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.

“If these findings can be replicated in clinical trials, the implications could be substantial,” says at the University of Reading in the UK, who wasn’t involved in the research. “Patients could avoid long-lasting sensory problems and chronic pain that often remain after cancer has been successfully treated.”

What’s more, “if nerve damage can be prevented, fewer patients may need dose reductions or interruptions of chemotherapy, potentially improving cancer outcomes”, she says.

But people with cancer shouldn’t take psilocybin, the psychedelic compound in magic mushrooms, without medical supervision. “Please don’t take psilocybin at home for chemotherapy-related pain,” says team member at the University of Texas MD Anderson Cancer Center in Houston. “It hasn’t been shown to be safe or effective in patients undergoing chemotherapy. It can interact dangerously with cancer medications.”

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 – each equivalent to a 25-milligram dose in people – 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’t receive cisplatin or psilocybin. The mice that received cisplatin without psilocybin seemed to be much more sensitive to the filament’s 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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Finally, the researchers confirmed the results in human neurons treated with either psilocybin or a saline solution before receiving cisplatin. “Psilocybin seemed to help nerves withstand the toxic effects of chemotherapy and maintain normal function,” 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. 

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’s 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’s cognitive skills. The researchers behind the approach hope to test it in people in the next few years.

“We can replace lost neurons and also reverse Alzheimer’s disease progression [in mice],” says at the University of South Carolina.

In Alzheimer’s 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’s disease and other neurodegenerative conditions. For instance, in 2020, scientists discovered that astrocytes – star-shaped cells that help neurons function – in the brains of mice with a version of Parkinson’s 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’t intend to target. “You can sometimes cut the wrong places, causing permanent genetic changes that may be harmful,” 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’s. 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’s 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’s, while the saline group showed no change. “There’s clearly an improvement, which is very thought-provoking,” says at the University of Cambridge.

When the researchers analysed samples of the mice’s 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.  

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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’s networks without disrupting their function over the long term, says at King’s College London. “We need to check [whether] these neurons [would] be beneficial, rather than screwing up the network.”

But with proper testing, the potential of this drug could be huge, he says. It “could have an enormous effect on the treatment of many brain diseases”, including schizophrenia, motor neuron disease (such as ALS) and Parkinson’s 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. “People 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,” says at Imperial College London, who wasn’t 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’t. 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 – a small but statistically significant difference.

“Even 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,” 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. “Our 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,” 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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, which may further lower the risk of cardiovascular problems, says Tregoning. “If you have a viral infection, you’ll then get inflammation in your body, and that will then put stress on your other organs, including the heart,” 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.

“It’s an important step forward in understanding the brain’s immune response,” says at the University of Oulu in Finland, who wasn’t involved in the study. As well as being applicable for cancer, “it’s relevant for understanding things like infections, inflammatory brain diseases, multiple sclerosis [and] neurodegenerative diseases”, 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. “These haven’t been described before,” 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. “It indicates the same is present in humans”, 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.  

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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. “We could figure out how to awaken and strengthen these [hubs],” he says.

Tiny versions of the cerebral cortex, a brain region involved in thinking and memory, have been grown for five years, making them the longest-lived brain organoids that have been studied in detail. Their genetic activity also mimicked that typically seen in the brain of a 4-year-old child, suggesting that the organoids could sense time passing.

“This demonstrates for the first time that not only can human brain organoids be grown for about five years, but they also show an ageing profile that corresponds with that of the developing brain of a similar age,” says at the University of Cambridge, who wasn’t involved in the study.

Brain organoids are clumps of brain cells grown in a lab dish. They are created by bathing stem cells in chemicals that coax them to form clumps resembling fetal brains. Studying them has already provided insights on autism and conditions like dementia. But the expense and manual labour involved means they are usually only grown for a few months, says Lakatos.

In 2021, researchers reported growing , with these structures mimicking the cerebral cortex from its development during pregnancy to nearly one year after birth.

