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Scientists have used an AI model to reassess the results of a completed clinical trial for an Alzheimer’s disease drug. They found the drug slowed cognitive decline by 46% in a group of patients with early stage, slow-progressing mild cognitive impairment – a condition that can progress to Alzheimer’s.

Using AI allowed the team to split trial participants into two groups: either slowly or rapidly progressing towards Alzheimer’s disease. They could then look at the effects of the drug on each group.

More precise selection of trial participants in this way could help select patients most likely to benefit from treatment, with the potential to reduce the cost of developing new medicines by streamlining clinical trials.

The AI model developed by researchers at the University of Cambridge predicts whether, and how quickly, people at early stages of cognitive decline will progress to full-blown Alzheimer’s. It gives predictions for patients that are three times more accurate than standard clinical assessments based on memory tests, MRI scans and blood tests.  

Using this patient stratification model, data from a completed clinical trial - which did not demonstrate efficacy in the total population studied - was re-analysed. The researchers found that the drug cleared a protein called beta amyloid in both patient groups as intended - but only the early stage, slow-progressing patients showed changes in symptoms. Beta amyloid is one of the first disease markers to appear in the brain in Alzheimer’s disease.

The new findings have significant implications: using AI to separate patients into different groups, such as slow versus rapidly progressing towards Alzheimer’s disease, allows scientists to better identify those who could benefit from a treatment approach - potentially accelerating the discovery of much-needed new Alzheimer’s drugs.

The results are published today in the journal Nature Communications.

Professor Zoe Kourtzi in the University of Cambridge’s Department of Psychology, senior author of the report, said: “Promising new drugs fail when given to people too late, when they have no chance of benefiting from them. With our AI model we can finally identify patients precisely, and match the right patients to the right drugs. This makes trials more precise, so they can progress faster and cost less, turbocharging the search for a desperately-need precision medicine approach for dementia treatment.”  

She added: “Our AI model gives us a score to show how quickly each patient will progress towards Alzheimer’s disease. This allowed us to precisely split the patients on the clinical trial into two groups – slow, and fast progressing, so we could look at the effects of the drug on each group.”

Health Innovation East England, the innovation arm of the NHS in the East of England, is now supporting Kourtzi to translate this AI-enabled approach into clinical care for the benefit of future patients.

Joanna Dempsey, Principal Advisor at Health Innovation East England, said: “This AI-enabled approach could have a significant impact on easing NHS pressure and costs in dementia care by enabling more personalised drug development - identifying which patients are most likely to benefit from treatment, resulting in faster access to effective medicines and targeted support for people living with dementia.”

Drugs like this are not intended as cures for Alzheimer’s disease. The aim is to reduce cognitive decline so that patients don’t get worse.

Dementia is the UK’s leading cause of death, and a major cause of mortality globally. It costs $1.3 tr per year, and the number of cases are expected to treble by 2050. There is no cure, and patients and families face high uncertainty.

Despite decades of research and development, clinical trials of treatments for dementia have been largely unsuccessful. The failure rate for new treatments is unreasonably high at over 95%, despite $43 bn having been spent on research and development. Progress has been hampered by the wide variation in symptoms, disease progression and responses to treatment among patients.

Although new dementia drugs have recently been approved for use in the US, their risk of side effects and insufficient cost effectiveness have prevented healthcare adoption in the NHS.

Understanding and accounting for the natural differences among individuals with a disease is crucial, so that treatments can be tailored to be most effective for each patient. Alzheimer’s disease is complex, and although some drugs are available to treat it they don’t work for everybody.

“AI can guide us to the patients who will benefit from dementia medicines, by treating them at the stage when the drugs will make a difference, so we can finally start fighting back against these cruel diseases. Making clinical trials faster, cheaper and better, guided by AI has strong potential to accelerate discovery of new precise treatments for individual patients, reducing side effects and costs for healthcare services,” said Kourtzi.

She added: “Like many people, I have watched hopelessly as dementia stole a loved one from me.  We’ve got to accelerate the development of dementia medicines. Over £40 billion has already been spent over thirty years of research and development - we can’t wait another thirty years.”

This research was funded by the Royal Society, Alan Turing Institute and Wellcome.

Reference 

Vaghari, D. V. et al: ‘AI-guided patient stratification improves outcomes and efficiency in the AMARANTH Alzheimer’s Disease clinical trial.’ Nature Communications, July 2025.  DOI: 10.1038/s41467-025-61355-3

Scientists have used AI to re-analyse a clinical trial for an Alzheimer’s medicine, and identified a group of patients who responded to treatment. The work demonstrates that AI can inform the design of future clinical trials to make them more effective and efficient, accelerating the search for new medicines.

