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But the study of adolescents in the US also showed that even those with better sleeping habits were not reaching the amount of sleep recommended for their age group.

Sleep plays an important role in helping our bodies function. It is thought that while we are asleep, toxins that have built up in our brains are cleared out, and brain connections are consolidated and pruned, enhancing memory, learning, and problem-solving skills. Sleep has also been shown to boost our immune systems and improve our mental health.

During adolescence, our sleep patterns change. We tend to start going to bed later and sleeping less, which affects our body clocks. All of this coincides with a period of important development in our brain function and cognitive development. The American Academy of Sleep Medicine says that the ideal amount of sleep during this period is between eight- and 10-hours’ sleep.

Professor Barbara Sahakian from the Department of Psychiatry at the University of Cambridge said: “Regularly getting a good night’s sleep is important in helping us function properly, but while we know a lot about sleep in adulthood and later life, we know surprisingly little about sleep in adolescence, even though this is a crucial time in our development. How long do young people sleep for, for example, and what impact does this have on their brain function and cognitive performance?”

Studies looking at how much sleep adolescents get usually rely on self-reporting, which can be inaccurate. To get around this, a team led by researchers at Fudan University, Shanghai, and the University of Cambridge turned to data from the Adolescent Brain Cognitive Development (ABCD) Study, the largest long-term study of brain development and child health in the United States.

As part of the ABCD Study, more than 3,200 adolescents aged 11-12 years old had been given FitBits, allowing the researchers to look at objective data on their sleep patterns and to compare it against brain scans and results from cognitive tests. The team double-checked their results against two additional groups of 13-14 years old, totalling around 1,190 participants. The results are published today in Cell Reports.

The team found that the adolescents could be divided broadly into one of three groups:

Group One, accounting for around 39% of participants, slept an average (mean) of 7 hours 10 mins. They tended to go to bed and fall asleep the latest and wake up the earliest.

Group Two, accounting for 24% of participants, slept an average of 7 hours 21 mins. They had average levels across all sleep characteristics.

Group Three, accounting for 37% of participants, slept an average of 7 hours 25 mins. They tended to go to bed and fall asleep the earliest and had lower heart rates during sleep.

Although the researchers found no significant differences in school achievement between the groups, when it came to cognitive tests looking at aspects such as vocabulary, reading, problem solving and focus, Group Three performed better than Group Two, which in turn performed better than Group One.

Group Three also had the largest brain volume and best brain functions, with Group One the smallest volume and poorest brain functions.

Professor Sahakian said: “Even though the differences in the amount of sleep that each group got was relatively small, at just over a quarter-of-an-hour between the best and worst sleepers, we could still see differences in brain structure and activity and in how well they did at tasks. This drives home to us just how important it is to have a good night’s sleep at this important time in life.”

First author Dr Qing Ma from Fudan University said: “Although our study can’t answer conclusively whether young people have better brain function and perform better at tests because they sleep better, there are a number of studies that would support this idea. For example, research has shown the benefits of sleep on memory, especially on memory consolidation, which is important for learning.”

The researchers also assessed the participants’ heart rates, finding that Group Three had the lowest heart rates across the sleep states and Group One the highest. Lower heart rates are usually a sign of better health, whereas higher rates often accompany poor sleep quality like restless sleep, frequent awakenings and excessive daytime sleepiness.

Because the ABCD Study is a longitudinal study – that is, one that follows its participants over time – the team was able to show that the differences in sleep patterns, brain structure and function, and cognitive performance, tended be present two years before and two years after the snapshot that they looked at.

Senior author Dr Wei Cheng from Fudan University added: “Given the importance of sleep, we now need to look at why some children go to bed later and sleep less than others. Is it because of playing videogames or smartphones, for example, or is it just that their body clocks do not tell them it’s time to sleep until later?”

The research was supported by the National Key R&D Program of China, National Natural Science Foundation of China, National Postdoctoral Foundation of China and Shanghai Postdoctoral Excellence Program. The ABCD Study is supported by the National Institutes of Health.

Reference

Ma, Q et al. Neural correlates of device-based sleep characteristics in adolescents. Cell Reports; 22 Apr 2025; DOI: 10.1016/j.celrep.2025.115565

Adolescents who sleep for longer – and from an earlier bedtime – than their peers tend to have improved brain function and perform better at cognitive tests, researchers from the UK and China have shown.

Even though the differences in the amount of sleep that each group got was relatively small, we could still see differences in brain structure and activity and in how well they did at tasksBarbara Sahakianharpazo_hope (Getty Images)Teenager asleep and wrapped in a blanket

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Scientists at the Medical Research Council (MRC) Mitochondrial Biology Unit, University of Cambridge, have worked out the structure of this machine and shown how it operates like the lock on a canal to transport pyruvate – a molecule generated in the body from the breakdown of sugars – into our mitochondria.

Known as the mitochondrial pyruvate carrier, this molecular machine was first proposed to exist in 1971, but it has taken until now for scientists to visualise its structure at the atomic scale using cryo-electron microscopy, a technique used to magnify an image of an object to around 165,000 times its real size. Details are published today in Science Advances.

Dr Sotiria Tavoulari, a Senior Research Associate from the University of Cambridge, who first determined the composition of this molecular machine, said: “Sugars in our diet provide energy for our bodies to function. When they are broken down inside our cells they produce pyruvate, but to get the most out of this molecule it needs to be transferred inside the cell’s powerhouses, the mitochondria. There, it helps increase 15-fold the energy produced in the form of the cellular fuel ATP.”

Maximilian Sichrovsky, a PhD student at Hughes Hall and joint first author of the study, said: “Getting pyruvate into our mitochondria sounds straightforward, but until now we haven’t been able to understand the mechanism of how this process occurs. Using state-of-the-art cryo-electron microscopy, we’ve been able to show not only what this transporter looks like, but exactly how it works. It’s an extremely important process, and understanding it could lead to new treatments for a range of different conditions.”

Mitochondria are surrounded by two membranes. The outer one is porous, and pyruvate can easily pass through, but the inner membrane is impermeable to pyruvate. To transport pyruvate into the mitochondrion, first an outer ‘gate’ of the carrier opens, allowing pyruvate to enter the carrier. This gate then closes, and the inner gate opens, allowing the molecule to pass through into the mitochondrion.

