙e not going to be going around transmitting organisms, so the outbreak ended very quickly,鈥� says Maiden.

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It is unclear exactly when these genetic changes occurred in the person believed to have initiated the outbreak, but they probably happened gradually, until there was the right combination of genetics and social mixing, says Maiden.

Such insights could support the development of better vaccines against N. meningitidis if we can target the features that make the bacterium particularly invasive, says Wall. But they won鈥檛 help us predict the next highly invasive strain. 鈥淸These bacteria are] inherently highly unpredictable,鈥� says Maiden.

Following the Kent outbreak, the UK government launched a for young people starting university or further education in September or October this year. Symptoms of IMD include fever, headache, a stiff neck, joint and muscle pain, and a rash that doesn鈥檛 fade when pressed with a glass.

Human brain organoids have been implanted into mice that are missing half their brain. Tiny versions of the human cerebral cortex 鈥� a region involved in memory, movement and thinking 鈥� were put into mice that lacked this major brain region. Not only did the organoids integrate into the mice鈥檚 brains, but they also restored most of their cognition.

鈥淭he mouse is [relatively] sick without a cortex, then you transplant these organoids in, and it behaves more like the normal mouse,鈥� says at the University of Cambridge, who wasn鈥檛 involved in the research.

at Stanford University in California and his colleagues genetically engineered mice to lack more than 90 per cent of their cortex, or about half their brain. These mice experience only some memory and movement deficits, since their brain adapts to compensate for their missing cortex, says Pa葯ca.

In about half of these mice, the team surgically implanted four human brain organoids, generated by bathing human stem cells in chemicals for about 40 days. These filled the cavity in each mouse鈥檚 skull, producing what the researchers called XCX mice. The remaining mice, apallial mice, didn鈥檛 receive the transplants.

A few months later, the apallial mice performed worse in a memory test, where they had to navigate a maze, than a third group of normal mice with intact brains. But this deficit was almost completely reversed in the XCX mice. The XCX mice also had a gait between that of the apallial and normal mice.

Scans revealed that the organoids had grown to form cortex-like grafts. 鈥淗alf the volume of the brain is [initially] gone, and now largely 90 per cent of that missing volume is covered by human cells,鈥� said Pa葯ca.

This builds on prior studies that have implanted human brain organoids into rat or mouse brains, but without such a large part of the rodent brain being missing initially, says Pa葯ca. These studies showed only that such organoids can alter cognition, rather than improving it, he says. For instance, in one study, light stimulated human brain organoids in rats to make them anticipate water.

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The grafts in the latest study were also the first to contain a kind of nerve cell, called von Economo neurons, that influences social skills, as well as neurons that extended from the cortex to the spinal cord. The latter could explain why these grafts reduced impairments in motor skills, says Balmu葯.

The team鈥檚 organoids were larger and more akin to the human cerebral cortex than those used in previous experiments, says Pa葯ca. But according to at the Institute of Molecular Biotechnology in Vienna, Austria, they still lack the proper arrangement and structure of the cortex. 鈥淚t鈥檚 a bit of a mishmash of neurons鈥� and other cells, he says. 鈥淢ost of the cell types are there, but they鈥檙e not separated into regions like in a normal cortex.鈥�

In another experiment, the team showed that human organoid transplants made mice respond to hypoxia, or low oxygen levels, in a way similar to people. Mice have evolved to be highly resilient to low oxygen levels, due to living underground, so it is hard to replicate this in a normal mouse, says Balmu葯. This suggests that these experimental animals could provide a better way to study cerebral palsy, a condition that causes movement problems and can be caused by hypoxia around birth, says Balmu葯.

But such experiments come with ethical concerns, says Knoblich. These mice 鈥渄eserve the same kind of protection that we ascribe to any animal experiment, meaning that we need to make absolutely sure that there鈥檚 no sensation of pain, that there is no unnecessary suffering, and that the risk of the experiment is matched to the medical gain,鈥� he says. The latest study achieved this, he says.