With our AI model we can finally identify patients precisely, and match the right patients to the right drugsZoe KourtziMichael Hewes/ Getty

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A case study of how AstraZeneca is nurturing the talent of the future through its funded PhD programmes.

New Cambridge laboratory supports the UK’s ambition of having the most advanced genomic healthcare system in the world.

Making advances in patient care through scientific collaboration and partnering on clinical trials.

A new study suggests that our ancestors’ close cohabitation with domesticated animals and large-scale migrations played a key role in the spread of infectious diseases.

The team, led by Professor Eske Willerslev at the Universities of Cambridge and Copenhagen, recovered ancient DNA from 214 known human pathogens in prehistoric humans from Eurasia.

They found that the earliest evidence of zoonotic diseases – illnesses transmitted from animals to humans, like COVID in recent times – dates back to around 6,500 years ago, with these diseases becoming more widespread approximately 5,000 years ago.

The study detected the world’s oldest genetic trace of the plague bacterium, Yersinia pestis, in a 5,500-year-old sample. The plague is estimated to have killed between one-quarter and one-half of Europe’s population during the Middle Ages.

In addition, the researchers found traces of many other diseases including:

Malaria (Plasmodium vivax) – 4,200 years ago

Leprosy (Mycobacterium leprae) – 1,400 years ago

Hepatitis B virus – 9,800 years ago

Diphtheria (Corynebacterium diphtheriae) – 11,100 years ago

This is the largest study to date on the history of infectious diseases and is published today in the journal Nature.

The researchers analysed DNA from over 1,300 prehistoric humans, some up to 37,000 years old. The ancient bones and teeth have provided a unique insight into the development of diseases caused by bacteria, viruses, and parasites.

“We’ve long suspected that the transition to farming and animal husbandry opened the door to a new era of disease – now DNA shows us that it happened at least 6,500 years ago,” said Willerslev.

He added: “These infections didn’t just cause illness – they may have contributed to population collapse, migration, and genetic adaptation.”

The significant increase in the incidence of zoonoses around 5,000 years ago coincides with a migration to north-western Europe from the Pontic Steppe – that is from parts of present-day Ukraine, south-western Russia and western Kazakhstan. The people embarking on this migration – and who to a large extent passed on the genetic profile found among people in north-western Europe today – belonged to the Yamnaya herders.

The findings could be significant for the development of vaccines and for understanding how diseases arise and mutate over time.

“If we understand what happened in the past, it can help us prepare for the future. Many of the newly emerging infectious diseases are predicted to originate from animals,” said Associate Professor Martin Sikora at the University of Copenhagen, and first author of the report.

Willerslev added: “Mutations that were successful in the past are likely to reappear. This knowledge is important for future vaccines, as it allows us to test whether current vaccines provide sufficient coverage or whether new ones need to be developed due to mutations.”

The sample material was primarily provided by museums in Europe and Asia. The samples were partly extracted from teeth, where the enamel acts as a lid that can protect the DNA against degradation as a result of the ravages of time. The rest of the DNA was primarily extracted from petrosa bones - the hardest bone in humans - located on the inside of the skull.

The research was funded by the Lundbeck Foundation.

Reference

Sikora, M. et al: ‘The spatiotemporal distribution of human pathogens in ancient Eurasia.’ Nature, July 2025. DOI: 10.1038/s41586-025-09192-8

Adapted from a press release by the University of Copenhagen.

Researchers have mapped the spread of infectious diseases in humans across millennia, to reveal how human-animal interactions permanently transformed our health today.

We’ve long suspected that the transition to farming and animal husbandry opened the door to a new era of disease – now DNA shows us that it happened at least 6,500 years agoEske WillerslevMarie Louise JørkovLate Neolithic skull from Madesø

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Researchers from every school and more than 20 departments across the University of Cambridge gathered in February to explore the links between air quality and climate, their impacts on human health, and the challenges and opportunities for Clean Air and Net Zero.

Cambridge researchers are working to undo a longstanding male bias in health research, to help drive more effective healthcare for all.

PFAS have been linked with a range of health issues including decreased fertility, developmental delays in children, and a higher risk of certain cancers and cardiovascular diseases.

Scientists at the University of Cambridge have identified a family of bacterial species, found naturally in the human gut, that absorb various PFAS molecules from their surroundings.  When nine of these bacterial species were introduced into the guts of mice to ‘humanise’ the mouse microbiome, the bacteria rapidly accumulated PFAS eaten by the mice - which were then excreted in faeces.