“It works like the locks on a canal but on the molecular scale,” said Professor Edmund Kunji from the MRC Mitochondrial Biology Unit, and a Fellow at Trinity Hall, Cambridge. “There, a gate opens at one end, allowing the boat to enter. It then closes and the gate at the opposite end opens to allow the boat smooth transit through.”

Because of its central role in controlling the way mitochondria operate to produce energy, this carrier is now recognised as a promising drug target for a range of conditions, including diabetes, fatty liver disease, Parkinson’s disease, specific cancers, and even hair loss.

Pyruvate is not the only energy source available to us. Our cells can also take their energy from fats stored in the body or from amino acids in proteins. Blocking the pyruvate carrier would force the body to look elsewhere for its fuel – creating opportunities to treat a number of diseases. In fatty liver disease, for example, blocking access to pyruvate entry into mitochondria could encourage the body to use potentially dangerous fat that has been stored in liver cells.

Likewise, there are certain tumour cells that rely on pyruvate metabolism, such as in some types of prostate cancer. These cancers tend to be very ‘hungry’, producing excess pyruvate transport carriers to ensure they can feed more. Blocking the carrier could then starve these cancer cells of the energy they need to survive, killing them.

Previous studies have also suggested that inhibiting the mitochondrial pyruvate carrier may reverse hair loss. Activation of human follicle cells, which are responsible for hair growth, relies on metabolism and, in particular, the generation of lactate. When the mitochondrial pyruvate carrier is blocked from entering the mitochondria in these cells, it is instead converted to lactate.

Professor Kunji said: “Drugs inhibiting the function of the carrier can remodel how mitochondria work, which can be beneficial in certain conditions. Electron microscopy allows us to visualise exactly how these drugs bind inside the carrier to jam it – a spanner in the works, you could say. This creates new opportunities for structure-based drug design in order to develop better, more targeted drugs. This will be a real game changer.”

The research was supported by the Medical Research Council and was a collaboration with the groups of Professors Vanessa Leone at the Medical College of Wisconsin, Lucy Forrest at the National Institutes of Health, and Jan Steyaert at the Free University of Brussels.

Reference

Sichrovsky, M, Lacabanne, D, Ruprecht, JJ & Rana, JJ et al. Molecular basis of pyruvate transport and inhibition of the human mitochondrial pyruvate carrier. Sci Adv; 18 Apr 2025; DOI: 10.1126/sciadv.adw1489

Fifty years since its discovery, scientists have finally worked out how a molecular machine found in mitochondria, the ‘powerhouses’ of our cells, allows us to make the fuel we need from sugars, a process vital to all life on Earth.

Drugs inhibiting the function of the carrier can remodel how mitochondria work, which can be beneficial in certain conditionsEdmund Kunjibob_bosewell (Getty Images)Bald young man, front view

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Around 3,100 people are diagnosed with acute myeloid leukaemia (AML) each year in the UK. It is an aggressive form of blood cancer that is very difficult to treat. Thanks to recent advances, individuals at high risk of AML can be identified years in advance using blood tests and blood DNA analysis, but there’s no suitable treatment that can prevent them from developing the disease.

In this study, Professor George Vassiliou and colleagues at the University of Cambridge investigated how to prevent abnormal blood stem cells with genetic changes from progressing to become AML. The work focused on the most common genetic change, which affects a gene called DNMT3A and is responsible for starting 10-15% of AML cases.

Professor Vassiliou, from the Cambridge Stem Cell Institute at the University of Cambridge and Honorary Consultant Haematologist at Cambridge University Hospitals NHS Foundation Trust (CUH) co-led the study. He said: “Blood cancer poses unique challenges compared to solid cancers like breast or prostate, which can be surgically removed if identified early. With blood cancers, we need to identify people at risk and then use medical treatments to stop cancer progression throughout the body.”

The research team examined blood stem cells from mice with the same changes in DNMT3A as seen in the pre-cancerous cells in humans. Using a genome-wide screening technique, they showed that these cells depend more on mitochondrial metabolism than healthy cells, making this a potential weak spot. The researchers went on to confirm that metformin, and other mitochondria-targeting drugs, substantially slowed the growth of mutation-bearing blood cells in mice. Further experiments also showed that metformin could have the same effect on human blood cells with the DNMT3A mutation.

Dr Malgorzata Gozdecka, Senior Research Associate at the Cambridge Stem Cell Institute and first author of the research said: “Metformin is a drug that impacts mitochondrial metabolism, and these pre-cancerous cells need this energy to keep growing. By blocking this process, we stop the cells from expanding and progressing towards AML, whilst also reversing other effects of the mutated DNMT3A gene.”

In addition, the study looked at data from over 412,000 UK Biobank volunteers and found that people taking metformin were less likely to have changes in the DNMT3A gene. This link remained even after accounting for factors that could have confounded the results such as diabetes status and BMI.

Professor Brian Huntly, Head of the Department of Haematology at the University of Cambridge, Honorary Consultant Haematologist at CUH, and joint lead author of the research, added: “Metformin appears highly specific to this mutation rather than being a generic treatment. That specificity makes it especially compelling as a targeted prevention strategy.

“We’ve done the extensive research all the way from cell-based studies to human data, so we’re now at the point where we have a made a strong case for moving ahead with clinical trials. Importantly, metformin’s lack of toxicity will be a major advantage as it is already used by millions of people worldwide with a well-established safety profile.”

The results of the study, funded by Blood Cancer UK with additional support from Cancer Research UK, the Leukemia & Lymphoma Society (USA) and the Wellcome Trust, are published in Nature.

Dr Rubina Ahmed, Director of Research at Blood Cancer UK, said: “Blood cancer is the third biggest cancer killer in the UK, with over 280,000 people currently living with the disease. Our Blood Cancer Action plan shed light on the shockingly low survival for acute myeloid leukaemia, with only around 2 in 10 surviving for 5 years, and we urgently need better strategies to save lives. Repurposing safe, widely available drugs like metformin means we could potentially get new treatments to people faster, without the need for lengthy drug development pipelines.”