A common concern is whether mice with human brain organoids will gain a human-like level of consciousness. 鈥淭he data so far doesn鈥檛 say that putting [a human organoid] in makes the mouse smarter or more conscious than a normal mouse,鈥� says Knoblich. 鈥淚t鈥檚 similar to taking a wheel from a car and putting it on a tree and saying that鈥檚 a car.鈥�

A brain implant has enabled people with paralysis to speak while gesturing, such as nodding or waving. These sorts of exchanges, done via an avatar, could help them communicate with more nuance.

鈥淚n our everyday life, gestures play an important role in communication,鈥� says at the University of California, San Francisco. 鈥淪aying 鈥榤aybe鈥� and nodding your head has a very different connotation than if you shake your head.鈥�

Experimental brain implants have boosted the ability to either speak or move among people with paralysis, but simultaneously haven鈥檛 been very successful. To achieve this, implants need to cover a large part of the sensorimotor cortex, a brain region involved in speech and movement, says Brosler.

Now, Brosler and her colleagues have tested an iPhone-sized implant in this part of the brain in two people with paralysis. The first participant, who the researchers call Bravo-1r, became paralysed after a stroke, while the second, Bravo-6, had amyotrophic lateral sclerosis, the most common form of motor neuron disease.

Both participants had lost almost all movement in their limbs. They also couldn鈥檛 speak and could only make unintelligible sounds.

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First, the team recorded the participants鈥� brain activity while they repeatedly attempted to say 10 phrases 鈥� such as 鈥渉ello鈥�, 鈥渘ice to meet you鈥� and 鈥渉ow鈥檚 it going?鈥� 鈥� or perform 10 gestures, like waving, clapping and shaking their head. In some cases, the participants attempted to do these separately, while in others they tried both simultaneously.

The team then used each of the participants鈥� brain recordings to train customised machine learning models to predict their intended phrases and gestures.

To put the models to the test, the participants attempted to repeat various pairs of phrases and gestures that were displayed on a screen. The models interpreted their brain activity and used that to control the movement of an avatar resembling the participants, while the speech predictions flashed up on the screen.聽

The team chose to use avatars, rather than attempting for the individuals themselves to speak and gesture, because this offered a relatively simple way to prove that both actions could be simultaneously decoded from brain activity, says Brosler.

Paralysed man can feel objects through another person鈥檚 hand

Keith Thomas, a man in his 40s with no sensation or movement in his hands, is able to feel and move objects by controlling another person's hand via a brain implant. The technique might one day even allow us to experience another person's body over long distances.

Bravo-1r鈥檚 intended gestures and speech were predicted with 88 and 84 per cent accuracy, respectively, while Bravo-6鈥檚 were predicted with 66 and 70 per cent accuracy. 鈥淚f those models were operating on complete chance, the accuracy would be like 9 per cent,鈥� says Brosler. 鈥淚t was really exciting.鈥�

鈥淚t鈥檚 a very nice piece of work, with robust results,鈥� says at the University of Lausanne in Switzerland. But it鈥檚 based on a very limited set of phrases and gestures, and these still need improving, he says. 鈥淔or daily use without frustration, there needs to be higher accuracy.鈥�

Brosler says the team is working to address this by further training the models and tweaking the algorithms. She also says that future models could move a person鈥檚 own body 鈥� if their joints and muscles are in a good enough condition 鈥� and produce a synthetic voice, rather than having to do this via an avatar.

Sleeping while listening to bursts of pink noise 鈥� background sounds akin to gentle radio static 鈥� seems to boost the flow of fluid through the brain, and so might enhance the clearance of waste products that are linked to conditions like Alzheimer鈥檚 disease. The pink noise seems to bolster the slow brainwaves that enhance the pumping of blood vessels, which drives the brain鈥檚 waste-disposal system.

We already knew that listening to bursts of pink noise during sleep , a kind of electrical activity that occurs during certain phases of聽non-REM聽sleep, known as聽N3 (deep sleep) and N2 (the lighter stage before it). This effect occurs when the bursts coincide with the peaks of slow brainwaves.

