Publisher Health

The sun-drenched paradise of Thailand’s Phi Phi islands isn’t the usual starting point for a PhD. But for Sarah Sajedi, those soft, sandy beaches – or rather, what she found under them -inspired her pivot from a business career to an academic one.
“I was standing there looking out at this gorgeous view of the Andaman Sea, and then I looked down and beneath my feet were all these pieces of plastic, most of them water bottles,” she says.
“I’ve always had a passion for waste reduction, but I realized that this was a problem with consumption.”
Sajedi, BSc ’91, decided to return to Concordia to pursue a PhD with a focus on plastic waste. As the co-founder of ERA Environmental Management Solutions, a leading provider of environmental, health and safety software, she brought decades of experience to complement her studies.
Her latest paper, published in the Journal of Hazardous Materials, looks at the science around the health risks posed by single-use plastic water bottles. They are serious, she says, and seriously understudied.
Tiny threats, little known
In her review of over 140 scientific articles, Sajedi writes that individuals on average ingest between 39,000 and 52,000 microplastic particles per year, and bottled water users consume 90,000 more particles than tap water consumers.

The particles are usually invisible to the naked eye. A microplastic particle can range between one micron — a thousandth of a millimeter — to five millimeters; nanoplastics are smaller than one micron.
They emerge as bottles are made, stored, transported and broken down over their lifespans. Because they are often made from low-quality plastic, they shed tiny pieces every time they are manipulated and exposed to sunlight and temperature fluctuations. And unlike other types of plastic particles, which enter human bodies through the food chain, these are ingested directly from the source.
As Sajedi notes, the health consequences can be severe. Once inside the body, these small plastics can cross biological boundaries, enter the bloodstream and reach vital organs. This can lead to chronic inflammation, oxidative stress on cells, hormonal disruption, impaired reproduction, neurological damage and various kinds of cancer. However, the long-term effects remain poorly understood due to a lack of widespread testing and standardized methods of measurement and detection.
Sajedi identifies multiple methods researchers have used to measure nano- and microplastics, each with their own strengths and weaknesses. Some, for instance, can detect very small particles but cannot identify their chemical composition. Others can provide details about their makeup but miss the smallest plastics. And the best, most advanced and most reliable tools are often extremely costly and not always available.
Education is the best prevention
Sajedi is encouraged by the legislative action that has been adopted by governments around the world aimed at limiting plastic waste. However, she notes that the most common targets are single-use plastic bags, straws and packaging. Very few address the pressing issue of single-use water bottles.
“Education is the most important action we can take,” she says. “Drinking water from plastic bottles is fine in an emergency but it is not something that should be used in daily life. People need to understand that the issue is not acute toxicity — it is chronic toxicity.”
Chunjiang An, associate professor, and Zhi Chen, professor, in the Department of Building, Civil and Environmental Engineering at the Gina Cody School of Engineering and Computer Science contributed to this paper.
This research was supported by the Natural Sciences and Engineering Research Council of Canada and Concordia University.

17 minutes agoShareSaveMichelle RobertsDigital health editorShareSaveGetty ImagesMore than 100 million people, including at least 15 million children, use e-cigarettes, fuelling a new wave of nicotine addiction, the World Health Organization (WHO) is warning. Children are, on average, nine times more likely than adults to vape, it says, based on available global figures. The WHO’s Dr Etienne Krug said e-cigarettes were fuelling a “new wave” of nicotine addiction. “They are marketed as harm reduction but, in reality, are hooking kids on nicotine earlier and risk undermining decades of progress.”WHO Director General, Dr Tedros, accused the tobacco industry of “agressively targeting” young people. Teens being ‘targeted'”Millions of people are stopping, or not taking up, tobacco use thanks to tobacco control efforts by countries around the world,” he said. “In response to this strong progress, the tobacco industry is fighting back with new nicotine products, aggressively targeting young people. Governments must act faster and stronger in implementing proven tobacco-control policies,” he added. The vaping figures are an estimate since some countries – 109 in all, and many in African and South-East Asia – do not gather data. According to the report, as of February this year, at least 86 million e-cigarette users were adults, mostly in high-income countries. And at least 15 million teenagers aged between 13 and 15 already vape, based on surveys from 123 countries.While many nations have made efforts to introduce e-cigarettes regulations to tackle child vaping in recent years, by the end of 2024, 62 countries still had no policy in place, and 74 countries had no minimum age at which e-cigarettes may be purchased, says the WHO. Meanwhile, tobacco use has been decreasing – from an estimated 1.38 billion users in 2000 to 1.2 billion in 2024.Prevalence of tobacco use among women dropped the most – from 11% in 2010 to 6.6% in 2024. Among men, the decrease was from 41.4% in 2010 to 32.5% in 2024.But one in five adults globally still uses tobacco. Smoking is linked to many diseases, including cancer. Experts say vaping is far less harmful than cigarettes, and can help you quit smoking. It is not recommended for non-smokers. E-cigarettes do not burn tobacco and do not produce tar or carbon monoxide, two of the most damaging elements in tobacco smoke. They contain nicotine, which can be addictive.

