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Working with Alzheimer’s mouse models, human cells, and donated human brain tissue, researchers found that reducing levels of a molecule called PU.1 can shift microglia into a more protective mode. Microglia are immune cells that live in the brain and help maintain its health. When PU.1 levels drop, these cells increase the production of certain lymphoid immunoregulatory receptor proteins, which are typically involved in managing immune responses in the body.
Although these protective microglia appear in relatively small numbers, the study showed that they have a powerful influence across the brain. Their presence helps calm harmful inflammation, supports cognitive abilities, and improves survival in mice. In contrast, when the team removed CD28 from this rare group of microglia, inflammation rose sharply and plaques associated with Alzheimer’s developed more quickly. This outcome demonstrated how essential CD28 is for enabling the helpful actions of these cells.
Microglia as Flexible and Protective Brain Cells
“Microglia are not simply destructive responders in Alzheimer’s disease — they can become the brain’s protectors,” explained Anne Schaefer, the senior author of the research and leader of the project. She noted that the findings build on earlier work showing that microglia can adopt a wide range of functional states, allowing them to play many different roles in brain health. According to Schaefer, the results also highlight how international scientific partnerships are crucial for making progress in complex fields like neurodegeneration.
Alexander Tarakhovsky added that it was striking to see immune-related molecules, long recognized for their roles in B and T lymphocytes, also influencing microglia. “This discovery comes at a time when regulatory T cells have achieved major recognition as master regulators of immunity, highlighting a shared logic of immune regulation across cell types,” he said. He also pointed out that understanding this shared system may open the door to new immunotherapeutic approaches for Alzheimer’s disease.
Genetic Clues That Connect PU.1 to Alzheimer’s Risk
The work expands on earlier genetic studies by senior co-author Alison Goate, who identified a common variant in SPI1 (the gene responsible for producing PU.1) that is associated with a lower risk of developing Alzheimer’s. Goate explained, “These results provide a mechanistic explanation for why lower PU.1 levels are linked to reduced Alzheimer’s risk,” offering a clearer picture of how genetics influence disease vulnerability.
Overall, the discovery of the PU.1-CD28 axis provides researchers with a new molecular framework for understanding how protective microglial states arise. It also emphasizes the promise of developing treatments that specifically target microglia in order to alter the course of Alzheimer’s disease.

Researchers at Washington University School of Medicine in St. Louis, working with scientists at Northwestern University, have created a noninvasive strategy to treat one of the most aggressive and deadly forms of brain cancer. Their method relies on carefully designed nanostructures made from extremely small materials that can carry potent cancer-fighting compounds into the brain through simple nasal drops. In studies involving mice, this approach successfully treated glioblastoma by stimulating the brain’s immune system. The technique also avoids the invasiveness seen in similar treatments now under development.
The findings were published this month in PNAS.
Why Glioblastoma Is So Difficult to Treat
Glioblastoma develops from astrocytes, a type of brain cell, and is the most common malignant brain tumor, affecting about three in every 100,000 people in the U.S. The disease advances rapidly and is almost always fatal. One of the biggest obstacles to treating it is the challenge of getting effective medicine into the brain.
“We wanted to change this reality and develop a noninvasive treatment that activates the immune response to attack glioblastoma,” said Alexander H. Stegh, PhD, a professor and vice chair of research in the WashU Medicine Taylor Family Department of Neurosurgery and a co-corresponding author of the study. Stegh also serves as research director of The Brain Tumor Center at Siteman Cancer Center, based at Barnes-Jewish Hospital and WashU Medicine. “With this research, we’ve shown that precisely engineered nanostructures, called spherical nucleic acids, can safely and effectively activate powerful immune pathways within the brain. This redefines how cancer immunotherapy can be achieved in otherwise difficult-to-access tumors.”
Reactivating the Immune System With STING Pathway Nanomedicine
Glioblastoma is often labeled a “cold tumor” because it does not naturally provoke a strong immune response. Unlike “hot tumors,” which are more responsive to immunotherapies, glioblastoma tends to evade detection. Scientists have been exploring ways to stimulate a pathway known as STING, short for stimulator of interferon genes. This pathway activates when cells detect foreign DNA, setting off immune defenses.