The researchers also found that as the mice were exposed to increasing levels of PFAS, the microbes worked harder, consistently removing the same percentage of the toxic chemicals. Within minutes of exposure, the bacterial species tested soaked up between 25% and 74% of the PFAS.

The results are the first evidence that our gut microbiome could play a helpful role in removing toxic PFAS chemicals from our body - although this has not yet been directly tested in humans.

The researchers plan to use their discovery to create probiotic dietary supplements that boost the levels of these helpful microbes in our gut, to protect against the toxic effects of PFAS.

The results are published in the journal Nature Microbiology.

PFAS (Perfluoroalkyl and Polyfluoroalkyl Substances) can’t be avoided in our modern world. These man-made chemicals are in many everyday items including waterproof clothing, non-stick pans, lipsticks and food packaging, used for their resistance to heat, water, oil and grease. But because they take thousands of years to break down, they are accumulating in large quantities in the environment – and in our bodies.

Dr Kiran Patil, in the University of Cambridge’s MRC Toxicology Unit and senior author of the report, said: “Given the scale of the problem of PFAS ‘forever chemicals’, particularly their effects on human health, it’s concerning that so little is being done about removing these from our bodies.”

“We found that certain species of human gut bacteria have a remarkably high capacity to soak up PFAS from their environment at a range of concentrations, and store these in clumps inside their cells. Due to aggregation of PFAS in these clumps, the bacteria themselves seem protected from the toxic effects.”

Dr Indra Roux, a researcher at the University of Cambridge’s MRC Toxicology Unit and a co-author of the study said: “The reality is that PFAS are already in the environment and in our bodies, and we need to try and mitigate their impact on our health now. We haven’t found a way to destroy PFAS, but our findings open the possibility of developing ways to get them out of our bodies where they do the most harm.”

There is increasing concern about the environmental and health impacts of PFAS, and in April 2025 the UK launched a parliamentary inquiry into their risks and regulation.

There are over 4,700 PFAS chemicals in widespread use. Some get cleared out of the body in our urine in a matter of days, but others with a longer molecular structure can hang around in the body for years.

Dr Anna Lindell, a researcher at the University of Cambridge’s MRC Toxicology Unit and first author of the study said: “We’re all being exposed to PFAS through our water and food – these chemicals are so widespread that they’re in all of us.

“PFAS were once considered safe, but it’s now clear that they’re not. It’s taken a long time for PFAS to become noticed because at low levels they’re not acutely toxic. But they’re like a slow poison.”

Lindell and Patil have co-founded a startup, Cambiotics, with serial entrepreneur Peter Holme Jensen to develop probiotics that remove PFAS from the body, and they are investigating various ways of turbo-charging the microbes’ performance. Cambiotics is supported by Cambridge Enterprise, the innovation arm of the University of Cambridge, which helps researchers translate their work into globally-leading economic and social impact.

While we wait for new probiotics to become available, the researchers say the best things we can do to help protect ourselves against PFAS are to avoid PFAS-coated cooking pans, and use a good water filter.

The research was funded primarily by the Medical Research Council, National Institute for Health Research, and Wellcome.

Reference

Lindell, AE: ‘Human gut bacteria bioaccumulate per- and polyfluoroalkyl substances.’ Nature Microbiology, July 2025. DOI: 10.1038/s41564-025-02032-5

Scientists have discovered that certain species of microbe found in the human gut can absorb PFAS - the toxic and long-lasting ‘forever chemicals.’ They say boosting these species in our gut microbiome could help protect us from the harmful effects of PFAS.

“Given the scale of the problem of PFAS ‘forever chemicals’, particularly their effects on human health, it’s concerning that so little is being done about removing these from our bodies.”Kiran PatilPeter Northrop / MRC Toxicology UnitPFAS accumulation in gut bacteria

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A team at Cambridge is helping to drive biological discovery through innovation in microscope technologies

Dr Alex Tsompanidis, senior researcher at the Autism Research Centre in the University of Cambridge, and the lead author of this new study, said: “Small variations in the prenatal levels of steroid hormones, like testosterone and oestrogen, can predict the rate of social and cognitive learning in infants and even the likelihood of conditions such as autism. This prompted us to consider their relevance for human evolution.”

One explanation for the evolution of the human brain may be in the way humans adapted to be social. Professor Robin Dunbar, an Evolutionary Biologist at the University of Oxford and joint senior author of this new study said: “We’ve known for a long time that living in larger, more complex social groups is associated with increases in the size of the brain. But we still don’t know what mechanisms may link these behavioural and physical adaptations in humans.”