The Nobel Prize in Physiology or Medicine 2025 has been awarded for discoveries that explain how the immune system attacks hostile infections, but not the body’s own cells.The prize is shared by Japan’s Shimon Sakaguchi and US researchers Mary Brunkow and Fred Ramsdell.They discovered “security guards” that eliminate parts of the immune system that could attack the body.Their work is being used to develop new treatments for autoimmune diseases and cancer.The winners share a prize fund worth 11m Swedish kronor (£870,000).”Their discoveries have been decisive for our understanding of how the immune system functions and why we do not all develop serious autoimmune diseases,” says Olle Kämpe, chair of the Nobel Committee.The Nobel panel added: “Their discoveries have laid the foundation for a new field of research and spurred the development of new treatments, for example for cancer and autoimmune diseases.”

Wounds that do not heal are often caused by bacterial infections and are particularly dangerous for the elderly and people with diabetes, cancer and other conditions.
Acetic acid (more commonly known as vinegar) has been used for centuries as a disinfectant, but it is only effective against a small number of bacteria, and it does not kill the most dangerous types.
New research led by researchers at University of Bergen in Norway, QIMR Berghofer and Flinders University in Australia has resulted in the ability to boost the natural bacterial killing qualities of vinegar by adding antimicrobial nanoparticles made from carbon and cobalt. The findings have been published in the international journal ACS Nano.
Molecular biologists Dr Adam Truskewycz and Professor Nils Halberg found these particles could kill several dangerous bacterial species, and their activity was enhanced when added to a weak vinegar solution.
As part of the study, Dr Truskewycz and Professor Halberg added cobalt-containing carbon quantum dot nanoparticles to weak acetic acid (vinegar) to create a potent antimicrobial treatment. They used this mixture against several pathogenic species, including the drug resistant Staphylococcus aureus, Escherichia coli (E. coli) and Enterococcus faecalis.
Dr Truskewycz said the acidic environment from the vinegar made bacterial cells swell and take up the nanoparticle treatment.
“Once exposed, the nanoparticles appear to attack dangerous bacteria from both inside the bacterial cell and also on its surface, causing them to burst. Importantly, this approach is non-toxic to human cells and was shown to remove bacterial infections from mice wounds without affecting healing,” he said.
The anti-bacterial boost in vinegar found in the study could potentially be an important contribution towards the ongoing battle against the rising antimicrobial resistance levels worldwide, with an estimated 4.5 million deaths associated with a direct infectious disease.
Professor Halberg said this study showed how nanoparticles could be used to increase the effectiveness of traditional bacterial treatments.
“Combination treatments such as the ones highlighted in this study may help to curb antimicrobial resistance. Given this issue can kill up to 5 million people each year, it’s vital we look to find new ways of killing pathogens like viruses, bacteria and fungi or parasites,” he said.