Previous research showed that drugs activating the STING pathway can prime the immune system to attack glioblastoma. The drawback is that these drugs degrade quickly and must be injected directly into the tumor to be effective. Since multiple doses are needed, this requires highly invasive procedures.
“We really wanted to minimize patients having to go through that when they are already ill, and I thought that we could use the spherical nucleic acid platforms to deliver these drugs in a noninvasive way,” said Akanksha Mahajan, PhD, a postdoctoral research associate in Stegh’s lab and first author of the study.
Building Gold-Core Nanostructures for Nose-to-Brain Delivery
To address this challenge, Stegh’s group partnered with co-corresponding author Chad A. Mirkin, PhD, director of the International Institute for Nanotechnology and the Rathmann Professor of Chemistry at Northwestern University. Mirkin developed spherical nucleic acids, which are nanoscale particles coated densely with DNA or RNA. These structures have been shown to be more effective than traditional delivery systems.
Together, the teams designed a specialized version of spherical nucleic acids featuring gold nanoparticle cores and short DNA fragments that activate the STING pathway in targeted immune cells. To move these compounds into the brain, the researchers used the nasal passages as the entry point.
Intranasal delivery has been studied before for brain-targeted treatments, but no nanoscale therapy had previously shown the ability to activate immune responses against brain tumors using this route.

“This is the first time that it has been shown that we can increase immune cell activation in glioblastoma tumors when we deliver nanoscale therapeutics from the nose to the brain,” Mahajan said.
Tracking Nanodrops as They Travel to the Brain
The researchers aimed to demonstrate both selective delivery to the brain and proper activation of the target immune cells. They added a molecular tag to the spherical nucleic acids that glowed under near-infrared light. After administering the nanodrops to mice with glioblastoma, they observed the particles traveling along the pathway of the main nerve connecting the facial region to the brain.
Once there, the immune response triggered by the nanomedicine concentrated in specific immune cells within the tumor. Some activity was also detected in nearby lymph nodes. Importantly, the therapy did not spread widely throughout the body, helping reduce the likelihood of unwanted side effects.
Further examination showed that immune cells in and around the tumor had activated the STING pathway, enabling them to mount a stronger attack against the cancer.
Combining Treatments to Eradicate Tumors and Prevent Recurrence
When the nanotherapy was paired with medicines that help activate T lymphocytes, another key type of immune cell, the two-dose treatment eliminated tumors in mice and produced long-lasting immunity that prevented the cancer from returning. These outcomes were significantly better than those seen with current STING-targeting therapies.
Stegh noted that stimulating the STING pathway alone is unlikely to cure glioblastoma. The tumor uses several tactics to weaken or shut down the immune response. His group is exploring ways to build additional immune-activating features into their nanostructures, which could allow multiple therapeutic targets to be addressed through a single treatment.
“This is an approach that offers hope for safer, more effective treatments for glioblastoma and potentially other immune treatment-resistant cancers, and it marks a critical step toward clinical application,” Stegh said.
Study Funding and Disclosures
This work was supported by the National Cancer Institute of the NIH (grant numbers P50CA221747 and R01CA275430), the NIH (grants R01CA120813, R01NS120547, and R01CA272639), the Melanoma Research Foundation, the Chicago Cancer Baseball Charities at the Lurie Cancer Center of Northwestern University and grants from Cellularity, Alnylam, and AbbVie. Imaging at Siteman Cancer Center Small Animal Cancer Imaging was supported by NIH instrumentation grants S10OD027042, S10OD025264, and National Cancer Institute Cancer Center grant P30CA091842. PET and MRI imaging was supported by Robert H. Lurie Comprehensive Cancer Center Grant P30CA060553.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Competing interests: Alexander Stegh is a shareholder of Exicure Inc., which develops SNA therapeutic platforms. Mirkin is a shareholder in Flashpoint, which develops SNA-based therapeutics. Stegh and Mirkin are co-inventors on patent US20150031745A1, which describes SNA nanoconjugates to cross the blood-brain barrier.

