Around 200 lives have been saved in England so far thanks to a vaccine which protects against cervical cancer, according to analysis published in the Lancet.
The first study of its kind showed that deaths have fallen sharply since school-age girls were offered the human papillomavirus (HPV) jab in 2008.
Between 2020 and 2024, no cervical cancer deaths were recorded in women aged 20 to 24 – the first time that had happened over a five-year period.
Without vaccination, around 23 deaths would have been expected.
“It’s incredible to think that a single jab can almost eliminate a particular type of cancer,” said Prof Peter Sasieni, the lead researcher at Queen Mary University of London.
The study also found that those children vaccinated at age 12 or 13 now have close to zero risk of dying from the disease before the age of 30.
Before the HPV vaccination campaign, around 20 deaths every year were being recorded in that age group.
Overall, cervical cancer is still the 14th most common cancer among females in the UK, with 3,300 people diagnosed every year.
It is thought HPV, a virus which is spread through close skin-to-skin contact, causes 99% of those cases.
Most HPV infections clear up without any problems, but some cause abnormal cell changes and can lead to cancer years later.
The report’s authors expect the numbers dying from the disease to continue to fall as more are given a HPV jab and vaccinated people grow older.
Cancer Research UK, which funded the research, described the findings as an “incredible milestone” but warned that vaccination rates in England were running below recommended levels.
“We know the HPV vaccine is extremely effective at stopping cervical cancer before it starts and for the first time these findings show it is saving lives,” said the organisation’s chief executive Michelle Mitchell.
‘I’m a real advocate for this vaccine’
Alexandra Legg left school just before the HPV vaccine was introduced in England.
In 2021, just as she was planning her wedding, she was diagnosed with cervical cancer aged 30.
“I remember hearing the words and I just couldn’t really breathe very well,” she says.
“I was so upset – everything went through my head, it was so hard.”
Her treatment involved the removal of lymph nodes in her abdomen, although surgeons were able to preserve a small part of her cervix, giving her a chance of becoming pregnant.
Just a year later, Ivy was born. Her middle name is Marvella – meaning “miracle”.
“Those nine months were so scary because I was at such risk of losing her at any point,” she says.
Alexandra says her life could have been far less traumatic if she had been offered the HPV vaccine and urged those eligible to get it.
“I’m a real advocate for this vaccine and when Ivy is old enough, she’ll be first in the queue,” she adds.
Reduction in deaths ‘tip of the iceberg’
Prof Sasieni, who specialises in cancer epidemiology at Queen Mary University of London, describes the reduction in deaths since the introduction of the vaccine as the “tip of the iceberg”.
“As vaccinated generations grow older, we’ll see many more lives saved from cervical cancer,” he adds.
“New research shows just how vital it is to keep HPV vaccination levels high so more people are protected.”
The UK government has pledged to eliminate cervical cancer as a public health problem by 2040.
But the latest data shows vaccination rates across the country have fallen below recommended levels.
Data from the UK Health Security Agency shows that 76% of girls in England were vaccinated by the age of 15 in 2024-25, well below the 90% that the World Health Organization (WHO) says is needed to eliminate cervical cancer.
“It’s essential that the UK Government and health systems urgently address this with targeted action to reach communities where uptake is the lowest,” says Michelle Mitchell at Cancer Research UK.
Despite the rollout of the HPV vaccine, women aged 25 to 64 are still advised to attend cervical screening (formerly known as a smear test).
Boys have also been given the HPV vaccine since 2019, which helps to protect them against anal, penis, throat and mouth cancers, and reduces the risk of them passing the virus on to girls.
HPV self-testing kits are also being sent out to women who have not yet come forward for screening, he added.

Lifestyle
‘BUTTON OF DESPAIR’
Little-Known ‘Syndrome’ Causes Distress Among Some Women
One woman’s viral video sparked debate over a phenomenon called “sad nipples.”
Millions of women are discovering they may share a strange symptom they once assumed was unique: a sudden wave of sadness, dread, or even “impending doom” triggered by something as simple as a nipple brushing against clothing.