鈥淭hey really don鈥檛 sound like much, they鈥檙e just little staticky beeps,鈥� says at Boston University in Massachusetts.

Prior research has also shown that boosting slow brainwaves 鈥� using drugs, for instance 鈥� can enhance the flow of the brain鈥檚 cerebrospinal fluid (CSF), which bathes the brain and carries away waste products.

But it was unknown whether listening to pink noise has the same effect. That鈥檚 because measuring the brain鈥檚 CSF flow involves imaging it with MRI scans, but MRI interferes with EEG, the technique used to measure waves of electrical activity in the brain. One consequence of this interference is that slow waves recorded via EEG during MRI scans can鈥檛 be detected fast enough to align bursts of pink noise with their peaks.

鈥淵ou have to do a lot of extensive processing of the EEG signals to detect slow brainwaves, so it鈥檚 hard to do that fast enough in real-time,鈥� says at the Massachusetts Institute of Technology.

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To overcome this problem, Levitt, Lewis and their colleagues used EEG data collected during MRI scans from prior studies to train an AI model to rapidly predict when the brain鈥檚 slow waves will peak. 鈥淸The AI] says, 鈥業n about 70 milliseconds, a slow wave peak is coming,鈥� so now we should schedule our sound stimulation to arrive in accordance with that,鈥� says Levitt.

鈥淭his, methodologically, really moves the field forward,鈥� says at the University of New Mexico.

The researchers then recruited 27 healthy adults, aged 29 on average, to wear EEG electrodes on their scalp while taking an afternoon nap in an MRI scanner. Of these, 14 managed to fall asleep and enter N2 sleep. 鈥淚t鈥檚 a difficult place to fall asleep,鈥� says Lewis.

At the peak of half of each participant鈥檚 slow brainwaves, the researchers used the AI model to play 50-millisecond bursts of pink noise. During the remaining slow brainwaves, they played no noise as a control.

By analysing the MRI and EEG recordings, they found that bursts of pink noise strengthened the slow waves they coincided with and briefly boosted the flow of CSF into the brain, compared with no sonic stimulation. This suggests the pink noise also enhanced the flow of CSF through, and out of, the brain. 鈥淲e know that the flow in is usually balanced with the flow that comes out,鈥� says Lewis.

The increased CSF flow seemed to be driven by enhanced pumping of the brain鈥檚 blood vessels, which is known to push fluid through the brain鈥檚 waste-disposal system, called the glymphatic system.

Off the back of these results, the team is exploring whether the approach also works in older adults and whether it can boost the clearance of proteins, such as beta-amyloid, that are linked to conditions like Alzheimer鈥檚 disease. If the results are positive, the researchers hope to test whether the technique can slow cognitive decline in people during normal ageing, mild cognitive impairment 鈥� a condition that often precedes dementia 鈥� and the early stages of Alzheimer鈥檚 disease.

Exercise may create new neurons by making other brain cells contract

Physical activity causes a type of brain cell called astrocytes to contract, which then leads to the formation of new neurons, according to a study in mice

There is reason to think this could work. Exposing people to sounds and flickering lights 鈥� while they are awake 鈥� has previously shown promise at slowing cognitive decline in people with Alzheimer鈥檚, potentially by boosting the glymphatic system.

But one benefit of the new approach is that it could eventually be delivered via a portable device while people are sleeping, which could be less disruptive, says Ryman.

We cannot live without soil. It provides us with building materials, most of our antibiotics and 95 per cent of our food.

In, photographer and soil ecologist Frank Ashwood urges us to better appreciate and protect the soil we rely on. He does so with stunning images of the creatures that call soil home.