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Now, at Harvard University and her colleagues have analysed the genetic activity of five-year-old cortical organoids grown from human stem cells. The team has grown the same kind of organoids for seven years, but there are too few of these older organoids to reliably analyse them, she says.

The researchers analysed the genetic activity and epigenetic marks – chemical tags added to DNA that regulate gene activity and shift with age – in cells within the five-year-old organoids. When comparing these measurements against those recorded from the brains of fetuses in previous research, they found that, at three to six months, the organoids resembled the fetal brain at around three to six months post-conception.

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With time, the organoids resembled the later stages of brain development, with the activity of five-year-old organoids mimicking that seen in the cerebral cortex of a typical 4-year-old child. “They were recording the passage of time in their epigenetic signatures [and gene activity],” says Arlotta.

Such long-lived organoids could offer a way to study how autism and conditions such as epilepsy emerge during the later stages of brain development, says Lakatos. Arlotta says she and her colleagues are using their organoids for this purpose, as well as to screen for drugs that may be able to alter the progression of conditions like epilepsy.

Other groups of researchers won’t be readily able to do this, due to the challenges of growing organoids, says Lakatos. Finding ways to speed up organoid ageing will be important for research, he says.

Our memories may persist even when half of the brain connections that store them are wiped out, according to a study in dormant mice. The “remarkable” discovery tells us more about how memory works and could one day reveal ways to improve it.

“Memories may be harder to break than we thought,” says at Boston University, who wasn’t involved in the study. “This absolutely, substantially advances our understanding of how memory works.”

When we experience a stimulus, neurons in our sensory organs, like our eyes, transmit electrical signals to our brain. Neurons then process this information by firing electrical signals to each other via junctions called synapses.

These neurons, called engram neurons, encode information into a memory by forming new synapses and strengthening existing ones. Recalling a memory .

Many scientists think a memory persists as long as the specific pattern of synapses on the engram neurons encoding that memory is maintained. This is partly based on experiments that have used drugs or genetic tools to , says at the Okinawa Institute of Science and Technology in Japan.

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But recent studies suggest a memory persists in location or number. This has called into question “what’s necessary and sufficient to have a memory preserved”, says at Yale University.

To address this, Tanaka and his colleagues took inspiration from hibernating animals. “Under hibernation, brain activity seems to drop significantly,” he says. “But studies in natural hibernators show that somehow those animals, after arousal in the spring, seem to remember their friends and the location of food they hid before hibernation.”

By examining how memory is retained during hibernation, a situation in which the brain changes dramatically, the researchers hoped to unpick basic principles by which the mammalian brain stores memories long term. “The [researchers] very cleverly and creatively get at the question of memory by using hibernation as a way to poke and prod at the brain,” says Ramirez.

They applied weak electric shocks to the feet of mice – which don’t naturally hibernate – while they were in a chamber that smelled of alcohol, creating a fearful memory associated with that scent. The next day, the mice froze in fear upon being placed in the same chamber, without receiving shocks.

The researchers induced an artificial state of hibernation in about half the mice for two days. This was done by injecting them with drugs that slow metabolism and placing them in a dark chamber.

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Five days later, mice that had artificially hibernated still froze when placed in the alcohol-smelling chamber. This was despite brain scans revealing that more than half of the synapses within the engram neurons in their hippocampus – a brain region crucial for memory – disappeared during hibernation. “Despite massive brain remodelling during hibernation, the memories were retained,” says Tanaka.

Dragoi says the findings are relevant to people, since prior research has shown that our brains store information very similarly to mice. “It tells us something about how our mammalian brains may work,” says Ramirez.

The team also found that the hibernating rodents’ brains retained synapses that clustered closely together on the surface of engram neurons, while those outside these clusters disappeared. This suggests that clustered synapses specifically are crucial for retaining memory in the brain, says Tanaka.

Non-clustered synapses that were wiped out by hibernation reappeared within a day post-hibernation, indicating that, while clustered engram synapses are necessary to retain the information within memories, the non-clustered synapses may be important for accessing memories, he says.

