The healthcare industry isn’t built for coming off medication

Top view of assorted prescription pills and capsules in colorful blister packs. Pharmaceutical medication background representing healthcare, drug treatment, medical industry, overmedication and pharmacy concept.
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Modern medicine has an impressive array of drugs in its arsenal. If you are unwell, there is a very good chance your doctor will prescribe a pill to get you back to health. What our medical system is less good at, however, is stopping medication.

Take antidepressants. The drugs aren’t effective for everyone, but they work well for some. Once the medication does its job, though, or the life circumstances that brought on depression grow easier – what then? We don’t yet have a good answer.

Because antidepressants are relatively safe drugs, they can often be dispensed for months or years on end, without much consideration about the long-term implications, as we discuss. But thousands of people struggle to stop taking them, with little help from doctors.

The problem starts long before doctors write out the prescription, though. Clinical trials are typically short-term, lasting only a matter of weeks, and there are few financial rewards or even resources for those who want to study long-term use or when medication should be stopped. This lack of evidence then informs clinical guidance – or rather, its absence.

Few industries want to help people stop using their products, but healthcare should

Antidepressants are just one example. The opioid crisis was spawned, in part, by a flippant attitude to prescribing drugs, and a failure to regulate how often physicians should review patients’ doses. Medications from beta-blockers to acid-reducing stomach drugs, though beneficial for heart or stomach issues in the short term, can cause serious long-term problems. When such issues do come up, physicians have a tendency to prescribe more medications to help combat any side effects – a problem known as a “prescription cascade”, which can be especially difficult for people managing health issues later in life.

Few industries are invested in getting people to stop using their products, but healthcare should be an exception. We need to pay attention to the problems that arise when people stop taking medication, and develop detailed guidance and support, so that when it is the right time to make a change, deprescribing is a valid option, too.

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Nanoparticles ease Alzheimer’s by making neurons from other cells

A micrograph of neurons, with the different colours representing the cells’ various roles
JOE MCKELLAR/SCIENCE PHOTO LIBRARY

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 Peisheng Xu at the University of South Carolina.


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In Alzheimer’s disease, which affects around 24 million people worldwide, 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 – can be converted into neurons 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.

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 András Lakatos 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 Benedikt Berninger 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.

Journal reference:

Cell Biomaterials
DOI: 10.1016/j.celbio.2026.100575 

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Workout patch delivers some of the benefits of exercise with no exertion

Exercise is important for good health, but some people, like those with certain medical conditions, find it difficult to be active
Connect Images/Alamy

Some of the benefits of a rigorous workout might one day be achievable without any physical exertion. A study in mice shows that injecting muscle cells beneath the skin creates a patch of these cells that continuously contracts, delivering some of the benefits of exercise around the clock. While this should never replace physical activity, it may be helpful for people who are unable to exercise, such as those in hospital.

Initially, Ng Shyh-Chang at the Beijing Institute for Stem Cell and Regenerative Medicine in China and his colleagues injected muscle cells into mice with the aim of increasing their muscle mass, but this had an unexpected result. “This thing was contracting under the skin continuously, and we thought, ‘This thing is like non-stop exercise’,” says Shyh-Chang.


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They started by taking samples of muscle stem cells from live mice, which they cultured until the cells differentiated into mature, contractile muscle cells known as myocytes. They then injected these just beneath the skin on the backs of the same mice. “The original intention was to increase muscle mass by injecting muscle cells,” says Shyh-Chang.

With an injection of about 6 million myocytes, a patch of cells formed, creating its own network of mini blood vessels. This then began to pulse continuously, even when the mice were asleep.

Various experiments showed the patches had widespread effects around the mice’s bodies. For instance, the mice given the muscle patches had a higher whole-body muscle mass and better immune function compared with those that got a sham injection. All the mice were free to move around their cages as normal during the study.

What’s more, in mice that were 18 months old (roughly equivalent to a person in their late 50s or 60s) and those fed to induce obesity, the patches improved muscle mass, bone density, physical strength and endurance.

These mice also showed reversal in signs of liver damage, as well as reduced inflammation and the ability to navigate a maze faster. “So, it also has effects on its brain,” says Shyh-Chang. “This is known from exercise, but here, we’re seeing it from a small muscle graft.”

The patch’s wide-ranging effects may be due to it mimicking how muscles work like endocrine tissue during exercise. “What I find particularly interesting is that the effects appear to go beyond the graft itself,” says Tang Hong-Wen at Duke-NUS Medical School in Singapore. “The study suggests that the contracting muscle can act as an endocrine organ, with changes in circulating factors that may contribute to effects in other tissues.”

Imaging showed that the muscle patches survived for at least 81 days, when the researchers stopped taking measurements, but Shyh-Chang says that follow-up work indicates they are still stable after six months. “So far, there’s no limit to its lifespan as far as I can tell,” he says. There also seems to be very little reduction in volume over time and no evidence of tumour growth, which can be a risk after implanting stem cells.

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Shyh-Chang hopes the patch could help people with medical conditions that stop them from exercising. The researchers are talking to several hospitals about starting clinical trials in people with limited mobility, which could begin within a year, he says. “We always say we should exercise to keep muscle mass, but the folks that need exercise the most are actually the ones least likely to be able to exercise,” he says.

“The idea of mimicking exercise for people who can’t exercise is amazing,” says Matthew Stroud at King’s College London, but he questions how comfortable a continuously contracting graft like this would be.

Tang stresses that the patch should be thought of as mimicking some aspects of exercise, rather than replacing it. “Exercise has many other effects – including cardiovascular, neuromuscular, mechanical and bone-loading effects – that a small subcutaneous muscle graft cannot fully reproduce,” he says.

Journal Reference:

Nature Aging
DOI: 10.1038/s43587-026-01190-3

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Shingles vaccine may lower risk of stroke and heart failure

An illustration of the the varicella zoster virus, which causes chickenpox and shingles
The varicella-zoster virus causes chickenpox and shingles
SCIENCE PHOTO LIBRARY

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 John Tregoning at Imperial College London, who wasn’t involved in the study.


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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, affects a third of people in the US at least once.

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 Max Taquet 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.

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 third of those eligible for the vaccine get it. The UK’s National Health Services offer it to anyone who turned 65 on or after 1 September 2023.

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

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Shingrix also prevents shingles more effectively than Zostavax, 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 ongoing trial, 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.

Journal Reference:

Nature Medicine
DOI: 10.1038/s41591-026-04606-0

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