The adorable velvet worm in the main image was found under a log in a misty beech forest on the South Island of New Zealand. 鈥淭hey look like little worms rolled in sequins,鈥� says Ashwood. But looks can be deceiving: 鈥淭hey crawl around and shoot glue out of special organs on their heads to immobilise their pray, which they鈥檒l then go and eat while alive.鈥�

A droplet of sperm deposited by a male springtail, a tiny insect-like creature, sits atop a delicate stem made of protein-rich secretions in the image below. 鈥淚t鈥檚 like a lollipop, basically, with a bit of sperm-rich fluid on the top, which the males leave for the females to come and find,鈥� says Ashwood.

But beware any marauding rivals. 鈥淚f a male finds another springtail鈥檚 spermatophore, they will actually eat it to destroy it,鈥� he says.

Below, a beautiful woodlouse spider stares straight down the lens of Ashwood鈥檚 camera. Its large fangs have evolved to better hunt woodlice. 鈥淭hey鈥檒l come at a woodlouse from the top or the side, grasp it, then reach underneath with those sharp bits of the fangs and pierce into the soft underbelly,鈥� he says.

A bright yellow slime mould stretches across a decaying log in the shot below. 鈥淚t鈥檚 a big, sprawling mass of a single cell, essentially; they branch out looking for food,鈥� says Ashwood. The mould鈥檚 efficient networks have been used to map road networks, the fastest way out of an IKEA showroom and dark matter throughout the universe, he says.

This gorgeous giant springtail, below, was found in a forest in New Zealand. Its orange spines help it camouflage against logs. 鈥淏ecause they鈥檙e rare, when you do see one, it鈥檚 a moment of pure exhilaration,鈥� says Ashwood. 鈥淭hey鈥檙e an indicator of the forest being in really good condition.鈥�

Ashwood, who is based at Lincoln University in New Zealand, snapped the silvery springtail below while in the UK. During the Victorian period in the 1800s, their iridescent scales were used to test microscopes. 鈥淭hey鈥檝e got really ornate, tiny sculpturing on them, so the better detail you could see, the better your microscope,鈥� he says.

Ashwood hopes his book will encourage people to protect soil, for instance by reducing deforestation and farming more sustainably. 鈥淥ver half of the world鈥檚 biodiversity is in soil, and we鈥檙e losing it at a rate that is not sustainable,鈥� he says.

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Psilocybin may prevent a debilitating side effect of chemotherapy: nerve damage that can cause lasting numbness, tingling or pain in the hands and feet. In tests in nerve samples from mice and humans, the psychedelic seemed to maintain the energy supply in nerve endings that is commonly disrupted by chemotherapy, resulting in less damage and fewer complications.

This is the first time a therapy has been shown to prevent this common side effect, which lacks effective treatments and can limit access to cancer drugs.

鈥淚f these findings can be replicated in clinical trials, the implications could be substantial,鈥� says at the University of Reading in the UK, who wasn鈥檛 involved in the research. 鈥淧atients could avoid long-lasting sensory problems and chronic pain that often remain after cancer has been successfully treated.鈥�

What鈥檚 more, 鈥渋f nerve damage can be prevented, fewer patients may need dose reductions or interruptions of chemotherapy, potentially improving cancer outcomes鈥�, she says.

But people with cancer shouldn鈥檛 take psilocybin, the psychedelic compound in magic mushrooms, without medical supervision. 鈥淧lease don鈥檛 take psilocybin at home for chemotherapy-related pain,鈥� says team member at the University of Texas MD Anderson Cancer Center in Houston. 鈥淚t hasn鈥檛 been shown to be safe or effective in patients undergoing chemotherapy. It can interact dangerously with cancer medications.鈥�

Chemotherapy-induced peripheral neuropathy (CIPN) affects about 75 per cent of cancer patients who undergo the treatment to some extent, said , also at the University of Texas MD Anderson Cancer Center, in a press briefing. It is usually treated with duloxetine, an antidepressant that provides moderate pain relief. But no drug had been shown to prevent CIPN, said Amit at the briefing.

CIPN occurs when chemotherapy drugs enter nerve cells and . These are railway-like structures that usually transport mitochondria from the main body of neurons, near the spinal cord, to nerve endings in the skin. The mitochondria supply energy to maintain nerve endings, but the disruption means they wear out and retract, causing issues like tingling.