Researchers recreated a nearly forgotten yogurt recipe that was once was once common across the Balkans and Turkey — using ants. Reporting in the Cell Press journal iScience on October 3, the team shows that bacteria, acids, and enzymes in ants can kickstart the fermentation process that turns milk into yogurt. The work highlights how traditional practices can inspire new approaches to food science and even add creativity to the dinner table.
“Today’s yogurts are typically made with just two bacterial strains,” says senior author Leonie Jahn from the Technical University of Denmark. “If you look at traditional yogurt, you have much bigger biodiversity, varying based on location, households, and season. That brings more flavors, textures, and personality.”
Red wood ants (Formica species) can be found crawling through the forests of the Balkans and Turkey, where this yogurt-making technique was once popular. To better understand how to use these ants to make yogurt, the researchers visited co-author and anthropologist Sevgi Mutlu Sirakova’s family village in Bulgaria, where her relatives and other locals remember the tradition.
“We dropped four whole ants into a jar of warm milk by the instruction of Sevgi’s uncle and community members,” recalls lead author Veronica Sinotte of the University of Copenhagen, Denmark. The jar was then tucked into an ant mound to ferment overnight. By the next day, the milk had started to thicken and sour. “That’s an early stage of yogurt, and it tasted that way as well.”
The researchers, who tested the yogurt during their trip, described it as slightly tangy, herbaceous, and having flavors of grass-fed fat.
Back in Denmark, the team dissected the science behind the ant yogurt. They found that the ants carry lactic and acetic acid bacteria. Acids produced by these bacteria help coagulate the dairy. One type of these bacteria was similar to that found in commercial sourdough.
The insects themselves also help in the yogurt-making process. Formic acid, which is part of the ant’s natural chemical defense system, acidifies the milk, affects its texture, and likely creates an environment for yogurt’s acid-loving microbes to thrive, say the researchers. Enzymes from the ant and the microbes work in tandem to break down milk proteins and turn milk into yogurt.

The researchers compared yogurts made with live, frozen, and dehydrated ants. Only live ants seeded the right microbial community, meaning they are best suited for yogurt making. However, the team found that caution was necessary to make sure the ant products were safe to consume: live ants can harbor parasites, and freezing or dehydrating ants can sometimes allow harmful bacteria to flourish.
To test out the contemporary culinary possibilities of ant yogurt, the team then partnered with chefs at Alchemist, a two-star Michelin restaurant in Copenhagen, Denmark, who gave the traditional yogurt a modern twist. They served guests several concoctions including yogurt ice-cream sandwiches shaped like an ant, mascarpone-like cheeses with a pungent tang, and cocktails clarified with a milk wash — all inspired by ant yogurt and using the insect as a key ingredient.
“Giving scientific evidence that these traditions have a deep meaning and purpose, even though they might seem strange or more like a myth, I think that’s really beautiful,” says Jahn.
“I hope people recognize the importance of community and maybe listen a little closer when their grandmother shares a recipe or memory that seems unusual,” says Sinotte. “Learning from these practices and creating space for biocultural heritage in our foodways is important.”