The next phase of this research will focus on clinical trials to test metformin’s effectiveness in people with changes in DNMT3A at increased risk of developing AML.  With metformin already approved and widely used for diabetes, this repurposing strategy could dramatically reduce the time it takes to bring a new preventive therapy to patients.

Tanya Hollands, Research Information Manager at Cancer Research UK, who contributed funding for the lab-based screening in mice, said: “It's important that we work to find new ways to slow down or prevent AML in people at high risk. Therefore, it’s positive that the findings of this study suggest a possible link between a commonly-used diabetes drug and prevention of AML progression in some people. While this early-stage research is promising, clinical trials are now needed to find out if this drug could benefit people. We look forward to seeing how this work progresses.”

Reference
Gozdecka, M et al. Mitochondrial metabolism sustains DNMT3A-R882-mutant clonal haematopoiesis. Nature; 16 Apr 2025; DOI: 10.1038/s41586-025-08980-6

Adapted from a press release from Blood Cancer UK

Metformin, a widely used and affordable diabetes drug, could prevent a form of acute myeloid leukaemia in people at high risk of the disease, a study in mice has suggested. Further research in clinical trials will be needed to confirm this works for patients.

We’ve done the extensive research all the way from cell-based studies to human data, so we’re now at the point where we have a made a strong case for moving ahead with clinical trialsBrian HuntlyUniversity of CambridgeBrown lab mouse on blue gloved hand

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Yes

In a paper published today in Nature Genetics, scientists at the University of Cambridge and NIHR Cambridge Biomedical Research Centre analysed the full DNA sequence of 4,775 tumours from seven types of cancer. They used that data from Genomics England’s 100,000 Genomes Project to create an algorithm capable of identifying tumours with faults in their DNA that makes them easier to treat.

The algorithm, called PRRDetect, could one day help doctors work out which patients are more likely to have successful treatment. That could pave the way for more personalised treatment plans that increase people’s chances of survival.

The research was funded by Cancer Research UK and the National Institute for Health and Care Research (NIHR).

Professor Serena Nik-Zainal  from the Early Cancer Institute at the University of Cambridge, lead author of the study, said: “Genomic sequencing is now far faster and cheaper than ever before. We are getting closer to the point where getting your tumour sequenced will be as routine as a scan or blood test.

“To use genomics most effectively in the clinic, we need tools which give us meaningful information about how a person’s tumour might respond to treatment. This is especially important in cancers where survival is poorer, like lung cancer and brain tumours.

“Cancers with faulty DNA repair are more likely to be treated successfully. PRRDetect helps us better identify those cancers and, as we sequence more and more cancers routinely in the clinic, it could ultimately help doctors better tailor treatments to individual patients.”

The research team looked for patterns in DNA created by so-called ‘indel’ mutations, in which letters are inserted or deleted from the normal DNA sequence.  

They found unusual patterns of indel mutations in cancers that had faulty DNA repair mechanisms – known as ‘post-replicative repair dysfunction’ or PRRd. Using this information, the scientists developed PRRDetect to allow them to identify tumours with this fault from a full DNA sequence.

PRRd tumours are more sensitive to immunotherapy, a type of cancer treatment that uses the body’s own immune system to attack cancer cells. The scientists hope that the PRRd algorithm could act like a ‘metal detector’ to allow them to identify patients who are more likely to have successful treatment with immunotherapy.

The study follows from a previous ‘archaeological dig’ of cancer genomes carried out by Professor Nik-Zainal, which examined the genomes of tens of thousands of people and revealed previously unseen patterns of mutations which are linked to cancer.

This time, Professor Nik-Zainal and her team looked at cancers which have a higher proportion of tumours with PRRd. These include bowel, brain, endometrial, skin, lung, bladder and stomach cancers. Whole genome sequences of these cancers were provided by the 100,000 Genomes Project - a pioneering study led by Genomics England and NHS England which sequenced 100,000 genomes from around 85,000 NHS patients affected by rare diseases or cancer.

The study identified 37 different patterns of indel mutations across the seven cancer types included in this study. Ten of these patterns were already linked to known causes of cancer, such as smoking and exposure to UV light. Eight of these patterns were linked to PRRd. The remaining 19 patterns were new and could be linked to causes of cancer that are not fully understood yet or mechanisms within cells that can go wrong when a cell becomes cancerous.

Executive Director of Research and Innovation at Cancer Research UK, Dr Iain Foulkes, said: “Genomic medicine will revolutionise how we approach cancer treatment. We can now get full readouts of tumour DNA much more easily, and with that comes a wealth of information about how an individual’s cancer can start, grow and spread.

“Tools like PRRDetect are going to make personalised treatment for cancer a reality for many more patients in the future. Personalising treatment is much more likely to be successful, ensuring more people can live longer, better lives free from the fear of cancer.”

NIHR Scientific Director, Mike Lewis, said: “Cancer is a leading cause of death in the UK so it's impressive to see our research lead to the creation of a tool to determine which therapy will lead to a higher likelihood of successful cancer treatment.”

Chief Scientific Officer at Genomics England, Professor Matt Brown, said: “Genomics is playing an increasingly important role in healthcare and these findings show how genomic data can be used to drive more predictive, preventative care leading to better outcomes for patients with cancer.

“The creation of this algorithm showcases the immense value of whole genome sequencing not only in research but also in the clinic across multiple diverse cancer types in advancing cancer care.”

Reference

Koh, GCC et al. Redefined indel taxonomy reveals insights into mutational signatures. Nat Gen; 10 Apr 2025; DOI:

Adapted from a press release from Cancer Research UK

Cambridge researchers have created a ‘metal detector’ algorithm that can hunt down vulnerable tumours, in a development that could one day revolutionise the treatment of cancer.

Genomic sequencing is now far faster and cheaper than ever before. We are getting closer to the point where getting your tumour sequenced will be as routine as a scan or blood testSerena Nik-ZainalUniversity of CambridgeSerena Nik-Zainal at the Early Cancer Institute

The text in this work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License. Images, including our videos, are Copyright ©University of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

YesLicence type: Attribution

The gene in question, FLCN, is linked to a condition known as Birt-Hogg-Dubé syndrome, symptoms of which include benign skin tumours, lung cysts, and an increased risk of kidney cancer.