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“This study is a remarkable step forward because it addresses a long-standing puzzle in memory research: how the brain retains long-term memories,” says at Vrije University Amsterdam in the Netherlands.

The team is exploring the molecular pathways through which clustered engram synapses store information and plans to dig into how non-clustered ones reappear, says Tanaka.

Targeting such pathways with drugs could even reveal ways to prevent or slow memory impairment, says Ramirez. “It gives hope that even in instances where information seems to be lost in the brain, whether it’s amnesia or Alzheimer’s disease, memory may nonetheless persist.”

Protein-rich products – from cereal to crisps to coffee – are all over supermarket shelves, but mounting evidence in non-human animals suggests that restricting our intake could slow ageing and extend lifespan. So, does that mean eating too much protein is harmful?

“We have this impression that dietary protein is sort of a universally good thing,” says at the University of Wisconsin-Madison. But according to the latest review of the evidence, “increasing dietary protein, beyond what’s needed, for sedentary individuals or animals leads to metabolic problems and can lead to shorter lifespan as well”, he says.

But others point out that nutritional studies in animals like mice and rats don’t readily translate to people, and a high protein intake has been linked to benefits in humans.

Lamming and his colleagues sifted through more than 300 studies, mostly in sedentary rodents, that explored how restricting protein intake to the minimum required to prevent deficiency affects ageing and lifespan.

In these studies, rodents generally either ate the equivalent of the minimum protein requirement recommended by US guidelines – 0.8 grams of protein per kilogram of body weight – or about double that. The latter is similar to the intake recently recommended by US dietary guidelines for optimal health, 1.2 to 1.6 grams of protein per kilogram of body weight.

In one study, rats that ate around the minimum protein intake lived nearly 120 days, or more than 50 per cent, longer than those that ate about double that.

This may be because protein restriction increases levels of the hormone FGF21, says Lamming. In rodents, this acts on the brain, fat tissue and the liver to improve blood sugar levels and reduce the number of senescent cells. These cells, which accumulate with age, have stopped dividing and cause chronic inflammation.

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Restricting protein intake has also been shown to dampen the activity of a protein called mTORC1 in mice. mTORC1 ordinarily stimulates cell growth, but reducing its activity boosts cellular repair. “It essentially switches cells from a proliferative state, where they’re growing and engaging a lot of metabolism, to one where they’re dividing more slowly, if at all, and focusing on repair,” says Lamming. Studies suggest this in mice, he says.

All this suggests that the recent trend to up our protein intake is probably fine among people who exercise regularly, because they may need more protein to repair muscle damage, but eating more than is needed could cause harm in sedentary individuals, says Lamming.

But at the University of Illinois Urbana-Champaign points out that rodents vary hugely from people when it comes to protein metabolism. For instance, mTORC1 is activated by feeding, and while people tend to a have a few big meals a day, rodents graze more regularly. Protein restriction may therefore affect mTORC1 pathways differently between the different species, he says. We are also more exposed to factors that accelerate ageing, like infections and extreme heat, than lab animals, says Layman.

What’s more, the review does not include most of the studies in people that suggest that upping our protein intake beyond the minimum , he says.

Lamming says no studies were intentionally omitted. “We were focused on protein restriction, not the many studies looking at higher levels of protein intake,” he says. Beyond building muscle and preventing frailty, there is mixed evidence on whether a higher protein intake helps with ageing, says Lamming.

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For instance, one study linked this to a reduced risk of age-related muscle loss, or sarcopenia, among . But the rates of sarcopenia were so low that the link is unreliable, says at the University of Sheffield in the UK.

Still, some studies showed that restricting intake of certain amino acids – such as isoleucine and valine, which are highest in meat, fish and dairy – in mice has a similar effect to limiting overall protein intake, says at the University of Nottingham, UK.

Atherton says he is planning a study to investigate whether drugs that deplete specific amino acids in people improve outcomes like blood sugar control, with results expected in the next few years.