To play this video you need to enable JavaScript in your browser.This video can not be playedMike HensonBBC Sport rugby union news reporter51 minutes agoFormer England captain Lewis Moody has revealed he has been diagnosed with motor neurone disease and admitted he cannot yet face the full implications of the muscle-wasting condition that killed fellow rugby players Doddie Weir and Rob Burrow.The 47-year-old, who was part of the 2003 Rugby World Cup-winning side and lifted multiple English and European titles with Leicester, spoke to BBC Breakfast two weeks after learning he has the disease.”There’s something about looking the future in the face and not wanting to really process that at the minute,” he said.”It’s not that I don’t understand where it’s going. We understand that. But there is absolutely a reluctance to look the future in the face for now.”Moody, speaking alongside his wife Annie, says instead he feels “at ease” as he concentrates on his immediate wellbeing, his family and making preparations for when the disease worsens.”Maybe that’s shock or maybe I process things differently, and once I have the information, it’s easier,” he added.Moody discovered he had MND after noticing some weakness in his shoulder while training in the gym.After physiotherapy failed to improve the problem, a series of scans showed nerves in his brain and spinal cord had been damaged by MND.”You’re given this diagnosis of MND and we’re rightly quite emotional about it, but it’s so strange because I feel like nothing’s wrong,” he added.”I don’t feel ill. I don’t feel unwell”My symptoms are very minor. I have a bit of muscle wasting in the hand and the shoulder.”I’m still capable of doing anything and everything. And hopefully that will continue for as long as is possible.”Rex FeaturesMND can progress quickly.According to the charity MND Association, the disease kills a third of people within a year and more than half within two years of diagnosis, as swallowing and breathing become more difficult.Treatment can only slow deterioration.”It’s never me that I feel sad for,” added an emotional Moody.”It’s the sadness around having to tell my mum – as an only child – and the implications that has for her.”Speaking from the family home with his wife and their pet dog by his side, Moody was overcome with emotion when he spoke about telling his sons – 17-year-old Dylan and 15-year-old Ethan – the devastating news, saying: “It was the hardest thing I’ve ever had to do.” “They are two brilliant boys and that was pretty heartbreaking,” Moody said.”We sat on the couch in tears, Ethan and Dylan both wrapped up in each other, then the dog jumped over and started licking the tears off our faces, which was rather silly.”Moody said the emphasis was staying in the moment.”There is no cure and that is why you have to be so militantly focused on just embracing and enjoying everything now,” he said.”As Annie said, we’ve been really lucky that the only real decision I made when I retired from playing was to spend as much time with the kids as possible. We don’t get those years back.”Getty ImagesA knee problem prevented Moody taking up an invitation to play in the inaugural 745 Game last autumn.The fundraising cross-code match, which brings together league and union stars, was the brainchild of Burrow and Ed Slater, the former Leicester and Gloucester second row who also lives with the disease.Burrow died in June 2024, while Slater is now in a wheelchair and struggles to speak without the help of a computer programme.Moody finds it hard to reconcile that he is now part of the match’s cause, rather than a supporter.”It is daunting because I love being active and embracing life, whether it’s on the rugby pitch, watching the kids, whatever it is,” he said.”There’s a lot of questions around what we need to put in place for the future. It’s still so new, I found out two weeks ago.”I feel slightly selfish in a way that I’ve been reluctant to reach out to anyone, to Ed.”But there will be a time when I can. And I would like to as well.”If they’re watching – I’m not ready yet, but I absolutely will [be].”Getty ImagesElite athletes are disproportionately affected by MND, with a study of Italian footballers suggesting the rate of the disease is up to six times higher than in the general population.It is thought that by limiting the oxygen available and causing damage to motor neurone cells, regular, strenuous exercise can trigger the disease in those already genetically susceptible.Moody, who won 71 England caps and toured with the British and Irish Lions in New Zealand in 2005, was nicknamed ‘Mad Dog’ during his playing career, in honour of his fearless, relentless approach to the game.He played through a stress fracture of his leg for a time with Leicester and once sparked a training-ground scuffle with team-mate and friend Martin Johnson when, frustrated, he abandoned a tackle pad and started throwing himself into tackles.After coming on as a replacement in the Rugby World Cup final win over Australia in 2003, he claimed a ball at the back of the line-out in the decisive passage of play, setting a platform for scrum-half Matt Dawson to snipe and Jonny Wilkinson to kick the match-winning drop-goal.Moody has already told Johnson, who captained England to that title, and a couple of other former team-mates about his diagnosis, but the rest will be learning his news with the rest of the public.”There will be a time when we’ll need to lean on their support but, at the minute, just having that sort of love and acknowledgment that people are there is all that matters,” he said.”Rugby is such a great community.”I said to the kids the other day, I’ve had an incredible life.”Even if it ended now, I’ve enjoyed all of it and embraced all of it and got to do it with unbelievable people.”When you get to call your passion your career, it’s one of the greatest privileges.”To have done it for so long with the teams that I did it with was a pleasure. And I know they will want to support in whatever way they can and I look forward to having those conversations.”Related topicsEngland Rugby UnionRugby Union

In a review of 246 deceased drivers, 41.9% tested positive for active THC in their blood, with an average level of 30.7 ng/mL — far exceeding most state impairment limits. The high rate of THC positivity remained consistent over six years and was unaffected by the state’s legalization of recreational cannabis during the study period. Messaging around the dangers of smoking cannabis and driving needs to be stronger, authors argue.New study findings show that over 40% of drivers who died in motor vehicle collisions tested positive for active delta-9-tetrahydrocannabinol (THC) in their system, with average blood levels far exceeding those considered to cause impairment. The research highlights a significant and persistent public health risk that is unchanged by the legalization of recreational cannabis, the authors said.The research will be presented at the American College of Surgeons (ACS) Clinical Congress 2025 in Chicago, October 4-7.
Researchers analyzed coroner records from Montgomery County in Ohio from January 2019 to September 2024, focusing on 246 deceased drivers who were tested for THC following a fatal crash. When autopsies are performed, drug screening is typically part of the process. The study period included the state’s legalization of recreational cannabis in 2023.
“I was surprised to see that level,” said lead author Akpofure P. Ekeh, MBBS, FACS, a professor of surgery at Wright State University in Dayton, Ohio. “An average level of 30.7 ng/mL generally means those people must have consumed marijuana at some time close to driving. This isn’t about residual use; it’s about recent consumption.”
Key Study Findings High Prevalence: 103 drivers (41.9%) overall tested positive for THC, with yearly rates ranging from 25.7% to 48.9%. No Effect from Legalization: The rate of drivers who tested positive for THC did not change significantly before or after legalization (42.1% vs. 45.2%), indicating that legal status did not influence the behavior of those who chose to drive after use. Consistent Over Time: The high rate of THC positivity showed no significant change over the six-year study period.The study notes that blood THC levels are typically drawn by the coroner within hours of death, providing an accurate snapshot of a driver’s state at the time of the crash. Most states that have set legal limits for driving range from 2 to 5 nanograms per milliliter (ng/mL) — a threshold the average level in this study (30.7 ng/mL) far exceeded.