In the United States, age-related macular degeneration is one of the most common causes of permanent vision loss in adults who are 60 and older. It affects the macula, the central region of the retina that contains tightly packed cells used for sharp, detailed color vision.
Roughly 20 million adults in the country are living with some form of AMD. People with this condition typically lose the ability to see objects directly in front of them, although their peripheral vision remains intact. Available therapies can slow how the disease progresses, but none of them can restore lost vision.
Exploring a New Cell-Based Approach
In a study published in Cell Stem Cell, scientists tested retinal pigment epithelial stem cells in a phase 1/2a clinical trial. The cells were obtained from adult postmortem eye tissue. These early-stage trials are designed to determine whether a treatment can be safely administered.
AMD occurs in two forms: dry and wet. More than 90% of patients have the dry type, which develops when retinal pigment epithelial cells begin to malfunction and eventually die.
In the early stages of AMD, these cells no longer work correctly. At more advanced stages, they die and cannot regenerate. As the condition worsens, multiple regions in the central retina lose these essential cells.
Transplanting Specialized Stem Cells
In the current study, individuals with advanced dry AMD received transplants of specialized stem cells originally sourced from eye-bank tissue. These adult stem cells were limited in function and could only mature into retinal pigment epithelial cells.

Six participants were given the lowest dose of the treatment (50,000 cells) during an eye surgery. The procedure proved safe, with no serious inflammation or tumor growth reported in any of the patients.
Early Signs of Vision Improvement
Participants also showed vision improvements in the treated eye, while their untreated eye did not show the same changes. This difference suggests that the technique itself may hold therapeutic potential. “Although we were pleased with the safety data, the exciting part was that their vision was also improving,” said Rajesh C. Rao, M.D., Leonard G. Miller Professor of Ophthalmology & Visual Sciences, and an associate professor of pathology and human genetics. “We were surprised by the magnitude of vision gain in the most severely affected patients who received the adult stem cell-derived RPE transplants. This level of vision gain has not been seen in this group of patients with advanced dry AMD.”
When tested on a standard eye chart, the low-dose group was able to read 21 additional letters one year after treatment.
Next Steps in the Clinical Trial
The research team is now monitoring 12 more participants who received higher doses of 150,000 and 250,000 cells. If no safety issues are identified, the investigators plan to move on to later stages of the clinical trial.

“We are grateful to all our participants who are allowing to better understand whether this intervention is safe enough to be a future therapy,” Rao said. “These kinds of NIH-funded studies can help us offer advanced treatments in the field of regenerative medicine, and we are happy we can offer this first-in-human, cutting-edge clinical trial at the University of Michigan.”
About Age-Related Macular Degeneration
Age-related macular degeneration is a condition that gradually damages the macula, the small but vital area at the back of the eye that supports sharp central vision. The disease typically develops as people get older, and it is more common in individuals over 60.
There are two primary forms of AMD. The dry form appears most often and involves the slow breakdown of retinal cells that help the eye process detail and color. The wet form is less common but progresses more quickly and involves abnormal blood vessel growth under the retina.
Over time, both types can cause blind spots in central vision, making activities such as reading and identifying faces increasingly difficult. While current treatments can slow the disease, scientists have been searching for ways to restore the lost cells, which is why stem cell research has become a promising direction.

Available for over a yearBaroness Hallett, Chair of the Inquiry, delivers her second report into the way the four governments of the UK responded to the pandemic. Summarising her conclusions as ‘too little, too late’, she outlines a failure by each government “to appreciate the scale of the threat or the urgency of the response it demanded”. Jim Reed reports.Programme WebsiteShow less