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The researchers wondered whether psilocybin, , could preserve these nerve endings.

To find out, they studied a group of mice with abdominal tumours, half of which were given two doses of psilocybin 鈥� each equivalent to a 25-milligram dose in people 鈥� via injections into the abdomen, one week apart. The remaining mice had saline injections. All of them then received daily injections of cisplatin, a type of chemotherapy that commonly causes CIPN, for one week.

After receiving cisplatin, the mice underwent pain-sensitivity tests, where they were touched with a thin plastic filament to see how they responded. Those that received psilocybin before cisplatin responded similarly to a third group of mice with cancer that didn鈥檛 receive cisplatin or psilocybin. The mice that received cisplatin without psilocybin seemed to be much more sensitive to the filament鈥檚 touch.

To explore how psilocybin may be having this effect, the team analysed nerve samples from the mice. This showed that, after the psychedelic is processed to its active ingredient, psilocin, it activates a receptor called 5HT2A, . But it also revealed that this receptor sends molecular signals that prevent chemotherapy-related disruption of mitochondrial transport.

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Psilocybin appears to alter brain networks linked to repetitive negative thoughts, which may explain how the drug helps to treat some mental health conditions

Finally, the researchers confirmed the results in human neurons treated with either psilocybin or a saline solution before receiving cisplatin. 鈥淧silocybin seemed to help nerves withstand the toxic effects of chemotherapy and maintain normal function,鈥� says Maiaru.

They now plan to begin a . This will be made up of about 80 people with breast, colorectal or head and neck cancer, testing two doses of psilocybin before chemotherapy. Results are expected in about five years.聽

Psilocybin has already been shown to relieve symptoms of depression and anxiety in people with cancer. Although not a psychedelic, cannabis is also approved to treat in the UK. The US Food and Drug Administration has also that are made up of chemicals similar to those in cannabis to relieve chemotherapy-related nausea and vomiting.

Neurons have been created from a different type of brain cell that usually supports them. Nerve cell death is a hallmark of Alzheimer鈥檚 disease, but a cage of nanoparticles containing antibodies converted astrocytes, another type of brain cell, into neurons in mice with a version of the condition. This boosted the mice鈥檚 cognitive skills. The researchers behind the approach hope to test it in people in the next few years.

鈥淲e can replace lost neurons and also reverse Alzheimer鈥檚 disease progression [in mice],鈥� says at the University of South Carolina.

In Alzheimer鈥檚 disease, which , the proteins beta-amyloid and tau misfold and form clumps, known as plaques and tangles. This leads to neuroinflammation and, ultimately, nerve cell death.

Researchers are increasingly exploring whether stimulating the growth of new neurons could treat Alzheimer鈥檚 disease and other neurodegenerative conditions. For instance, in 2020, scientists discovered that astrocytes 鈥� star-shaped cells that help neurons function 鈥� in the brains of mice with a version of Parkinson鈥檚 disease, which improved their motor skills.

This involved using CRISPR to genetically engineer the mice to deplete levels of a protein called PTBP1. This usually acts like a master switch that stops astrocytes from turning into neurons.

But such genetic approaches can alter regions of the genome you didn鈥檛 intend to target. 鈥淵ou can sometimes cut the wrong places, causing permanent genetic changes that may be harmful,鈥� says Xu.

To address this issue, he and his colleagues have developed another way to deplete PTBP1. They designed a drug called TN-PTBP1 that packages PTBP1-targeting antibodies within a cage of nanoparticles that shuttles them across the blood-brain barrier.

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The drug enters cells in the brain, including astrocytes, where the antibodies bind to and substantially deplete PTBP1. After about a week, the antibodies are recycled by the cell, says Xu.

The team has now tested this in brain organoids made up of clumps of astrocytes and neurons, which were grown from human stem cells in a lab dish. This showed that TN-PTBP1 converts astrocytes into neurons.