In this new paper, published today in Evolutionary Anthropology, the researchers now propose that the mechanism may be found in prenatal sex steroid hormones, such as testosterone or oestrogens, and the way these affect the developing brain and behaviour in humans.

Using ‘mini-brains’ – clusters of human neuronal cells that are grown in a petri dish from donors’ stem cells – other scientists have been able to study, for the first time, the effects of these hormones on the human brain. Recent discoveries have shown that testosterone can increase the size of the brain, while oestrogens can improve the connectivity between neurons.

In both humans and other primates such as chimpanzees and gorillas, the placenta can link the mother’s and baby’s endocrine systems to produce these hormones in varying amounts.

Professor Graham Burton, Founding Director of the Loke Centre of Trophoblast Research at the University of Cambridge and coauthor of the new paper, said: “The placenta regulates the duration of the pregnancy and the supply of nutrients to the fetus, both of which are crucial for the development of our species’ characteristically large brains. But the advantage of human placentas over those of other primates has been less clear.”

Two previous studies show that levels of oestrogen during pregnancy are higher in human pregnancies than in other primate species.

Another characteristic of humans as a species is our ability to form and maintain large social groups, larger than other primates and other extinct species, such as Neanderthals. But to be able to do this, humans must have adapted in ways that maintain high levels of fertility, while also reducing competition in large groups for mates and resources.

Prenatal sex steroid hormones, such as testosterone and oestrogen, are also important for regulating the way males and females interact and develop, a process known as sex differentiation. For example, having higher testosterone relative to oestrogen leads to more male-like features in anatomy (e.g., in physical size and strength) and in behaviour (e.g., in competition).

But in humans, while these on-average sex differences exist, they are reduced, compared to our closest primate relatives and relative to other extinct human species (such as the Neanderthals). Instead, anatomical features that are specific to humans appear to be related more to aspects of female rather than male biology, and to the effects of oestrogens (e.g., reduced body hair, and a large ratio between the second and fourth digit).

The researchers propose that the key to explain this may lie again with the placenta, which rapidly turns testosterone to oestrogens, using an enzyme called aromatase. Recent discoveries show that humans have higher levels of aromatase compared to macaques, and that males may have slightly higher levels compared to females.

Bringing all these lines of evidence together, the authors propose that high levels of prenatal sex steroid hormones in the womb, combined with increased placental function, may have made human brains larger and more interconnected. At the same time, a lower ratio of androgens (like testosterone) to oestrogens may have led to reductions in competition between males, while also improving fertility in females, allowing humans to form larger, more cohesive social groups.

Professor Simon Baron-Cohen, Director of the Autism Research Centre at the University of Cambridge and joint senior author on the paper, said: “We have been studying the effects of prenatal sex steroids on neurodevelopment for the past 20 years. This has led to the discovery that prenatal sex steroids are important for neurodiversity in human populations. This new hypothesis takes this further in arguing that these hormones may have also shaped the evolution of the human brain.”

Dr Tsompanidis added: “Our hypothesis puts pregnancy at the heart of our story as a species. The human brain is remarkable and unique, but it does not develop in a vacuum. Adaptations in the placenta and the way it produces sex steroid hormones may have been crucial for our brain’s evolution, and for the emergence of the cognitive and social traits that make us human.”

Reference

Tsompanidis, A et al. The placental steroid hypothesis of human brain evolution. Evolutionary Anthropology; 20 June 2025; DOI: 10.1002/evan.70003

The placenta and the hormones it produces may have played a crucial role in the evolution of the human brain, while also leading to the behavioural traits that have made human societies able to thrive and expand, according to a new hypothesis proposed by researchers from the Universities of Cambridge and Oxford.

Our hypothesis puts pregnancy at the heart of our story as a speciesAlex TsompanidisNadzeya Haroshka (Getty Images)Models of a fetus in the womb and of the brain

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Yes

Today, all non-Africans are known to have descended from a small group of people that ventured into Eurasia around 50,000 years ago. However, fossil evidence shows that there were numerous failed dispersals before this time that left no detectable traces in living people.

In a new study published today in the journal in Nature, scientists say that from around 70,000 years ago, early humans began to exploit different habitat types in Africa in ways not seen before.

At this time, our ancestors started to live in the equatorial forests of West and Central Africa, and in the Sahara and Sahel desert regions of North Africa, where they encountered a range of new environmental conditions.

As they adapted to life in these diverse habitats, early humans gained the flexibility to tackle the range of novel environmental conditions they would encounter during their expansion out of Africa.