An extensive review of nearly two dozen long-term studies shows that people who smoke only a small number of cigarettes still face a much higher chance of heart disease and early death than those who have never smoked. This elevated risk remains for years after quitting. Michael Blaha of the Johns Hopkins Ciccarone Center for Prevention of Cardiovascular Disease, USA, and his team published the findings on November 18th in the open-access journal PLOS Medicine.
Previous research has already established that smoking raises the likelihood of cardiovascular disease, but the connection between smoking intensity and specific health consequences has been harder to clarify, particularly for light smokers. As more individuals smoke fewer cigarettes than in past decades, understanding both the risks tied to low-intensity smoking and the long-term benefits of quitting has become increasingly important, even for people who do not consider themselves heavy smokers.
Large Multi-Study Review Reveals Long-Term Damage
Blaha’s group examined information from more than 300,000 adults who participated in 22 longitudinal studies (which follow individuals over extended periods) for as long as 19.9 years. During that time, more than 125,000 deaths and 54,000 cardiovascular events were recorded, including heart attacks, strokes and heart failure. The results showed that smoking only two to five cigarettes per day was linked to a 50 percent higher risk of heart failure and a 60 percent higher risk of death from any cause compared with people who had never smoked. The greatest reduction in cardiovascular risk occurred within the first 10 years after quitting and continued to improve the longer a person remained smoke-free. Even so, former smokers still had higher risk levels than lifelong non-smokers for as long as three decades after they quit.
Quitting Completely Offers the Strongest Protection
Because even occasional or low-level smoking can sharply increase the chance of heart disease and premature death, the researchers emphasize that stopping entirely at a younger age is the most effective way to reduce long-term harm. Simply cutting back on the number of cigarettes smoked each day does not provide the same protective benefits. These findings support long-standing public health recommendations that encourage early and complete cessation and highlight the need for robust smoking prevention efforts.
Researchers Stress the Impact of Early Cessation
The authors add, “This is one of the largest studies of cigarette smoking to date using the highest quality data in the cardiovascular epidemiology literature. It is remarkable how harmful smoking is — even low doses of smoking confer large cardiovascular risks. As far as behavior change, it is imperative to quit smoking as early in life as possible, as the among of time passed since complete cessation from cigarettes is more important prolonged exposure to a lower quantity of cigarettes each day.”

Scientists have known for many years that hormones can shape how the brain works, affecting emotions, mental energy, and everyday choices. What remains unclear is exactly how these chemical signals bring about such changes.
A recent investigation offers new insight by examining the role of estrogen, a hormone central to the female reproductive cycle. Through controlled experiments using laboratory rats, researchers found that the brain processes involved in learning and decision-making shift naturally throughout the cycle. These shifts appear to stem from molecular changes linked to dopamine, the chemical messenger behind the “reward” signals that help the brain learn.
The study appears in the journal Nature Neuroscience.
How Estrogen May Shape Cognitive Function
“Despite the broad influence of hormones throughout the brain, little is known about how these hormones influence cognitive behaviors and related neurological activity,” explains Christine Constantinople, a professor in New York University’s Center for Neural Science and the senior author of the paper. “There is a growing realization in the medical community that changes in estrogen levels are related to cognitive function and, specifically, psychiatric disorders.”
Carla Golden, an NYU postdoctoral fellow and the paper’s lead author, adds, “Our results provide a potential biological explanation that bridges dopamine’s function with learning in ways that better inform our understanding of both health and disease.”
Laboratory Tests Reveal Estrogen’s Effects
The research team, which also included scientists from NYU Grossman School of Medicine’s Neuroscience Institute and Virginia Commonwealth University’s Department of Pharmacology and Toxicology, monitored brain activity in rats while the animals completed a set of learning tasks.