The phenomenon, informally dubbed “sad nipple syndrome” online, went viral after one woman described a “feeling of deep and unexplainable overwhelming sadness and guilt” whenever her nipple grazed something.
The video has racked up more than 9 million views, with women flooding the comments in disbelief that others experience the same thing.
Others dubbed the area the “button of despair,” describing the nauseating sensation as “maybe the worst feeling ever.”
Though the phenomenon is not recognized as a formal medical condition, experts say there may be biological explanations for why some women experience an intense emotional reaction to nipple stimulation.
Dr. Susanna Unsworth, an intimate health expert at Intimina, told Tyla that hormonal shifts could play a role.
“Nipple and breast stimulation are known to affect oxytocin levels, so it is biologically plausible that similar mechanisms could contribute to these emotional responses in some non-lactating individuals too,” she said.
Unsworth pointed to the closest known medical comparison: dysphoric milk ejection reflex, or D-MER, a condition experienced by some breastfeeding mothers that causes sudden feelings of sadness, anxiety, dread, or other negative emotions when milk is released.
Researchers believe D-MER may be linked to a brief drop in dopamine—a neurotransmitter associated with pleasure and reward—that occurs as milk production hormones are activated.
Although several women experiencing the viral phenomenon say they are not breastfeeding, experts say the overlap is worth exploring.
A study published in the National Library of Medicine found that nipple stimulation can increase oxytocin levels even in nonlactating women.
That finding has prompted some experts to wonder whether a similar hormonal mechanism could be involved for women suffering from “sad nipples.”
“This raises a biologically plausible—though as yet unstudied—question about whether the same dopamine mechanism may be at play in women who have never breastfed,” OB/GYN Dr. Melissa Walsh told the New York Post.
Many women sharing their experiences online said the feeling began long before pregnancy or breastfeeding entered the picture.
“Happened to me since I was a kid, and it was awful once I had a kid,” one commenter wrote in response to suggestions that the phenomenon could be linked exclusively to D-MER.
Dr. Ari Hoschander, a plastic surgeon in New York, told the Post that the reports sound more like physiological responses than psychological ones.
“What [they’re] describing sounds like that dopamine drop hitting particularly hard,” he speculated.
Walsh said recognizing a possible biological explanation can be reassuring for women who experience the phenomenon.
Many women in the comments appeared to agree.
“I didn’t experience [sexual trauma] and I have this feeling. I don’t think it’s a trauma response,” one woman wrote.
Hoschander noted that the nipple-areola complex is among the most neurologically dense areas of the body, meaning stimulation can trigger surprisingly powerful reactions.
The good news, he said, is that the feelings typically pass as quickly as they arrive.
While women have found community online around the experience, research into the phenomenon remains limited.
For those struggling with recurring symptoms, Unsworth recommends identifying potential triggers—including certain clothing fabrics—and practicing relaxation techniques. In more severe cases, she said cognitive behavioral therapy may help.
“This is an area that highlights how much more research is needed into women’s hormonal and neurobiological experiences,” Unsworth said.
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A copper-based drug could offer a new route to tackling Alzheimer’s disease, after researchers found it reduced toxic proteins in the brain while improving memory in laboratory studies.
Scientists at Monash University reported that the compound, known as Cu(ATSM), not only lowered levels of amyloid-beta—a protein strongly linked to Alzheimer’s—but also improved long-term spatial memory.
Their findings, published in ACS Chemical Neuroscience, point to a treatment that targets the brain’s waste-removal system, a process known to break down in people with the disease.
Read More on Health
How Toxic Proteins Build Up in Alzheimer’s
Alzheimer’s develops in part due to the build-up of amyloid-beta in the brain. Under normal conditions, these proteins are cleared away through the blood-brain barrier, a protective layer that controls what enters and leaves the brain.
However, this system becomes less efficient over time in Alzheimer’s patients, allowing harmful proteins to accumulate.
A central role in this process is played by P-glycoprotein (P-gp) pumps—transport proteins that help move waste products out of the brain and into the bloodstream. When these pumps lose function, the brain’s ability to clear toxic material is significantly reduced.