“The messaging over the last few years has been just the push towards recreational legalization,” Dr. Ekeh noted. “The problem is that from a public health standpoint, there has not been enough emphasis on some of the downsides and the dangers that can occur. People should treat smoking marijuana just like they treat alcohol: don’t smoke and drive.”
Co-authors are Lois Nguapa, BS; Clara Mussin Phillips, BS; and Ann Cardosi, BS, MPH.
Citation: Ekeh A, et al. Cannabis Prevalence in Drivers Involved in Motor Vehicle Crash Fatalities over a 6-Year Period, Scientific Forum, American College of Surgeons (ACS) Clinical Congress 2025.
Note: This research was presented as an abstract at the ACS Clinical Congress Scientific Forum. Research abstracts presented at the ACS Clinical Congress Scientific Forum are reviewed and selected by a program committee but are not yet peer reviewed.

Scientists at Montefiore Einstein Comprehensive Cancer Center (MECCC) and Albert Einstein College of Medicine have shown for the first time that glioblastoma — the deadliest form of brain cancer — affects not just the brain but also erodes the skull, alters the makeup of skull marrow, and interferes with the body’s immune response. Drugs intended to inhibit skull-bone loss made the cancer more aggressive, according to results published on October 3 in Nature Neuroscience.
“Our discovery that this notoriously hard-to-treat brain cancer interacts with the body’s immune system may help explain why current therapies — all of them dealing with glioblastoma as a local disease — have failed, and it will hopefully lead to better treatment strategies,” said the paper’s corresponding author Jinan Behnan, Ph.D., assistant professor in the Leo M. Davidoff Department of Neurological Surgery and in the department of microbiology & immunology at Einstein, and a member of the National Cancer Institute (NCI)-designated MECCC.
According to the NCI, approximately 15,000 people are diagnosed with glioblastoma each year. The median survival of those who receive standard treatment of surgery, chemotherapy, and radiation is approximately 15 months.
A Matter of Marrow
As is true for many other bones, the skull contains marrow in which immune cells and other blood cells form. Dr. Behnan’s research on glioblastoma and the skull was prompted by recent studies revealing extremely thin channels that connect the skull with its underlying brain, allowing molecules and cells to travel between the skull’s marrow and the brain.
Dr. Behnan and colleagues used advanced imaging techniques on mice that developed two different types of glioblastomas. They found that the tumors caused skull bones to erode, especially along the sutures where skull bones fuse. Such erosions seem to be unique to glioblastoma and other malignant intracranial tumors, since they don’t occur with strokes, other types of brain damage, or even other systemic cancers. Computerized-tomography (CT) images of patients with glioblastoma revealed that decreases in skull thickness were present in the same anatomic areas as in mice.
The skull erosions in the mice were found to have increased the number and diameter of the skull-to-bone channels. The researchers hypothesized that these channels might allow the glioblastoma to transmit signals to the skull marrow that could profoundly change its immune landscape.