The rats learned to reach a “reward” — in this case, access to water — after recognizing audio cues that indicated when water would be available and how much they would receive.
Performance improved when estrogen levels were elevated. According to the authors, estrogen increases dopamine activity in regions of the brain responsible for reward processing, strengthening the signals that support learning.
Lower Estrogen Levels Reduce Learning Ability
When estrogen activity was reduced, limiting its influence on dopamine regulation, the rats learned less effectively. These findings suggest a possible link between hormone fluctuations and symptoms seen in certain neuropsychiatric disorders. The team also emphasized that estrogen’s influence did not extend to decision making; only learning was affected.
“All neuropsychiatric disorders show fluctuations in symptom severity over hormonal states, suggesting that a better understanding of how hormones influence neural circuits might reveal what causes these diseases,” notes Constantinople.
This research was funded by the National Institutes of Health (DP2MH126376, F32MH125448, 5T32MH019524, 1S10OD010582-01A1), the National Cancer Institute (P30CA016087), NYU Langone Health, and the Simons Foundation. The authors state that the content is solely their responsibility and does not necessarily represent the official views of the National Institutes of Health.

A research team at Mass General Brigham has released new evidence directly comparing how well tirzepatide (Mounjaro, Zepbound) and semaglutide (Ozempic, Wegovy) protect the heart. According to the analysis, both medications lowered the chances of heart attack, stroke, and death from any cause. The study appears in Nature Medicine, and the findings were also presented at the American Heart Association Scientific Sessions 2025.
Earlier studies had already shown that semaglutide lowers the likelihood of major cardiovascular events such as heart attacks and strokes. What had remained uncertain was whether tirzepatide, another widely used treatment for type 2 diabetes, offers similar protection.
Large Real-World Dataset Offers New Clarity
To investigate this, researchers examined national health insurance claims and compared cardiovascular outcomes among nearly one million adults using tirzepatide, semaglutide, or other type 2 diabetes therapies.
“Randomized controlled trials are often considered the reference standard in the medical evidence generation process. However, not all questions can be answered using this time- and resource-intensive method,” said first author Nils Krüger, MD, a research fellow in the Division of Pharmacoepidemiology and Pharmacoeconomics in the Mass General Brigham Department of Medicine. “Data generated in clinical practice and used secondarily for research allow us to address a wide range of clinically relevant questions time- and resource-effectively — when applied correctly. Moreover, we can study patients who reflect the reality of everyday clinical care, in contrast to the highly selected participants of randomized experiments.”
Risk Reductions Seen in Both Medications
The results showed measurable cardiovascular benefits among people with type 2 diabetes who were at higher risk for heart-related complications. When compared with sitagliptin, a diabetes medication known to have a neutral effect on cardiovascular outcomes, semaglutide lowered the combined risk of heart attack and stroke by 18 percent. Tirzepatide produced a 13 percent reduction in the risk of heart attack, stroke, and death when compared with dulaglutide, another GLP-1 receptor agonist that has been on the market for many years.

“Both drugs show strong cardioprotective effects. Our data also indicate that these benefits occur early, suggesting that their protective mechanisms go beyond weight loss alone,” said Krüger. Although the study highlights strong results, the biological pathways behind these heart-protective effects are still not fully understood.
Head-to-Head Comparisons Show Only Small Differences
Since these medications are relatively new, scientists continue to investigate how they protect the heart, especially in studies that directly compare tirzepatide and semaglutide. Krüger noted that “According to recently presented database analyses by the respective manufacturers, each company’s own drug appears to reduce cardiovascular risk much more effectively than the competitor’s.” He added, “However, our study found only small differences between tirzepatide and semaglutide in cardiovascular protection among populations at risk of adverse events, underscoring that both agents provide protective benefit and could be integrated into clinical cardiovascular practice.”
“We hope that our study will help clinicians better understand how these new medications work in clinical practice. Our transparent and open science practices, including pre-registration of a public protocol and shared analytic code, are designed to support scientific discussion,” said last author Shirley Wang, PhD, an associate epidemiologist in the Division of Pharmacoepidemiology and Pharmacoeconomics in the Mass General Brigham Department of Medicine.
Authorship: In addition to Krüger, Mass General Brigham authors include Sebastian Schneeweiss, Rishi J. Desai, Sushama Kattinakere Sreedhara, Anna R. Kehoe, Kenshiro Fuse, Georg Hahn, and Shirley V. Wang. Additional authors include Heribert Schunkert.
Disclosures: Schneeweiss reported personal fees from Aetion Inc, a software-enabled analytics company, and grants from Bayer, UCB, and Boehringer Ingelheim to Brigham and Women’s Hospital outside the submitted work. Schunkert reported personal fees from AstraZeneca, Bayer Vital GmbH, Boehringer Ingelheim, Bristol Myers Squibb, Daiichi Sankyo, MSD, Novartis, Pharmacosmos, Sanofi, Servier, Synlab, Amgen, and Amarin outside the submitted work. Wang reported personal fees from MITRE, a federally funded research and development center for the Centers for Medicare & Medicaid Services and personal fees from Cytel Inc during the conduct of the study. No other disclosures were reported.
Funding: This work was funded by the National Institutes of Health (R01-HL141505, R01-AR080194) and the German Heart Foundation (S/02/24, SRF-HF/24).