In a study published today in the journal Thorax, a team from the University of Cambridge examined data from UK Biobank, the 100,000 Genomes Project, and East London Genes & Health – three large genomic datasets encompassing more than 550,000 people.

They discovered that between one in 2,710 and one in 4,190 individuals carries the particular variant of FLCN that underlies Birt-Hogg-Dubé syndrome. But curiously, whereas patients with a diagnosis of Birt-Hogg-Dubé syndrome have a lifetime risk of punctured lung of 37%, in the wider cohort of carriers of the genetic mutation this was lower at 28%. Even more striking, while patients with Birt-Hogg-Dubé syndrome have a 32% of developing kidney cancer, in the wider cohort this was only 1%.

Punctured lung – known as pneumothorax – is caused by an air leak in the lung, resulting in painful lung deflation and shortness of breath. Not every case of punctured lung is caused by a fault in the FLCN gene, however. Around one in 200 tall, thin young men in their teens or early twenties will experience a punctured lung, and for many of them the condition will resolve itself, or doctors will remove air or fluid from their lungs while treating the individual as an outpatient; many will not even know they have the condition.

If an individual experiences a punctured lung and doesn’t fit the common characteristics – for example, if they are in their forties – doctors will look for tell-tale cysts in the lower lungs, visible on an MRI scan. If these are present, then the individual is likely to have Birt-Hogg-Dubé syndrome.

Professor Marciniak is a researcher at the University of Cambridge and an honorary consultant at Cambridge University Hospitals NHS Foundation Trust and Royal Papworth Hospital NHS Foundation Trust. He co-leads the UK’s first Familial Pneumothorax Rare Disease Collaborative Network, together with Professor Kevin Blyth at Queen Elizabeth University Hospital and University of Glasgow. The aim of the Network is to optimise the care and treatment of patients with rare, inherited forms of familial pneumothorax, and to support research into this condition. 

Professor Marciniak said: “If an individual has Birt-Hogg-Dubé syndrome, then it’s very important that we’re able to diagnose it, because they and their family members may also be at risk of kidney cancer.

“The good news is that the punctured lung usually happens 10 to 20 years before the individual shows symptoms of kidney cancer, so we can keep an eye on them, screen them every year, and if we see the tumour it should still be early enough to cure it.”

Professor Marciniak says he was surprised to discover that the risk of kidney cancer was so much lower in carriers of the faulty FLCN gene who have not been diagnosed with Birt-Hogg-Dubé syndrome.

“Even though we’ve always thought of Birt-Hogg-Dubé syndrome as being caused by a single faulty gene, there’s clearly something else going on,” Professor Marciniak said. “The Birt-Hogg-Dubé patients that we've been caring for and studying for the past couple of decades are not representative of when this gene is broken in the wider population. There must be something else about their genetic background that’s interacting with the gene to cause the additional symptoms.”

The finding raises the question of whether, if an individual is found to have a fault FLCN gene, they should be offered screening for kidney cancer. However, Professor Marciniak does not believe this will be necessary.

“With increasing use of genetic testing, we will undoubtedly find more people with these mutations,” he said, “but unless we see the other tell-tale signs of Birt-Hogg-Dubé syndrome, our study shows there's no reason to believe they’ll have the same elevated cancer risk.”

The research was funded by the Myrovlytis Trust, with additional support from the National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Reference
Yngvadottir, B et al. Inherited predisposition to pneumothorax: Estimating the frequency of Birt-Hogg-Dubé syndrome from genomics and population cohorts. Thorax; 8 April 2025; DOI: 10.1136/thorax-2024-221738

As many as one in 3,000 people could be carrying a faulty gene that significantly increases their risk of a punctured lung, according to new estimates from Cambridge researchers. Previous estimates had put this risk closer to one in 200,000 people.

If an individual has Birt-Hogg-Dubé syndrome, then it’s very important that we’re able to diagnose it, because they and their family members may also be at risk of kidney cancerStefan Marciniakwildpixel (Getty Images)Chest pain

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Yes

AI has the potential to transform health and medicine. It won't be straightforward, but if we get it right, the benefits could be enormous. Andres Floto, Mihaela van der Schaar and Eoin McKinney explain.

Cambridge researchers are looking at ways that AI can transform everything from drug discovery to Alzheimer's diagnoses to GP consultations.

Dr. Ayla Selamoglu is an expert on psychedelic medicine. Her work shows how nature’s most mysterious compounds provide new ways to combat mental illness.

A machine learning algorithm developed by Cambridge scientists was able to correctly identify in 97 cases out of 100 whether or not an individual had coeliac disease based on their biopsy, new research has shown.

Scientists have developed a new technique that has enabled ultra-powerful MRI scanners to identify tiny differences in patients’ brains that cause treatment-resistant epilepsy. It has allowed doctors at Addenbrooke’s Hospital, Cambridge, to offer the patients surgery to cure their condition.

Today sees the launch of the POrtal for Patient and Public Engagement in Dementia Research (POPPED) website, where anyone can give their feedback on dementia research projects.

Dementia affects 50 million people worldwide and 1 million people in the UK. Current treatments are limited, but research has led to some significant recent advances. For example, the first drugs which slow down the disease are now licensed in the UK and potential dementia blood tests are being trialled.

Scientists are also turning to existing drugs to see if they may be repurposed to treat dementia. As the safety profile of these drugs is already known, the move to clinical trials can be accelerated significantly. Researchers want to ask members of the public which drugs they would like to see prioritised for these clinical trials.

Dr Ben Underwood, from the Department of Psychiatry at the University of Cambridge and Cambridgeshire and Peterborough NHS Foundation Trust, said: “One thing that always improves research into medical conditions is the involvement of people with experience of them – in many respects, you are the experts, rather than us.

“As dementia is common, almost everyone has some experience of it, either through family, friends, work or meeting people with dementia in general life. It’s a problem across society and we want a wide range of opinions for the best way to tackle it.”

Dr Underwood has teamed up with Linda Pointon, a Programme Manager at the Department of Psychiatry, to create a website where everyone can give their feedback on dementia research projects. Linda herself has experience of caring for her mother-in-law, who had frontotemporal dementia and passed away in 2020.