A Tilt Towards Inflammation
Using single-cell RNA sequencing, the researchers found that glioblastoma had dramatically shifted the skull marrow’s immune-cell balance in favor of pro-inflammatory myeloid cells — nearly doubling the levels of inflammatory neutrophils, while nearly eliminating several types of antibody-producing B cells as well as other B cells.
“The skull-to-brain channels allow an influx of these numerous pro-inflammatory cells from the skull marrow to the tumor, rendering the glioblastoma increasingly aggressive and, all too often, untreatable,” said study co-author E. Richard Stanley, Ph.D., professor of developmental and molecular biology at Einstein. “This indicates the need for treatments that restore the normal balance of immune cells in the skull marrow of people with glioblastoma. One strategy would be suppressing the production of pro-inflammatory neutrophils and monocytes while at the same time restoring the production of T and B cells.”
Interestingly, and adding to evidence that glioblastoma is a systemic rather than local disease, the marrows of the skull and femur reacted differently to the cancer. Glioblastoma activated several genes in the skull marrow that boosted production of inflammatory immune cells; but in femur marrow, the cancer suppressed genes needed to produce several types of immune cells.
The researchers wondered if administering anti-osteoporosis drugs that prevent bone loss would affect skull-bone erosion, glioblastoma, or both. To find out, they gave mice with glioblastoma tumors two different drugs approved by the U.S. Food and Drug Administration for treating osteoporosis. Both drugs (zoledronic acid and denosumab) halted skull erosion — but one of them (zoledronic acid) also fueled tumor progression in one type of glioblastoma. Both drugs also blocked the beneficial effects of anti-PD-L1, an immunotherapy drug that boosts levels of tumor-fighting T cells.
The Nature Neuroscience paper is titled “Brain Tumors Induce Widespread disruption of Calvarial Bone and Alteration of Skull Marrow Immune Landscape.” Additional MECCC and Einstein authors include Abhishek Dubey, Biljana Stangeland, Imane Abbas, David Fooksman, Ph.D., Wade R. Koba, B.S., Jinghang Zhang, M.D., Benjamin T. Himes, Ph.D., Derek Huffman, Ph.D., Zhiping Wu, Rachel Welch, David Reynolds, B.S., Kostantin Dobrenis, Ph.D., Qinge Ye, Kevin Fisher, and Emad Eskandar, M.D. Other authors include Erika Yamashita, Yutaka Uchida and Masaru Ishii, at Osaka University, Osaka, Japan, Robert A. Harris at Karolinska Hospital Solna, Stockholm, Sweden, Gregory M Palmer at Duke University Medical Center, Durham, North Carolina, Olivia R. Lu and Winson S. Ho at University of California, San Francisco, CA, and Alexander F. Fiedler at German Rheumatism Research Center (DRFZ) and Freie Universität Berlin, Berlin, Germany.