2 days agoShareSaveRuth CleggHealth and Wellbeing reporterShareSaveBBCIn my many years as a journalist, I never thought I would be asking someone how it feels to have trout sperm injected into their face.And yet, here I am.Abby is lying on a large, black padded chair at a small aesthetics clinic in south Manchester. She winces as a small cannula is delicately inserted into her cheek.”Ouch. Ouch,” she exclaims.I should make it clear that 29-year-old Abby is not actually receiving a pure dose of trout sperm. The lower part of her face is being injected with tiny fragments of DNA, known as polynucleotides, which have been extracted from either trout or salmon sperm.Why? Well, interestingly, our DNA is pretty similar to that of a fish.So the hope is Abby’s body will not only welcome these tiny strands of fish DNA, her skin cells will be spurred into action, producing more collagen and elastin, two proteins which are vital for maintaining the structural integrity of our skin.For Abby, the aim is to freshen her skin, keep it healthy, and hopefully, treat the acne she’s lived with for many years by reducing scarring and redness.”I just want to target those problem areas,” she explains.Polynucleotides are being touted as the next big skincare “miracle” and are rapidly gaining popularity after a number of celebrities have spoken candidly about their “salmon sperm facials”.Earlier this year, Charli XCX told her nine million Instagram followers that she felt “fillers are kind of over now”, and explained she had moved onto polynucleotides, which are “kinda like deep vitamins”.Kim and Khloe Kardashian are also reportedly avid fans. And when asked about her skincare routine on a recent episode of Jimmy Kimmel Live, Jennifer Aniston responded: “Don’t I have beautiful salmon skin?”EPA-EFE/REX/ShutterstockSo, despite their fishy beginnings, are polynucleotides transforming skincare?”We are having a Benjamin Button moment,” Suzanne Mansfield, who works for aesthetics company Dermafocus, tells me.That’s a reference to the 2008 film The Curious Case of Benjamin Button, where Brad Pitt plays a man who ages backwards. By the time he’s in his later years, he has the skin of a baby’s bottom.While such an effect is highly unlikely and would probably be a tad disconcerting, Ms Mansfield says polynucleotides are forging the way when it comes to regenerative skincare.A small but growing body of research and clinical trials suggest that injecting polynucleotides can rejuvenate skin, not only making it healthier but potentially reducing fine lines, wrinkles and scars.”All we are doing, by using it in the aesthetics industry,” she says, “is enhancing something the body already does. That’s why these are so special.”But they also come with a pretty hefty price tag.A single session of polynucleotide injections can cost anywhere from £200 to £500 – and it’s recommended you have three of these over several weeks. After that clinics tend to advise you need to top up every six to nine months to maintain the look.Back at the clinic, Abby’s treatment is almost finished.”Just one area left,” Helena Dunk, the aesthetic nurse practitioner who owns the clinic, Skin HD, reassures her.She says polynucleotides have massively increased in popularity over the past 18 months.”Half my clients really notice a huge difference – their skin feels more hydrated, healthier, younger – while the other half don’t see such a big change. But their skin does tend to feel tighter and fresher.”Abby has already had the area under her eyes injected as part of a three-course treatment at the clinic – and she’s really pleased with the results.She received lots of tiny injections of polynucleotides, which was a “pretty painful procedure”, but says it’s helped reduce the dark circles under her eyes.Charlotte BickleyWhile a growing number of studies consider it a safe and effective treatment, it is still relatively new and some experts warn the hype may be outpacing the science.Consultant dermatologist Dr John Pagliaro, based in Brisbane, Australia, says that while we know that nucleotides play an important role in our bodies – they are the building blocks of our DNA for a start – he questions whether “injecting salmon DNA, cut into little pieces” into our faces is going to work as well as our own nucleotides.”We do not have good, strong data,” he says. “As a medical specialist, I would want to see at least a few more years of big, credible studies showing safety and efficacy before I started using them in my practice. We’re just not there yet.”Charlotte Bickley describes her foray into the world of polynucleotides as “salmon-gate”. The 31-year-old from New York had the treatment last year as part of her “wedding glow up”, shortly before she was due to get married.But Charlotte ended up with a skin infection, inflammation and darker rings under her eyes than before she had the treatment.”I got the complete opposite of what I wanted,” she says. “I trusted that doctor, but he’s left me scarred.”Charlotte believes she was injected too deeply under her eyes, causing a negative reaction. There can be side effects – such as redness, swelling and bruising but these tend to be temporary.In some cases, people can have an allergic reaction, or, if polynucleotides are not injected properly, there are longer term risks, such as skin pigmentation and infections.Polynucleotides are widely used across the UK. They are registered as medical devices with the Medicines Health and Regulatory Authority (MHRA) but they are not regulated like medicines. They have not been approved by the UK’s equivalent in the US, the Food and Drug Administration (FDA).”I just keep thinking, ‘Why did I go through with it?'” Charlotte says. “When something goes wrong on my face I hyperfixate on it.”She’s paid thousands in medical bills to try to rectify the situation, but 10 months on, there’s still some scarring below her eyes.”I would never have salmon DNA injected into my face again,” Charlotte says, “ever.”Ashton Collins, director of Save Face, an organisation which campaigns for better regulation of the cosmetic industry and who runs a government-approved register of clinics in the UK, says polynucleotides are generally considered a safe treatment when administered by a medically-trained professional and the brand of polynucleotides used is from a reputable company.”But, we are now seeing products coming onto the market that haven’t been tested properly, that’s the worry,” she says.Dr Sophie Shotter, president of the British College of Aesthetic Medicine, agrees.”Due to the lack of regulation, anyone can use products that have not been robustly tested. It is a real issue.”In her opinion, are polynucleotides effective though?”I have them on my shelf, in my toolbox. I definitely offer them to clients, who want a natural look and want to potentially invest long-term,” Dr Shotter says.”Polynucleotides as a treatment is not the panacea. There are plenty of other treatments out there that can do similar, and have more data behind them.”There is no one treatment that will work for everyone, she adds.”We all respond differently to different things, and that is not always predictable.”More weekend picks