Linda said: “We’re launching our website because we want as many people as possible to share their views and help us guide the direction of our research. It’s a great opportunity for all of us who have been affected by dementia, either directly or caring for a friend or relative, to help researchers understand what aspects of these potential treatments are important and meaningful, both in terms of benefits and side-effects.”

The information collected by the POPPED team will be used to help inform AD-SMART, a trial to be led by Imperial College London, which will test several existing drugs alongside a placebo to quickly determine if any can slow early Alzheimer’s progression.

Dr Underwood added: “Instead of asking a few people what might be helpful, our website gives us the opportunity to ask thousands of people. The more people who use it, the more powerful it will be, so I’d encourage everyone to visit the site and tell us what they think. We can use it to work together to beat dementia, a condition whose effects I see in my clinic every day.”

Cambridge researchers are seeking the views of people with lived experience of dementia – patients and their friends and families – on which existing drugs should be repurposed for clinical trials to see whether they can slow or halt the progress of dementia.

One thing that always improves research into medical conditions is the involvement of people with experience of them – in many ways, they are the experts, not usBen UnderwoodToa55 (Getty Images)Elderly woman putting pills into pill box for the week - stock photo

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Yes

The technique – known as deep brain stimulation – is to be trialled at Addenbrooke’s Hospital, Cambridge, and King’s College Hospital, London. The team behind the Brain-PACER: Brain Pacemaker Addiction Control to End Relapse study is currently recruiting individuals with severe alcohol or opioid addiction who are interested in taking part.

Deep brain stimulation (DBS) is a neurosurgical procedure that delivers ongoing stimulation to the brain. DBS acts as a brain pacemaker to normalise abnormal brain activity. It is well-tolerated, effective and widely used for neurological disorders and obsessive compulsive disorder.

Although there have been several proof-of-concept studies that suggest DBS is effective in addictions, Brain-PACER – a collaboration between the University of Cambridge, Kings College London and the University of Oxford – is the first major, multicentre study to use DBS to treat craving and relapse in severe addiction.

Chief Investigator Professor Valerie Voon, from the Department of Psychiatry at the University of Cambridge, said: “While many people who experience alcohol or drug addiction can, with the right support, control their impulses, for some people, their addiction is so severe that no treatments are effective. Their addiction is hugely harmful to their health and wellbeing, to their relationships and their everyday lives.

“Initial evidence suggests that deep brain stimulation may be able to help these individuals manage their conditions. We’ve seen how effective it can be for other neurological disorders from Parkinson’s to OCD to depression. We want to see if it can also transform the lives of people with intractable alcohol and opioid addiction.”

The primary aim of the Brain-PACER study is to assess the effects of DBS to treat alcohol and opioid addiction in a randomised controlled trial study. Its mission is twofold: to develop effective treatments for addiction and to understand the brain mechanisms that drive addiction disorders.

DBS is a neurosurgical treatment that involves implanting a slender electrode in the brain and a pacemaker under general anaesthesia. These electrodes deliver electrical impulses to modulate neural activity, which can help alleviate symptoms of various neurological and psychiatric disorders.

Keyoumars Ashkan, Professor of Neurosurgery at King’s College Hospital and the lead surgeon for the study, said: “Deep brain stimulation is a powerful surgical technique that can transform lives. It will be a major leap forward if we can show efficacy in this very difficult disease with huge burden to the patients and society.”

During surgery, thin electrodes are carefully placed in precise locations of the brain. These locations are chosen based on the condition being treated. For addiction, the electrodes are placed in areas involved in reward, motivation, and decision-making.

Harry Bulstrode, Honorary Consultant Neurosurgeon at Cambridge University Hospitals NHS Foundation Trust and Clinical Lecturer at the University of Cambridge, said: "We see first-hand how deep brain stimulation surgery can be life-changing for patients with movement disorders such as Parkinson’s disease and essential tremor. Thanks to this trial, I am now hopeful that we can help patients and their families – who have often struggled for years – by targeting the parts of the brain linked to addiction."

Dr David Okai, Visiting Senior Lecturer from the Institute of Psychiatry, Psychology & Neuroscience, King’s College London, added: “DBS is safe, reversible and adjustable, so it offers a flexible option for managing chronic conditions. We hope it will offer a lifeline to help improve the quality of life for patients whose treatment until now has been unsuccessful.”

Details on the trial, including criteria for participation and how to sign up, can be found on the Brain-PACER website.

The research is supported by the Medical Research Council, UK Research & Innovation.

People suffering from severe alcohol and opioid addiction are to be offered a revolutionary new technique involving planting electrodes in the brain to modulate brain activity and cravings and improve self-control.

We’ve seen how effective deep brain stimulation can be for neurological disorders from Parkinson’s to OCD to depression. We want to see if it can also transform the lives of people with intractable alcohol and opioid addictionValerie VoonShamir R, Noecker A and McIntyre CGraphic demonstrating deep brain stimulation

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Using real world data from 1,600 patients, available through a database created for speeding up research and innovation, the team also found that its reliability differs significantly in winter compared to autumn.

Asthma is a common lung condition that can cause wheezing and shortness of breath, occasionally severe. Around 6.5% of people over six years old in the UK are affected by the condition. Treatments include the use of inhalers or nebulisers to carry medication into the lungs.

The majority of asthma attacks occur at nighttime or early in the morning. Although this may in part be due to cooler nighttime air and exposure to dust mites and allergens, it also suggests that circadian rhythms – our ‘body clocks’ – likely play a role.

Researchers at the Victor Phillip Dahdaleh Heart and Lung Research Institute, a collaboration between the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust (RPH), wanted to explore whether these circadian rhythms may also have an impact on our ability to diagnose asthma, using routinely performed clinical testing.

Typically, people with suspected asthma will be offered a spirometry test, which involves taking a deep breath in, then breathing out hard and fast for as long as possible into a tube to assess lung function. They will then be administered the drug salbutamol via an inhaler or nebuliser, and shortly afterwards retake the spirometry test.

Salbutamol works by opening up the airways, so a positive test result – that is, a difference in readings between the initial and follow-up spirometry tests – means that the airways must have been narrower or obstructed to begin with, suggesting that the patient could have asthma.