Next, the researchers tried the approach in 12 mice that had been genetically engineered to develop a condition mimicking Alzheimer鈥檚. Prior to receiving TN-PTBP1, brain imaging revealed that these mice had lost a substantial number of neurons, similar to what is seen in moderate-to-severe Alzheimer鈥檚 disease, says Xu. The mice struggled to build nests and performed poorly in a memory test that involved navigating a maze.

The team intravenously injected half of the mice with TN-PTBP1 twice over two weeks, while the rest received saline injections. Two weeks later, the mice that received TN-PTBP1 were able to nest and navigate the maze at a similar level to another group of mice without the version of Alzheimer鈥檚, while the saline group showed no change. 鈥淭here鈥檚 clearly an improvement, which is very thought-provoking,鈥� says at the University of Cambridge.

When the researchers analysed samples of the mice鈥檚 hippocampi, an area of the brain involved in memory and learning, they found that TN-PTBP1 had caused new neurons to sprout in the brain. 聽

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They are now planning more studies in mice where astrocytes are labelled with fluorescent tags to track whether TN-PTBP1 is really behind those cells converting into neurons, says Xu. The researchers also hope to test the approach in monkeys and people in the next few years, he says.

The mice showed no signs of side effects, but future work should explore whether the newly formed neurons safely integrate into the brain鈥檚 networks without disrupting their function over the long term, says at King鈥檚 College London. 鈥淲e need to check [whether] these neurons [would] be beneficial, rather than screwing up the network.鈥�

But with proper testing, the potential of this drug could be huge, he says. It 鈥渃ould have an enormous effect on the treatment of many brain diseases鈥�, including schizophrenia, motor neuron disease (such as ALS) and Parkinson鈥檚 disease, he says.

Getting vaccinated against shingles could significantly reduce your risk of cardiovascular problems. A study of more than 72,000 people suggests that those who have received the latest shingles vaccine are less likely to develop conditions like stroke or heart failure than individuals who got an older version of the jab. This may be because the latest vaccine contains a chemical that boosts the immune response and may reprogram immune cells to cause less inflammation.

The same vaccine has previously been linked to a significantly lower risk of dementia. 鈥淧eople should get their shingles vaccine not only because it stops them getting shingles, which in [and] of itself can be very unpleasant and quite dangerous, but also it potentially gives you protection against dementia and heart disease,鈥� says at Imperial College London, who wasn鈥檛 involved in the study.

Shingles is an infection caused by reactivation of the varicella-zoster virus, which causes chickenpox. The condition, which causes a painful rash that can get infected, .

In 2025, a study linked being vaccinated against shingles to having a reduced risk of cardiovascular conditions, but this was based on comparing people who choose to get vaccinated with those who don鈥檛. Vaccinated people tend to have healthier lifestyles in general, making it unclear whether shingles vaccination itself really boosts cardiovascular health, said at the University of Oxford during a press briefing.

To address this, Taquet and his colleagues made use of the fact that, in October 2017, the standard shingles vaccine administered in the US switched from Zostavax to Shingrix. The former contains a live, weakened version of the varicella-zoster virus, while Shingrix is made up of a protein from the virus, along with a chemical that strongly stimulates immunity, called AS01.

The team analysed the medical records of more than 72,000 people aged 60 and older, about half of whom received Zostavax between April and September 2017. Nearly all the remaining participants received Shingrix the following year.

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By 3.5 years after vaccination, 10.9 per cent of participants who had Zostavax had developed at least one of three conditions: heart failure, stroke or clogged arteries in the heart. This is compared with 9.6 per cent in the Shingrix group 鈥� a small but statistically significant difference.

鈥淓ven though the percentage changes are small, the absolute numbers of heart disease cases are high, so it can lead to a large actual number of people being protected,鈥� says Tregoning.

This benefit waned over the next 3.5 years but was still higher in the Shingrix group.

This is the best evidence yet that being vaccinated against shingles reduces the risk of cardiovascular disease, says Taquet. 鈥淥ur study leverages a natural experiment that mitigates many of [the] biases [associated with observational research] and provides a more reliable estimate of the effect of Shingrix on cardiovascular disease,鈥� he says.