6 hours agoShareSaveKellie BrightPresenter, BBC Panorama andDoug FaulknerBBC NewsShareSaveKellie BrightI’ve been desperate to make a documentary about special educational needs and disabilities (Send) for ages.You might know me as EastEnders’ Linda Carter but I’m also a mum to my autistic son. He’s also dyslexic and has ADHD.It took months of perseverance and hard work from my husband and I to try to get the right education for him. At times, it felt like a battle.That is why I wanted to make this film for Panorama, so I could meet other families who were going through the same thing, and speak to teachers, councils and the government about how Send children are educated in England.There are more than 1.7 million children in England with Send. It is a broad group, including autistic children and people who struggle with speech and language, have ADHD and physical disabilities, among other conditions.Schools in England already provide some support to these students but if parents think their child needs extra help they can make an application to their council for what’s called an Education, Health and Care Plan (EHCP).An EHCP is a crucial document because it is legally binding, states where a child should go to school and outlines how much extra support they should get.My husband and I spent hours filling in the forms to request an EHCP and many families find the process very frustrating.Buddy and TundeNot long after I meet 15-year-old Buddy, he shows me his favourite cuddly toy, Reindeer Dog.Buddy’s autistic, meaning his brain experiences and reacts to the world in a different way from many people’s. He struggles with meeting people his own age, understanding his emotions and anxiety. Buddy likes to keep Reindeer Dog close to him.After moving to London from Scotland in October 2024, Buddy’s mum, Tunde, started applying for schools. She says she tried at least 11 schools but many of them didn’t get back to her, and those that did said they were full or could not give Buddy extra support without an EHCP.At the start of this year more than 638,000 EHCPs had been issued to children and young people in England, a 10.8% rise on the year before and an 80% increase in six years.The increase is partly because parents and schools have got better at identifying children who have special educational needs, especially autism, as opposed to there being more children with Send.It is the second time Buddy and Tunde have applied for an EHCP. Their first application was turned down before Buddy was assessed. Councils reject about a quarter of EHCP applications at the assessment stage, according to the Department for Education.When they lived in Scotland, Tunde says they did not have to apply for the equivalent of an EHCP. Buddy’s comprehensive school arranged support for his learning, although not for his emotional needs.Scotland has a different system for helping children with Send; schools there aim to deliver more support without the need for parents to apply for the equivalent of an EHCP.”It’s a madness,” Tunde says. “[Getting extra support] was so easily done, and it could be easily done again.”While Buddy is not able to go to school, the council is providing him with 19 hours of lessons per week in the local library.Tunde tells me the process of applying for an EHCP has been so time consuming she had to stop working as a midwife and health visitor for a time.”I can’t do the parenting. I can’t get him to these appointments, and work at the same time… I couldn’t get my son seen in the right amount of time and see other people’s babies in the right amount time. And it was a toss up – and my son won,” she says.We catch up with Buddy after a lengthy speech and language assessment.”Draining… that’s all I’ve got for you,” he says as he leans against a fence, Reindeer Dog tucked under his arm.A school for BuddyIt’s September and as millions of children start term, Buddy is still being taught in the library. Two months after I first met him, he’s getting an EHCP but his education is still not settled.The council agreed to Tunde’s request that he go to an independently run school that works with children who struggle in mainstream schools.Before Buddy can start there, the school has already taken over the lessons he receives in the library. But Tunde’s now not sure the school will be able to deliver what she believes her son needs to improve his social skills and confidence with children his own age.”We were all prepared for September… and he’s still not at school, he’s still having one-to-one,” she said.”I think … preparing to be around other kids and then still just being one-to-one with adults has really knocked him back and made him not want to go to school.”Southwark Council says it takes Tunde’s concerns very seriously and it will continue to support her family to ensure they receive the provision they need without further delay.It says it knows how hard it can be for families to navigate the system, and how distressing delays in securing support can be.It says it has invested in a specialist information and advice team, and now ensures children are assessed by specialist teachers at the earliest stage, and it is open to reviewing the situation when parents are concerned about education placements.’The current system is broken’I know there is another side to this story.The huge rise in the number of EHCPs is putting councils under severe financial pressure. It is estimated by the Department for Education that English councils are set to run up a total accumulated Send deficit between £4.3bn and £4.9bn by March 2026.The government says it has invested a billion pounds to help councils pay for EHCPs and £740m on new Send school places.I went to West Sussex County Council to interview one of few people in local government prepared to talk to me on the record about Send funding.Jacquie Russell is a Conservative councillor and cabinet member for children, young people and learning.”The current system is actually very adversarial. Our parents are increasingly tired and anxious and fed up of fighting… Staff sickness levels are really, really high at the moment,” she says.”The current system doesn’t work. It is broken. It’s not delivering the best outcomes for children.”Demand for EHCPs is now outstripping funding in West Sussex. In 2015, the council had about 3,400 children with an EHCP. Today there are more than 10,000.As a result the Send deficit has been growing year-on-year, so that at the end of 2025 it stands at more than £123m.”That [money] is really essentially meant to be for local services. That would have ordinarily gone to repair your roads… and other local services,” she says.”The current position is not sustainable.”The government agrees. It is planning major reforms of the Send system, though final plans have not yet been agreed.The minister for school standards, Georgia Gould, told me the upcoming reforms were “not taking support away from families”.”We’re wanting to put more support in earlier,” she said. “Where people have fought for support, and that’s in place, we want to make sure that that support continues.”She also told me she wanted to work with parents to get the reforms right and to get support at the “earliest possible point rather than having to battle”. The minister added that parents would still have a “legal basis” to get support.

In the realm of memories, “where” holds special importance. Where did I leave my keys? Where did I eat dinner last night? Where did I first meet that friend? Recalling locations is necessary for daily life, yet spatial memory — which keeps track of “where” — is one of the first cognitive abilities to fade in old age. And deficits earlier in life can be a telltale sign of dementia.
Now, researchers at Stanford Medicine and their colleagues are uncovering what goes awry in older brains when spatial memory falters and whether these changes can be prevented.
In a new study comparing young, middle-aged and old mice, the researchers found that activity in the medial entorhinal cortex — sometimes likened to the Global Positioning System of the brain — becomes less stable and less attuned to the environment in elderly animals. Those with the most impaired activity in this brain region were the most confused on a spatial memory test.
“You can think of the medial entorhinal cortex as containing all the components you need to build a map of space,” said Lisa Giocomo, PhD, professor of neurobiology and senior author of the study to publish Oct. 3 in Nature Communications.
“Before this study, there was extremely limited work on what actually happens to this spatial mapping system during healthy aging.”
Although, on average, elderly mice were noticeably worse than their younger counterparts at navigating their environments, there was wide variation among them — a sign that spatial memory decline may not be an inevitable part of advanced age.
Mental maps
The medial entorhinal cortex is an essential part of the brain’s navigation system. It contains a variety of cells that track different information, including the animal’s speed and head direction, as well as the dimensions and borders of a space. For the new study, the researchers focused on so-called grid cells, which create a map of the environment, almost like a longitude and latitude system.