Cambridge University Hospitals NHS Foundation Trust (CUH) has recently set up the Electronic Patient Record Research and Innovation (ERIN) database so that researchers can access patient data in a secure environment to help in their research and speed up improvements in patient care.

Using this resource, the Cambridge team analysed data from 1,600 patients referred to CUH between 2016 and 2023, adjusted for factors such as age, sex, body mass index (BMI), smoking history, and the severity of the initial impairment in lung function.

In findings published today in Thorax, the researchers found that starting at 8.30am, with every hour that passed during the working day, the chances of a positive response to the test – in other words, the patient’s lungs responding to treatment, suggesting that they could have asthma – decreased by 8%.

Dr Ben Knox-Brown, Lead Research Respiratory Physiologist at RPH, said: “Given what we know about how the risk of an asthma attack changes between night and day, we expected to find a difference in how people responded to the lung function test, but even so, we were surprised by the size of the effect.

“This has potentially important implications. Doing the test in the morning would give a more reliable representation of a patient's response to the medication than doing it in the afternoon, which is important when confirming a diagnosis such as asthma.”

The researchers also discovered that individuals were 33% less likely to have a positive result if tested during autumn when compared to those tested during winter.

Dr Akhilesh Jha, a Medical Research Council Clinician Scientist at the University of Cambridge and Honorary Consultant in Respiratory Medicine at CUH, said that there may be a combination of factors behind this difference.

“Our bodies have natural rhythms – our body clocks,” Jha said. “Throughout the day, the levels of different hormones in our bodies go up and down and our immune systems perform differently, for example. Any of these factors might affect how people respond to the lung function test.

“The idea that the time of day, or the season of the year, affects our health and how we respond to treatments is something we’re seeing increasing evidence of. We know, for example, that people respond differently to vaccinations depending on whether they’re administered in the morning or afternoon. The findings of our study further support this idea and may need to be taken into account when interpreting the results of these commonly performed tests.”

Reference
Knox-Brown, B et al. The effect of time of day and seasonal variation on bronchodilator responsiveness: The SPIRO-TIMETRY study. Thorax; 12 March 2025; DOI: 10.1136/thorax-2024-222773

A lung function test used to help diagnose asthma works better in the morning, becoming less reliable throughout the day, Cambridge researchers have found.

Throughout the day, the levels of different hormones in our bodies go up and down and our immune systems perform differently. Any of these factors might affect how people respond to the lung function testAkhilesh JhaKoldunov (Getty Images)Man testing breathing function by spirometry - stock photo

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Yes

Clare Bryant, Professor of Innate Immunity, is a molecular detective. Clare allows us to see how inflammation functions across species, and when our defence systems go too far.

A study involving over 3,000 participants – both patients and clinicians – found that these misdiagnoses (sometimes termed “in your head” by patients) were often associated with long term impacts on patients’ physical health and wellbeing and damaged trust in healthcare services.

The researchers are calling for greater awareness among clinicians of the symptoms of such diseases, which they recognise can be difficult to diagnose, and for more support for patients.

Autoimmune rheumatic diseases such as rheumatoid arthritis, lupus and vasculitis are chronic inflammatory disorders that affect the immune system and can damage organs and tissues throughout the body. They can be very difficult to diagnose as people report a wide range of different symptoms, many of which can be invisible, such as extreme fatigue and depression.

Dr Melanie Sloan from the University of Cambridge led a study exploring patient-reported experiences from two large groups, each of over 1,500 patients, and in-depth interviews with 67 patients and 50 clinicians. The results are published today in Rheumatology.

Patients who reported that their autoimmune disease was misdiagnosed as psychosomatic or a mental health condition were more likely to experience higher levels of depression and anxiety, and lower mental wellbeing. For example, one patient with multiple autoimmune diseases said: “One doctor told me I was making myself feel pain and I still can’t forget those words. Telling me I’m doing it to myself has made me very anxious and depressed.”

More than 80% said it had damaged their self-worth and 72% of patients reported that the misdiagnosis still upset them, often even decades later. Misdiagnosed patients also reported lower levels of satisfaction with every aspect of medical care and were more likely to distrust doctors, downplay their symptoms, and avoid healthcare services. As one patient reported, it “has damaged my trust and courage in telling doctors very much. I even stopped taking my immunosuppressive medicine because of those words”.

Following these types of misdiagnoses, patients often then blamed themselves for their condition, as one individual described: “I don’t deserve help because this is a disease I’ve brought on myself. You go back to those initial diagnosis, you’ve always got their voices in your head, saying you’re doing this to yourself. You just can’t ever shake that. I’ve tried so hard.”

One patient described the traumatising response their doctor’s judgement had on them: “When a rheumatologist dismissed me I was already suicidal, this just threw me over the edge. Thankfully I am terrible at killing myself, it’s so much more challenging than you think. But the dreadful dismissiveness of doctors when you have a bizarre collection of symptoms is traumatizing and you start to believe them, that it’s all in your head.”

Dr Melanie Sloan, from the Department of Public Health and Primary Care at the University of Cambridge, said: “Although many doctors were intending to be reassuring in suggesting a psychosomatic or psychiatric cause for initially unexplainable symptoms, these types of misdiagnoses can create a multitude of negative feelings and impacts on lives, self-worth and care. These appear to rarely be resolved even after the correct diagnoses. We must do better at helping these patients heal, and in educating clinicians to consider autoimmunity at an earlier stage.”      

Clinicians highlighted how hard it was to diagnose autoimmune rheumatic diseases and that there was a high risk of misdiagnosis. Some doctors said they hadn’t really thought about the long-term problems for patients, but others talked about the problems in regaining trust, as one GP from England highlighted: “They lose trust in anything that anyone says…you are trying to convince them that something is OK, and they will say yes but a doctor before said that and was wrong.”

However, there was evidence that this trust can be rebuilt. One patient described having been “badly gaslit by a clinician”, but that when they told the clinician this, “She was shocked and had no idea … She was great. Took it on the chin. Listened and heard. Apologised profusely…For me, the scar of the original encounter was transformed into something much more positive.”

Mike Bosley, autoimmune patient and co-author on the study, said: “We need more clinicians to understand how a misdiagnosis of this sort can result in long-standing mental and emotional harm and in a disastrous loss of trust in doctors. Everyone needs to appreciate that autoimmune conditions can present in these unusual ways, that listening carefully to patients is key to avoiding the long-lasting harm that a mental health or psychosomatic misdiagnosis can cause.”