What the Study Found About Cu(ATSM)
The new study shows that Cu(ATSM) may help restore this system by increasing the number and activity of these pumps. Lead author Dr. Jae Pyun explained that the treatment works by improving the function of the brain’s blood vessels, leading to both lower toxic protein levels and better cognitive performance.
“This is the first study to show that Cu(ATSM) can increase the abundance of P-gp clearance pumps in an Alzheimer’s model, by 24.1 percent, effectively linking the repair of the blood-brain barrier to a reduction in toxic proteins and improved cognitive function,” Dr. Pyun said.
The team found that restoring this waste-removal pathway had a measurable effect. “By improving the pumps, the brain can finally clear out the trapped waste. Over 56 days, the treatment reduced toxic amyloid-beta by 42 percent and improved spatial learning by nearly 44 percent.”
The results suggest that repairing the blood-brain barrier could be key to slowing or reversing some of the damage seen in Alzheimer’s disease.
A Drug Already Tested in Other Conditions
Senior author Professor Joseph Nicolazzo said the drug could move toward human trials more quickly than some other experimental treatments. That is because Cu(ATSM) has already been tested for safety in other neurological conditions.
“Cu(ATSM) is a copper compound with anti-inflammatory and neuroprotective properties that has already progressed to clinical testing for conditions like Parkinson’s and ALS,” Nicolazzo said.
He added that the reduction of amyloid in the brain is a meaningful target for improving symptoms. “Because reducing amyloid burden is clinically proven to improve functional outcomes, these preclinical results strongly support the rationale for testing this drug in early symptomatic Alzheimer’s disease.”
What Remains Unknown
While the findings are promising, researchers are still working to understand exactly how amyloid-beta leaves the brain once the barrier is restored. One theory is that Cu(ATSM) may also boost the activity of microglia—immune cells that help break down toxic proteins.
Dr. Dayan Goodenowe, a Ph.D. neuroscientist who is not directly connected to this specific study, told Newsweek that targeting the blood-brain barrier and waste-clearance systems is a promising area because Alzheimer’s is not just a plaque-storage problem.
“Alzheimer’s involves the biological environment of the aging brain and including membrane biology, inflammation, vascular function, lipid metabolism and cellular resilience… All of those components…” he said. “So any SINGLE mechanism still has to be validated before we know whether it produces meaningful clinical benefit.”
According to Goodenowe, the biology suggests that amyloid may be influenced by the broader lipid environment of the brain.
“The key question is not simply whether amyloid changes, but whether the intervention improves cognition, function and outcomes in humans,” he said. “The research must move from mechanism and preclinical work to human safety, dose, efficacy and ultimately FDA governed validation.”
What This Could Mean for Future Treatment
Further studies will explore these pathways in more detail. For now, the results highlight the potential of therapies that target both blood vessel function and protein clearance mechanisms in the brain.

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For years, mainstream neurodevelopmental research overwhelmingly focused on abnormalities within the cerebral cortex—the brain region responsible for thinking, learning, and processing information—as the primary driver of autism.
However, a May 2026 study suggests that another part of the brain, the cerebellum, may play a much larger role than ever thought.
Highlights
New research suggests that autism may not originate solely in the brain’s thinking centers.
Scientists uncovered how changes in the cerebellum may influence the social difficulties associated with autism.
A second study identified two biological subtypes of autism that could reshape future diagnosis and treatment.
Researchers discovered that perineuronal nets (PNNs), the tiny supportive structures surrounding cerebellar neurons, help maintain healthy communication across brain networks involved in social behavior.
When these structures were disrupted, social interactions changed, offering a fresh perspective on the biological mechanisms that may contribute to autism spectrum disorder (ASD).
RELATED:
Disrupted cerebellar support cells were found to affect social behavior linked to autism
Image credits: Unsplash (Not the actual photo)
The study was conducted by Japan’s Kanazawa University, and the results were published in the journal Translational Psychiatry on May 13.
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The researchers examined two different mouse models of autism for the purpose.
Image credits: Pexels (Not the actual photo)
In one model, autism-like traits were induced by exposing mice to valproic acid before birth, while in the other, the mice carried a mutation in the autism-associated gene CHD8.
Despite their different origins, both models showed a significant loss of perineuronal nets (PNNs) in the cerebellum.