This increase in the human niche may have been the result of social adaptations, such as long-distance social networks, which allowed for an increase in cultural exchange. The process would have been self-reinforcing: as people started to inhabit a wider proportion of the African continent, regions previously disconnected would have come into contact, leading to further exchanges and possibly even greater flexibility. The final outcome was that our species became the ultimate generalist, able to tackle a wider range of environments.

Andrea Manica, Professor of Evolutionary Ecology in the University of Cambridge’s Department of Zoology, who co-led the study with Professor Eleanor Scerri from the Max Plank Institute of Bioanthropology in Germany, said: “Around 70,000-50,000 years ago, the easiest route out of Africa would have been more challenging than during previous periods, and yet this expansion was big - and ultimately successful.”

Manica added: “It’s incredibly exciting that we were able to look back in time and pinpoint the changes that enabled our ancestors to successfully migrate out of Africa.”

Dr Emily Hallett of Loyola University Chicago, co-lead author of the study, said: “We assembled a dataset of archaeological sites and environmental information covering the last 120,000 years in Africa. We used methods developed in ecology to understand changes in human environmental niches - the habitats humans can use and thrive in - during this time.” 

Dr Michela Leonardi at the University of Cambridge and London’s Natural History Museum, the study’s other lead author, said: “Our results showed that the human niche began to expand significantly from 70,000 years ago, and that this expansion was driven by humans increasing their use of diverse habitat types, from forests to arid deserts.” 

Many explanations for the uniquely successful dispersal out of Africa have previously been made, from technological innovations, to immunities granted by interbreeding with Eurasian hominins. But there is no evidence of technological innovation, and previous interbreeding does not appear to have helped the long-term success of previous attempts to spread out of Africa.

“Unlike previous humans dispersing out of Africa, those human groups moving into Eurasia after around 60-50,000 years ago were equipped with a distinctive ecological flexibility as a result of coping with climatically challenging habitats,” said Scerri. “This likely provided a key mechanism for the adaptive success of our species beyond their African homeland.”

Previous human dispersals out of Africa - which were not successful in the long term - seem to have happened during particularly favourable windows of increased rainfall in the Saharo-Arabian desert belt, which created ‘green corridors’ for people to move into Eurasia.

The environmental flexibility developed in Africa from around 70,000 years ago ultimately resulted in modern humans’ unique ability to adapt and thrive in diverse environments, and to cope with varying environmental conditions throughout life.

This research was supported by funding from the Max Planck Society, European Research Council and Leverhulme Trust.

Adapted from a press release by the Max Planck Institute of Geoanthropology, Germany

Reference: Hallett, E. Y. et al: ‘Major expansion in the human niche preceded out of Africa dispersal.’ Nature, June 2025. DOI: 10.1038/s41586-025-09154-0.

Before the ‘Out of Africa’ migration that led our ancestors into Eurasia and beyond, human populations learned to adapt to new and challenging habitats including African forests and deserts, which was key to the long-term success of our species’ dispersal.

It’s incredibly exciting that we were able to look back in time and pinpoint the changes that enabled our ancestors to successfully migrate out of Africa.Andrea ManicaOndrej Pelanek and Martin PelanekAfrican Bush Elephant

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YesLicence type: Attribution-Noncommerical

The successful Cambridge grantees’ work covers a range of research areas, including the development of next-generation semiconductors, new methods to identify dyslexia in young children, how diseases spread between humans and animals, and the early changes that happen in cells before breast cancer develops, with the goal of finding ways to stop the disease before it starts.

The funding, worth €721 million in total, will go to 281 leading researchers across Europe. The Advanced Grant competition is one of the most prestigious and competitive funding schemes in the EU and associated countries, including the UK. It gives senior researchers the opportunity to pursue ambitious, curiosity-driven projects that could lead to major scientific breakthroughs. Advanced Grants may be awarded up to € 2.5 million for a period of five years. The grants are part of the EU’s Horizon Europe programme. The UK agreed a deal to associate to Horizon Europe in September 2023.

This competition attracted 2,534 proposals, which were reviewed by panels of internationally renowned researchers. Over 11% of proposals were selected for funding. Estimates show that the grants will create approximately 2,700 jobs in the teams of new grantees. The new grantees will be based at universities and research centres in 23 EU Member States and associated countries, notably in the UK (56 grants), Germany (35), Italy (25), the Netherlands (24), and France (23).