The study authors recommend several measures for improving support for patients with autoimmune rheumatological diseases. These are likely to apply for many other groups of patients with chronic diseases that are often misunderstood and initially misdiagnosed.

They propose that clinicians should talk about previous misdiagnoses with patients, discuss and empathise with their patients as to the effects on them, and offer targeted support to reduce the long-term negative impacts. Health services should ensure greater access to psychologists and talking therapies for patients reporting previous misdiagnoses, which may reduce the long-term impact on wellbeing, healthcare behaviours, and patient-doctor relationships. Education may reduce misdiagnoses by encouraging clinicians to consider systemic autoimmunity when they assess patients with multiple, seemingly unconnected, physical and mental health symptoms.

Professor Felix Naughton, from the Lifespan Health Research Centre at the University of East Anglia, said: “Diagnosing autoimmune rheumatic diseases can be challenging, but with better awareness among clinicians of how they present, we can hopefully reduce the risk of misdiagnoses. And while there will unfortunately inevitably still be patients whose condition is not correctly diagnosed, with the correct support in place, we may be able to lessen the impact on them.”

The research was funded by LUPUS UK and The Lupus Trust.

Reference
Sloan, M, et al. “I still can’t forget those words”: mixed methods study of the persisting impacts of psychosomatic and psychiatric misdiagnoses. Rheumatology; 3 Mar 2025; DOI: 10.1093/rheumatology/keaf115

A ‘chasm of misunderstanding and miscommunication’ is often experienced between clinicians and patients, leading to autoimmune diseases such as lupus and vasculitis being wrongly diagnosed as psychiatric or psychosomatic conditions, with a profound and lasting impact on patients, researchers have found.

These types of misdiagnoses can create a multitude of negative feelings and impacts on lives, self-worth and careMel SloanAnnie SprattA person laying in a bed under a blanket

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The findings, published today in Science Advances, suggest that such individuals will need regular vaccine boosters to protect them and reduce the risk of infections that could be severe and also lead to new ‘variants of concern’ emerging.

Almost 16 million people worldwide are estimated to have died from Covid-19 during 2020 and 2021, though nearly 20 million deaths are thought to have been prevented as a result of the rapid rollout of vaccines against SARS-CoV-2, the virus that caused the pandemic.

During the pandemic, researchers discovered that immunocompromised individuals had difficulty clearing the virus, even when vaccinated. These are people whose immune systems are not functioning correctly, either as a direct result of disease or because they are on medication to dampen down their immune systems, for example to prevent organ transplant rejection. This meant that their infections lasted longer, giving the virus more opportunities to mutate.

Research from early in the pandemic showed that chronic infections can give rise to variants of concern that can then cause new waves of infection in the wider population.

When an individual is vaccinated, their immune systems produce antibodies that recognise and launch an attack on the virus. Such a process is known as seroconversion. Additional ‘booster’ vaccinations increase seroconversion and hence the likelihood of clearing infection.

However, although most immunocompromised individuals will have received three or more doses of the Covid-19 vaccine, they still account for more than a fifth of hospitalisations, admissions to intensive care units, and overall deaths associated with the disease.

To see why this is the case, scientists at the Cambridge Institute of Therapeutic Immunology and Infectious Disease (CITIID) at the University of Cambridge examined immunocompromised individuals who had been vaccinated against Covid-19. These patients, recruited from Cambridge University Hospitals NHS Foundation Trust, were living with vasculitis, a group of disorders that cause inflammation of blood vessels. Data from this group was compared against individuals who were not immunocompromised.

Treatments for vasculitis rely on immunosuppressant medicines. These include drugs such as rituximab, which depletes the number of B-cells in the body – but B-cells are the immune cells responsible for producing antibodies. As such, these individuals are a severely at-risk population.

When the researchers analysed bloods samples from the vasculitis patients, they found that even though vaccination induced seroconversion, this in itself was not always sufficient to neutralise the virus. Every immunocompromised individual required at least three doses of the vaccine to protect them across a range of variants up to and include Omicron (the variant that appeared towards the end of 2021 and caused a new wave of infections). In some cases, even four vaccinations were not sufficient to adequately protect them.

Kimia Kamelian, a Gates Cambridge Scholar at CITIID and St Edmund's College, Cambridge, said: “We know that immunocompromised individuals are particularly vulnerable to diseases such as Covid-19 because their immune systems struggle to clear infections. Vaccinations offer some protection, but our study shows that only repeated vaccinations – often four or more – offer the necessary protection.”

Professor Ravi Gupta, also from CITIID and a Fellow at Homerton College, Cambridge, added: “This of course has implications for the individual, who is more likely to have prolonged infection and a much greater risk of severe infection, but it also gives the virus multiple opportunities to mutate.

“We know from our previous work that at least some of the variants of concern probably emerged during chronic infections. That’s why these individuals must be given priority for updated vaccines against new variants.”

The research was funded by Wellcome, Gates Cambridge, Addenbrooke’s Charitable Trust and Vasculitis UK, with additional support by the National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Reference
Kamelian, K et al. Humoral responses to SARS-CoV-2 vaccine in vasculitis-related immune suppression. Sci Adv; 12 Feb 2025; DOI: 10.1126/sciadv.adq3342

Vaccinations alone may not be enough to protect people with compromised immune systems from infection, even if the vaccine has generated the production of antibodies, new research from the University of Cambridge has shown.

We know that immunocompromised individuals are particularly vulnerable to diseases such as Covid-19 because their immune systems struggle to clear infectionsKimia KamelianNoSystem imagesVaccination of an senior male

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Published today in Nature, this comprehensive resource, called HYPOMAP, provides an unparalleled view of the brain’s appetite centre and promises to accelerate the development of treatments for obesity and diabetes.

The hypothalamus is often described as the brain’s ‘control centre’, orchestrating many of the body’s most vital processes. While much of our knowledge of the hypothalamus comes from animal studies, especially in mice, translating these findings to humans has long been a challenge. HYPOMAP bridges this gap by providing an atlas of the individual cells within the human hypothalamus. This resource not only charts over 450 unique cell types but also highlights key differences between the human and mouse hypothalamus — differences that have major implications for drug development.