They studied mice in three age categories: young mice approximately 3 months old, middle-aged mice approximately 13 months old and old mice approximately 22 months old. These ages roughly correlate to human 20-year-olds, 50-year-olds and 75- to 90-year-olds.
The researchers recorded the brain activity of slightly thirsty mice as they ran virtual reality tracks looking for hidden rewards — a lick of water. They ran on a stationary ball surrounded by screens that displayed the virtual environment, like a mouse-sized treadmill in a mouse-sized Imax theater.
Each mouse ran the tracks hundreds of times over six days. (Mice are naturally avid runners, the researchers noted.)
With enough repetition, mice in all age groups could learn the location of a hidden reward on a particular track. By day six, they stopped only to lick at the reward locations. Accordingly, the grid cells in their medial entorhinal cortex developed distinct firing patterns for each track, as if building custom mental maps.
Switching tracks
But on a more challenging task in which the mice were randomly alternated between two different tracks they had already learned, each with a different reward location, the elderly mice were stymied — seemingly unable to determine which track they were on.

“In this case, the task was more similar to remembering where you parked your car in two different parking lots or where your favorite coffeeshop is in two different cities,” Giocomo said.
Unsure of where they were, the old mice tended to sprint the rest of the track without bothering to stop and search for rewards. A few took a different tactic and tried licking everywhere.
Their grid cells reflected their confusion. Despite having developed distinct firing patterns for each track, their grid cells fired erratically when the tracks were alternated.
“Their spatial recall and their rapid discrimination of these two environments was really impaired,” said Charlotte Herber, PhD, an MD-PhD student and lead author of the study.
The findings seem to align with human behavior. “Older people often can navigate familiar spaces, like their home or the neighborhood they’ve always lived in, but it’s really hard for them to learn to navigate a new place, even with experience,” Giocomo said.
In contrast, both young and middle-aged mice understood the assignment by day six, and their grid cell activity swiftly matched whichever track they were on.
“Over days one through six, they have progressively more stable spatial firing patterns that are specific to context A and specific to context B,” Herber said. “The aged mice fail to the develop these discrete spatial maps.”
The middle-aged mice had somewhat weaker patterns in their brain activity, but they performed very similarly to the young mice. “We think this is a cognitive capacity that at least until about 13 months old in a mouse, or maybe 50 to 60 years old in a human counterpart, is probably intact,” Herber said.
Super-ager
Though young and middle-aged mice performed uniformly within their age groups, the oldest set showed more variability in spatial memory.
Male mice generally performed better than female mice, though the researchers do not yet know why.
One elderly male mouse stood out: It aced the test, remembering the hidden reward locations on alternating tracks just as well as, if not better than, the young and middle-aged mice.
“It was the very last mouse I recorded and, honestly, when I was watching it run the experiment, I thought, ‘Oh no, this mouse is going to screw up the statistics,'” Herber said.
Instead, the super-ager mouse turned out to confirm the link between grid cell activity and spatial memory. Its grid cells were as unusually sprightly as its behavior, firing clearly and accurately in each environment.
“The variability in the aged group allowed us to establish these correlative relationships between neural function and behavior,” Herber said.
The super-ager mouse also encouraged the researchers to look for genetic differences that might underly variability in aging. They sequenced the RNA of young and old mice and found 61 genes that were more expressed in mice with unstable grid cell activity. These genes could be involved in either driving or compensating for spatial memory decline, the researchers said.
The gene Haplin4, for example, contributes to the network of proteins that surround neurons, known as the perineuronal net, which could help shore up grid cell stability and protect spatial memory in aging mice.
“Just like mice, people also exhibit a variable extent of aging,” Herber said. “Understanding some of that variability — why some people are more resilient to aging and others are more vulnerable — is part of the goal of this work.”
Researchers at the University of California, San Francisco, contributed to the study.
The study received funding from the Stanford University Medical Scientist Training Program, the National Institute on Aging, the National Institutes of Health BRAIN Initiative (grant U19NS118284), National Institute of Mental Health (grants MH126904 and MH130452), the National Institute on Drug Abuse (grant DA042012), the Vallee Foundation and the James S. McDonnell Foundation.