“Many congratulations to our Cambridge colleagues on these prestigious ERC funding awards,” said Professor Sir John Aston, Cambridge’s Pro-Vice-Chancellor for Research. “This type of long-term funding is invaluable, allowing senior researchers the time and space to develop potential solutions for some of biggest challenges we face. We are so fortunate at Cambridge to have so many world-leading researchers across a range of disciplines, and I look forward to seeing the outcomes of their work.”

The Cambridge recipients of 2025 Advanced Grants are:

Professor Clare Bryant (Department of Veterinary Medicine) for investigating human and avian pattern recognition receptor activation of cell death pathways, and the impact on the host inflammatory response to zoonotic infections.

Professor Sir Richard Friend (Cavendish Laboratory/St John’s College) for bright high-spin molecular semiconductors.

Professor Usha Goswami (Department of Psychology/St John’s College) for a cross-language approach to the early identification of dyslexia and developmental language disorder using speech production measures with children.

Professor Regina Grafe (Faculty of History) for colonial credit and financial diversity in the Global South: Spanish America 1600-1820.

Professor Judy Hirst (MRC Mitochondrial Biology Unit/Corpus Christi College) for the energy-converting mechanism of a modular biomachine: Uniting structure and function to establish the engineering principles of respiratory complex I.

Professor Matthew Juniper (Department of Engineering/Trinity College) for adjoint-accelerated inference and optimisation methods.

Professor Walid Khaled (Department of Pharmacology/Magdalene College) for understanding precancerous changes in breast cancer for the development of therapeutic interceptions.

Professor Adrian Liston (Department of Pathology/St Catharine’s College) for dissecting the code for regulatory T cell entry into the tissues and differentiation into tissue-resident cells.

Professor Róisín Owens (Department of Chemical Engineering and Biotechnology/Newnham College) for conformal organic devices for electronic brain-gut readout and characterisation.

Professor Emma Rawlins (Department of Physiology, Development and Neuroscience/Gurdon Institute) for reprogramming lung epithelial cell lineages for regeneration.

Dr Marta Zlatic (Department of Zoology/Trinity College) for discovering the circuit and molecular basis of inter-strain and inter-species differences in learning

“These ERC grants are our commitment to making Europe the world’s hub for excellent research,” said Ekaterina Zaharieva, European Commissioner for Startups, Research, and Innovation. “By supporting projects that have the potential to redefine whole fields, we are not just investing in science but in the future prosperity and resilience of our continent. In the next competition rounds, scientists moving to Europe will receive even greater support in setting up their labs and research teams here. This is part of our “Choose Europe for Science” initiative, designed to attract and retain the world’s top scientists.”

“Much of this pioneering research will contribute to solving some of the most pressing challenges we face - social, economic and environmental,” said Professor Maria Leptin, President of the European Research Council. “Yet again, many scientists - around 260 - with ground-breaking ideas were rated as excellent, but remained unfunded due to a lack of funds at the ERC. We hope that more funding will be available in the future to support even more creative researchers in pursuing their scientific curiosity.”

Eleven senior researchers at the University of Cambridge have been awarded Advanced Grants from the European Research Council – the highest number of grants awarded to any institution in this latest funding round.

Westend61 via Getty ImagesScientist pipetting samples into eppendorf tube

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

Research finds that appetite for bushmeat – rather than the black market for scales to use in traditional Chinese medicine – may be driving West Africa’s illegal hunting of one of the world’s most threatened mammals.

Why are there so many different kinds of animals and plants on Earth? One of biology’s big questions is how new species arise and how nature’s incredible diversity came to be.

Cichlid fish from Lake Malawi in East Africa offer a clue. In this single lake, over 800 different species have evolved from a common ancestor in a fraction of the time it took for humans and chimpanzees to evolve from their common ancestor.

What’s even more remarkable is that the diversification of cichlids happened all in the same body of water. Some of these fish became large predators, others adapted to eat algae, sift through sand, or feed on plankton. Each species found its own ecological niche.

Now, researchers from the Universities of Cambridge and Antwerp have determined how this evolution may have happened so quickly. Their results are reported in the journal Science.

The researchers looked at the DNA of over 1,300 cichlids to see if there’s something special about their genes that might explain this rapid evolution. “We discovered that, in some species, large chunks of DNA on five chromosomes are flipped – a type of mutation called a chromosomal inversion,” said senior author Hennes Svardal from the University of Antwerp.

Normally, when animals reproduce, their DNA gets reshuffled in a process called recombination – mixing the genetic material from both parents. But this mixing is blocked within a chromosomal inversion. This means that gene combinations within the inversion are passed down intact without mixing, generation after generation, keeping useful adaptations together and speeding up evolution.