“This is a game-changer for understanding the human hypothalamus,” said Professor Giles Yeo, senior author of the study from the Institute of Metabolic Science-Metabolic Research Laboratories (IMS-MRL) and MRC Metabolic Diseases Unit, University of Cambridge.

“HYPOMAP confirms the critical role of the hypothalamus in body-weight regulation and has already allowed us to identify new genes linked to obesity. It gives us a roadmap to develop more effective, human-specific therapies.”

Together with researchers at the Max Planck Institute for Metabolism Research in Cologne, Professor Yeo and colleagues used cutting-edge technologies to analyse over 400,000 cells from 18 human donors. HYPOMAP allows researchers to pinpoint specific cell types, understand their genetic profiles, and explore how they interact with neighbouring cells. This detailed cellular resolution offers invaluable insights into the circuits that regulate appetite and energy balance, as well as other functions such as sleep and stress responses.

Comparison with a mouse hypothalamus atlas revealed both similarities and critical differences. Notably, some neurons in the mouse hypothalamus have receptors for GLP-1 — targets of popular weight-loss drugs like semaglutide — that are absent in humans.

"While drugs like semaglutide have shown success in treating obesity, newer therapies target multiple receptors such as GLP-1R and GIPR. Understanding how these receptors function specifically in the human hypothalamus is now crucial for designing safer and more effective treatments," said Dr Georgina Dowsett from the Max Planck Institute for Metabolism Research and formerly at the IMS-MRL.

“Our map of the human hypothalamus is an essential tool for basic and translational research,” added Professor Jens C. Brüning, Director at the Max Planck Institute. “It allows us to pinpoint which mouse nerve cells are most comparable to human cells, enabling more targeted preclinical studies.”

HYPOMAP’s open-access nature ensures that it will be an invaluable resource for scientists worldwide. By offering insights into the hypothalamus’s role in conditions ranging from obesity to cachexia (a wasting condition associated with several illness, which involves extreme loss of muscle and fat), it provides a foundation for tackling some of the most pressing health challenges of our time.

Dr John Tadross, Consultant Pathologist at Addenbrooke’s Hospital and lead author from IMS-MRL, said: “This is just the beginning. The atlas itself is a milestone, but what could really make a difference for patients is understanding how the hypothalamus changes in people who are overweight or underweight. This could fundamentally shift our approach to metabolic health and enable more personalised therapies.”

With HYPOMAP, researchers have a new tool to unlock the secrets of the human brain’s metabolic control centre. By better understanding the human hypothalamus, science takes a significant step toward combating obesity, diabetes, and related conditions.

Reference
Tadross, JA, Steuernagel, L & Dowsett, GKC et al. A comprehensive spatio-cellular map of the human hypothalamus. Nature; 5 Feb 2025; DOI: 10.1038/s41586-024-08504-8

Adapted from a story by the Institute of Metabolic Science-Metabolic Research Laboratories and the Max Planck Institute for Metabolism Research

Scientists have created the most detailed map to date of the human hypothalamus, a crucial brain region that regulates body weight, appetite, sleep, and stress.

HYPOMAP confirms the critical role of the hypothalamus in body-weight regulation and has already allowed us to identify new genes linked to obesityGiles YeoSander DalhuisenPerson holding burger bun with vegetables and meat

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The Cambridge Awards for Research Impact and Engagement, formerly the Vice-Chancellor's Award, are held annually to recognise exceptional achievement, innovation, and creativity in developing research engagement and impact plans with significant economic, social, and cultural potential. Awarded in three categories, the winners for 2024 are:

Established Academic

Winner: Professor Sander van der Linden (Department of Psychology, School of Biological Sciences and Churchill College) and his team at the Cambridge Social Decision-Making Lab (Team application)

Project: A Psychological Vaccine Against Misinformation

Professor Sander van der Linden and team have developed a novel approach to countering the spread of harmful misinformation. This ‘psychological vaccine’ resulted in award winning public impact tools that have shown millions of people how to spot fake news online. These games have been adopted by the World Health Organisation, United Nations, UK Government and Google and led to key policy changes in the EU Digital Services Act.

Early Career Researcher

Winner: Dr Gabriel Okello (Cambridge Institute for Sustainability Leadership, School of Technology)

Project: Applying multidisciplinary, collaborative approaches to tackle air pollution in rapidly urbanising African cities

The project catalysed Uganda’s first-ever Air Quality Standards, advancing policy and public health. It drove transformative growth in the e-mobility sector and battery-swapping stations. The Clean Air Network was established as a multi-regional community of practice for air quality management across Africa. The platform now provides real-time air quality data enabling evidence-based decision-making in Uganda and eight other African countries.

Collolaboration Award

Winner: 

Lead: Prof Paul Fletcher (Department of Psychiatry, School of Clinical Medicine, Clare College), Dr Dervila Glynn (Cambridge Neuroscience IRC), Dominic Matthews (Ninja Theory Ltd), Sharon Gilfoyle (Cambridgeshire and Peterborough NHS Foundation Trust)

Project: Representing psychosis in video games: Communicating clinical science and tackling stigma

This work draws together expertise in video game design and clinical neuroscience, with lived experience of mental illness to co-produce two award-winning video games vividly conveying the nature of altered experience of reality in a character with psychosis. Within conversations around mental health, psychosis is neglected and highly stigmatised.

In creating a powerful character and telling her story through gameplay, the project has enabled sensitive and thoughtful conversations about psychosis, and mental illness in general. It has had a measurably positive impact on stigma.

Find out more about the winning projects and meet our runners-up here: www.cam.ac.uk/public-engagement/cambridge-awards-2024. 

From helping to inoculate the public against misinformation to tackling air pollution in rapidly urbanising African cities, researchers from across the University of Cambridge were honoured at the Cambridge Awards yesterday (Monday 3rd February) afternoon.

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Meet the winner of the Cambridge Awards 2024 for Research Impact and Engagement and learn more about their projects.

Medical students are taught about some of the rarest diseases, yet do not learn something as important as how to care for trans patients. This needs to change, says intensive care specialist Luke Flower.