Image credits: Pexels (Not the actual photo)
To understand the impact of this change, scientists deliberately disrupted PNNs in healthy mice.
This yielded striking results, with mice showing damaged PNNs exhibiting reduced social interaction and less interest in unfamiliar mice — behaviors commonly associated with ASD.
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Further experiments revealed why this happened.
Image credits: Pexels (Not the actual photo)
In healthy mice, social interactions activated neurons in the cerebellum, which then sent signals to other brain regions involved in processing social information. When PNNs were disrupted, this neural activity dropped significantly, weakening communication across multiple brain networks.
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Image credits: Unsplash (Not the actual photo)
The team also identified a key molecular player called ARNT2. Levels of this protein increased when PNNs were lost, making neurons less responsive.
Reducing ARNT2 activity restored both normal brain function and social behavior in the mice.
The findings suggest that autism-related social difficulties may not stem solely from changes in the brain’s thinking centers. Instead, structural changes in the cerebellum and the networks it controls could also play an important role.
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While more research is needed to determine whether the same mechanism exists in humans, the study offers a promising new direction for understanding the biology of autism.
The study came shortly before another research effort identified two subtypes of autism
Image credits: Unsplash (Not the actual photo)
This study, titled Autism Subtypes Identified Using Cross-Species Functional Connectivity Analyses, was led by researchers at the Instituto Italiano di Tecnologia in Rovereto, Italy, and the Child Mind Institute in New York, with additional contributions from the University of Trento.
Their findings were published in Nature Neuroscience on May 15.
Image credits: Pexels (Not the actual photo)
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Researchers examined brain scans from 20 different mouse models that showed autism-like traits, as well as scans from 940 children and young adults with autism and 1,036 neurotypical individuals.
They were looking for differences in how various parts of the brain communicate with one another.
The analysis revealed two main patterns.
Image credits: Unsplash (Not the actual photo)
First was a hypoconnectivity group, where autism was associated with reduced brain connectivity. Here, brain activity was linked to genes involved in synaptic junctions that enable brain cells to communicate.
Then there was a hyperconnectivity group, associated with increased connectivity across the brain. The group’s brain patterns were linked to genes related to the immune system and showed measures of slightly more severe autism.
Because the same patterns were found in both mice and humans and replicated across multiple datasets, the researchers believe these patterns may represent real biological subtypes of autism.
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If future research confirms these subtypes and reliable diagnostic methods are developed, it could lead to more personalized treatments tailored to each subtype.
This wasn’t the first time researchers tried to spot matching patterns and split autism into several types
Image credits: Unsplash (Not the actual photo)
A study published in July 2025 by researchers from Princeton University, the Simons Foundation, and the Flatiron Institute identified four types of autism in a group of 5,000 children.
Instead of using brain imaging, the researchers defined these types by analyzing more than 230 behavioral characteristics.
Other studies have suggested that autism can appear differently depending on when it develops, such as in early childhood, late childhood, adolescence, or young adulthood.
Together, these studies aim to improve how autism is identified and understood.
Image credits: Unsplash (Not the actual photo)
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The researchers believe that larger datasets and more advanced analysis methods will help uncover additional autism subtypes in the future.
The team behind Autism Subtypes Identified Using Cross-Species Functional Connectivity Analyses has made its data and analysis tools publicly available, enabling other scientists to build on its findings.
“Our cross-species approach provides an advanced translational framework for a multidimensional, biologically grounded stratification of autism,” the researchers wrote in the published paper.
“Our database is openly available to the research community, supporting future investigations into autism-related connectivity alterations,” they added.
“I have three kids, all diagnosed with autism. I am realizing I am also autistic. Genetics!” a netizen wrote
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Researchers at UC Davis have created an advanced brain-computer interface that can allow people with severe paralysis to communicate, work and interact with the digital world. In a new study published in Nature Medicine, a team of scientists at the University of California, Davis detailed a years-long study of a brain-computer interface (BCI) that has been equipped with “advanced decoding algorithms that translate neural signals into text and enable cursor control,” as stated in a press release shared by UC Davis Health. This means that the user can fully interact with a personal computer without the need for researcher support.