“It’s sort of like a toolbox where all the most useful tools are stuck together, preserving winning genetic combinations that help fish adapt to different environments,” said first author Moritz Blumer from Cambridge’s Department of Genetics.

These preserved sets of genes are sometimes called ‘supergenes. In Malawi cichlids, the supergenes seem to play several important roles. Although cichlid species can still interbreed, the inversions help keep species separate by preventing their genes from blending too much. This is especially useful in parts of the lake where fish live side by side – like in open sandy areas where there’s no physical separation between habitats.

The genes inside these supergenes often control traits that are key for survival and reproduction – such as vision, hearing, and behaviour. For example, fish living deep in the lake (down to 200 meters) need different visual abilities than those near the surface, require different food, and need to survive at higher pressures. Their supergenes help maintain those special adaptations.

“When different cichlid species interbred, entire inversions can be passed between them – bringing along key survival traits, like adaptations to specific environments, speeding up the process of evolution,” said Blumer.

The inversions also frequently act as sex chromosomes, helping determine whether a fish becomes male or female. Since sex chromosomes can influence how new species form, this opens new questions about how evolution works.

“While our study focused on cichlids, chromosomal inversions aren’t unique to them,” said co-senior author Professor Richard Durbin, from Cambridge’s Department of Genetics. “They’re also found in many other animals — including humans — and are increasingly seen as a key factor in evolution and biodiversity.”

“We have been studying the process of speciation for a long time,” said Svardal. “Now, by understanding how these supergenes evolve and spread, we’re getting closer to answering one of science’s big questions: how life on Earth becomes so rich and varied.”

Reference:
L. M. Blumer, V. Burskaia, I. Artiushin, J. Saha et al. ‘Introgression dynamics of sex- linked chromosomal inversions shape the Malawi cichlid radiation.’ Science (2025). DOI: 10.1126/science.adr9961

Researchers have found that chunks of ‘flipped’ DNA can help fish quickly adapt to new habitats and evolve into new species, acting as evolutionary ‘superchargers’.

banusevim via Getty ImagesDolphin cichlid (Cyrtocara moorii)

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Imagine a plant with entirely new abilities – more nutritious food, crops that survive heatwaves, or leaves that grow useful materials. With new ARIA funding Cambridge researchers hope to unlock the technology to fast-track crop development and enhance plants with new qualities, like drought-tolerance to reduce the amount of water they need, or the ability to withstand pests and diseases.

Their research has the potential to revolutionise the future of agriculture and offer a radical new approach to securing food supply in the face of climate change.

Programmable plants – a major leap in plant biology

“We’re building the tools to make plants programmable, just like software. This isn’t science fiction – it’s the future of agriculture,” said Professor Jake Harris, Head of the Chromatin and Memory group, and project lead for one of the ARIA-funded projects.

Harris’ team is awarded £6.5 million to build the world’s first artificial plant chromosome.

The ambitious aim of the Synthetic Plants programme is to develop artificial chromosomes and chloroplasts that can survive in a living plant. If the teams achieve this, it will be one the most significant advances in plant synthetic biology.

The international team involves collaborators from The University of Western Australia, biotech company Phytoform Labs and the Australian Genome Foundry at Macquarie University.

“Our idea is that instead of modifying an existing chromosome, we design it from the ground up,” Professor Harris said.

He added: “We’re rethinking what plants can do for us. This synthetic chromosome could one day help grow crops that are more productive, more resilient, and better for the planet.”

While synthetic chromosomes have been achieved in simpler organisms, such as bacteria and yeast, this will be the first attempt to create and deploy one entirely from scratch in a plant.

The project will use the moss Physcomitrium patens – a unique, highly engineerable plant – as a development platform to build and test a bottom-up synthetic chromosome, before transferring it into potato plants.

It also opens new possibilities for growing food and medicines in space, and for indoor agriculture. It could allow scientists to give elite crop varieties disease resistance, or to grow productively in new climates and environments.

Unlocking powerful applications in agriculture

The second funded project, led by Professor Alison Smith and Dr Paweł Mordaka in the Plant Metabolism group, aims to use the synthetic chloroplasts to enable plants to fix nitrogen, and produce vitamin B12. The use of fertilisers to supply nitrogen and promote good crop yields is the greatest cause of pollution from agriculture; reducing the need for these would promote more sustainable food production systems.

This builds on their previous work to design and build the entire chloroplast genome for the simple single-cell alga Chlamydomonas reinhardtii.

The Cambridge researchers are awarded almost £1 million, as part of a £9 million grant to this project. They are working with an international team of researchers from the UK, USA and Germany to transfer this technology to build synthetic chloroplasts in potato plants.