The availability of Shingrix in the US in October 2017 coincided with eligibility for a shingles vaccine being lowered from age 60 to 50. The researchers estimate that if everyone aged 50 and older in the US received Shingrix, it could delay or prevent hundreds of thousands of cases of cardiovascular problems within a decade, said Taquet. Currently, only about a get it. anyone who turned 65 on or after 1 September 2023.

How Shingrix curbs cardiovascular issues is unclear, but prior research suggests that AS01 reprograms immune cells known as monocytes to , called cytokines, said team member , also at the University of Oxford, during the press briefing. These promote the clogging of blood vessels, she said.

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We think of our body clock ticking over on a 24-hour cycle, but evidence is growing that it has seasonal rhythms, which could affect our response to vaccines

, which may further lower the risk of cardiovascular problems, says Tregoning. 鈥淚f you have a viral infection, you鈥檒l then get inflammation in your body, and that will then put stress on your other organs, including the heart,鈥� he says.

In an , more than 160,000 people aged 65 and older in Denmark will receive either Shingrix or no shingles vaccine. This should provide even stronger evidence for a causal link between Shingrix and a lower risk of both cardiovascular outcomes and dementia, said Taquet.

Initial results are expected in 2027. If positive, offering Shingrix as a booster vaccine every few years could significantly improve cardiovascular health and lower healthcare costs, he said.

Hubs of immune cells in the skull may help to defend our brain from ill health. A study into the brains of mice and human genetic data suggests that immune cells cluster in a particular area at the back of our skull. The discovery implies that targeting these hubs with drugs could bring new treatments for conditions where immune cells go rogue, such as brain cancer.

鈥淚t鈥檚 an important step forward in understanding the brain鈥檚 immune response,鈥� says at the University of Oulu in Finland, who wasn鈥檛 involved in the study. As well as being applicable for cancer, 鈥渋t鈥檚 relevant for understanding things like infections, inflammatory brain diseases, multiple sclerosis [and] neurodegenerative diseases鈥�, he says.

Immune cells called T-cells and B-cells are activated to act in the brain if they are presented with signs of threats, like fragments of tumours, in the lymphatic system. Now, at Washington University in St. Louis, Missouri, and his colleagues have uncovered another way these T- and B-cells are activated.

By imaging and analysing the skulls of mice, the team found that B- and T-cells cluster together with immune cells called antigen-presenting cells in immune hubs at the back of the skull. 鈥淭hese haven鈥檛 been described before,鈥� says Kiviniemi. These hubs resemble lymph nodes, where antigen-presenting cells expose threats like tumour fragments to T- and B-cells.

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The team thinks these immune hubs are also in people. This is based on gene activity data collected from human skulls in prior studies, which suggest that T-cells were activated and helped activate B-cells in this part of the body. 鈥淚t indicates the same is present in humans鈥�, says Kiviniemi, although further studies analysing the skulls of cadavers are needed to confirm this.

To explore whether these hubs launch protective immune responses, the researchers injected cancer cells into the brains of mice. They then injected half the mice beneath the scalp with an experimental drug that disrupts the activation of B- and T-cells in the skull. This works by blocking a protein called CD40L on antigen-presenting cells, which helps them activate these immune cells. The remaining mice received saline injections. 聽

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The mice that received the drug went on to live for about 25 days, on average, after the tumour injection, whereas those in the placebo group lived about 30 days. This suggests the immune hubs help to generate an anti-cancer immune response, says Kiviniemi.

In another experiment, a group of mice was given the same tumour injection, but this time, half received three drugs that enhanced the activation of B- and T-cells in their skull. These mice survived for about 10 days longer than others that got placebo injections.

If the same immune hubs are confirmed to exist in people, targeting them could bring new therapies for many brain-related conditions, says Kiviniemi. 鈥淲e could figure out how to awaken and strengthen these [hubs],鈥� he says.