7 hours agoShareSavePhilippa Roxby,Health reporter and Alison Holt,Social affairs editorShareSaveGetty ImagesDetails of a new UK clinical trial to assess the risks and benefits of puberty-blocking drugs in children who question their gender have been announced.It follows the banning of the drugs for gender treatment last year after a major review raised concerns about the lack of clinical evidence over their safety for under-18s.Researchers from King’s College London say the trial will involve around 220 children under the age of 16 who are going through puberty, and will examine the impact of the drugs on their physical, social and emotional wellbeing.Some clinicians and campaigners question whether the trial is ethical.Prof Emily Simonoff, study leader and professor of child and adolescent psychiatry at King’s College London (KCL), said: “We know there are ongoing societal discussions about gender transition, but this research is focused solely on informing and improving healthcare by better understanding how to support the physical and mental health of young people with gender incongruence.”Puberty blockers, also known as puberty suppressing hormones (PSH), are drugs used to delay or prevent puberty happening.They were used to treat some young people with gender incongruence – when someone’s gender identity doesn’t match the sex they were registered at birth – or with gender dysphoria, when it causes significant distress.As a result of the uncertainty over the safety of the drugs, highlighted by the Cass review into gender care, led by paediatrician Dr Hilary Cass, doctors can now only offer the treatment to under-18s as part of a research study.Last year, the government brought in a UK-wide indefinite ban on the drugs being prescribed privately or by the NHS to children and young people questioning their gender identity.The new clinical trial, called Pathway, will involve children who are currently accessing gender services and have a diagnosis of gender incongruence.They will all have reached puberty, but will be younger than 16 – and will have to meet strict criteria, undergo intensive medical and psychological screening before they are allowed to start taking puberty blockers.A team of specialist NHS doctors must have a full picture of the young person’s wellbeing before deciding if they think they are suitable for the treatment.The young person will also have to show they have a good enough understanding of the potential impact of taking puberty blockers to give their consent, and their parent or legal guardian will need to agree. They will be provided with ongoing psychological support.To explore the impact of the drugs, the researchers plan to start one group on the treatment straight away and another group 12 months later. The children in these groups will be chosen randomly.The KCL researchers said there would be no minimum age for taking the drugs, but puberty normally starts around the age of 11 for girls and 12 for boys.The trial will look at issues such as bone density, brain development and mental health and wellbeing over time.The research team said the trial had been given ethical approval and was expected to start in January, with five to six children recruited every month. The first results should be available in around four years.Alongside this, a larger observational study involving 3,000 children will research different types of support and how effective they are.The puberty blockers trial has already proved controversial, with campaigners threatening legal action.Keira Bell, who took the Tavistock gender clinic to court in 2020 after she was given puberty blockers and cross-sex hormones as a teenager, said the trial should be halted immediately. If it is not, she says she and another campaigner will start judicial review proceedings at the High Court.She said it was “disgusting” that children were being put on the drugs when they had already been banned because they were “unsafe”.In her case, the High Court ruled that under-16s were “unlikely to be able to give informed consent” to puberty blockers, but this was later overturned by the Court of Appeal which ruled that doctors can judge whether young people can give consent to the treatment.Some clinicians from the Clinical Advisory Network on Sex and Gender, which campaigns for rigorous science and improved treatment options for gender-questioning people, have also questioned whether the trial can be carried out ethically. A spokesperson for charity Stonewall, which campaigns for the rights of LGBTQ+ people, said all young people should have access to the very best medical care, guided by evidence.”We urge the government and policymakers to invest in delivering excellent healthcare for trans young people and to make sure the voices of trans young people and their families are at its core.”

1 hour agoShareSaveMark NormanSouth East health correspondent ShareSaveMark Norman/BBCA non-smoker who was diagnosed with lung cancer at the age of 37 is campaigning for better awareness of the condition in young women. Jules Fielder, from Hastings, East Sussex, has secured a meeting with Health Secretary Wes Streeting after a social media campaign. Ms Fielding, now 41, said she was challenging “outdated stereotypes” about the condition, particularly that it only affects older people or people who smoke.She is demanding “urgent action” about one of the UK’s biggest cancer killers.Ms Fielder said she was given a prognosis of six to nine months in August. She said: “I just thought, right, this is it, now is the final straw for me. “I’m just going to use my lifeline as a tool and use the power of social media to try to grant me what I’m after. “And that is why I wanted Wes Streeting’s attention – to express how lung cancer is UK’s number one killer but has the least amount of limelight on it.” @CharlotteamyphotographyMs Fielder has a following of almost 35,000 people for her cancer journey blog on Instagram. Taking to social media in a coordinated movement with Roy Castle Lung Cancer Foundation, she asked followers to take a black and white photo holding their finger to their lips with the hashtag BreakTheSilence.Ms Fielding said the response was “overwhelming” which led to an invite from the Health Secretary. @CharlotteamyphotographyShe said she was determined to break down “outdated stereotypes” about the disease.She said: “We still live in such a dated time where the stigma around lung cancer is associated to a man, a smoker.”I’m not prepared to sit anymore and wait for another decade of non-smokers to appear in order for lung cancer to have the awareness and the attention that it needs.”More on this storyRelated internet links