Professor Smith said: “Our success would unlock powerful applications in agriculture, like plants capable of nitrogen fixation or producing essential nutrients like vitamin B12, potentially reducing fertiliser dependence and addressing malnutrition. These traits have tremendous potential should they be engineered into plants.”

She added: “It will enable scientists to surpass what can be accomplished with gene editing and equip plants with new functions, from reducing agricultural water use to protecting crop yields in uncertain conditions.”

A unique opportunity

The ambitiousness of this project is outside the scope of most other UK funding schemes. Professor Harris believes this stems from ARIA’s unique approach to developing the research opportunity and goal along with the research community.

Harris said: “ARIA had a couple of events with synthetic biologists to look at what’s on the edge of possible, what could be useful as a moonshot approach that could really change things.”

He added: “It’s a totally different way of seeing things. We went from ‘here’s what we want to see in the world’ to ‘how are we going to get there?’ It catalysed a different team and a different way of thinking.”

“This work moves us beyond the limitations of natural genomes. It’s about designing entirely new capabilities in plants – from the molecular level up.”

Currently, it typically takes eight years to develop a new crop variety in the UK, but with this new technology it could be a matter of one year or even less. The speed of development would be dramatically increased, much in the way that revolutionary protein-folding technology like AlphaFold has massively accelerated the process of drug discovery.

Synthetic biology is already revolutionising the world of healthcare and could transform agriculture if applied to tailoring plant traits.

 

Two groups involving researchers from the University of Cambridge’s Department of Plant Sciences are among nine teams to have been awarded funding today from the UK’s Advanced Research + Invention Agency (ARIA)’s Synthetic Plants programme.

We’re building the tools to make plants programmable, just like software. This isn’t science fiction – it’s the future of agriculture.Jake Harrispkujiahe on GettyGloved hand holding plant in pot

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The new Fellows have been recognised for their remarkable contributions to advancing medical science, groundbreaking research discoveries and translating developments into benefits for patients and the wider public. Their work exemplifies the Academy’s mission to create an open and progressive research sector that improves health for everyone.

They join an esteemed Fellowship of 1,450 researchers who are at the heart of the Academy’s work, which includes nurturing the next generation of scientists and shaping research and health policy in the UK and worldwide.

One of Cambridge’s new Fellows, Professor Sam Behjati, is a former recipient of the Academy’s prestigious Foulkes Foundation medal, which recognises rising stars within biomedical research. Sam is Clinical Professor of Paediatric Oncology at the University and an Honorary Consultant Paediatric Oncologist at Addenbrooke’s Hospital, as well as Group Leader at the Wellcome Sanger Institute. His research is rooted in cancer genomics, phylogenetics, and single cell transcriptomics and spans a wide range of diseases and biological problems. More recently, his work has focused on the origin of cancers, in particular of childhood cancer. In addition, he explores how to use genomic data to improve the treatment of children. Sam is a Fellow at Corpus Christi College, Cambridge.

Also elected to the Academy of Medical Sciences Fellowship are:

Professor Clare Bryant, Departments of Medicine and Veterinary Medicine

Clare Bryant is Professor of Innate Immunity. She studies innate immune cell signalling during bacterial infection to answer fundamental questions about host-pathogen interactions and to search for new drugs to modify them. She also applies these approaches to study inflammatory signalling in chronic diseases of humans and animals.  Clare has extensive collaborations with many pharmaceutical companies, is on the scientific advisory board of several biotech companies, and helped found the natural product company Polypharmakos. Clare is a Fellow of Queens’ College, Cambridge.

Professor Frank Reimann, Institute of Metabolic Science-Metabolic Research Laboratories

Frank Reimann is Professor of Endocrine Signaling. The main focus of his group, run in close partnership with Fiona Gribble, is the enteroendocrine system within the gut, which helps regulate digestion, metabolism, and how full we feel. Their work has included the use of animal models and human cellular models to understand how cells function. One of these cells, glucagon-like peptide-1 (GLP-1) is the target of therapies now widely used in the treatment of diabetes mellitus and obesity. How cells shape feeding behaviour has become a major focus of the lab in recent years.

Professor Mina Ryten, UK Dementia Research Institute

Mina Ryten is a clinical geneticist and neuroscientist, and Director of the UK Dementia Research Institute at Cambridge since January 2024. She also holds the Van Geest Professorship and leads a lab focused on understanding molecular mechanisms driving neurodegeneration. Mina’s research looks at how genetic variation influences neurological diseases, particularly Lewy body disorders. Her work has advanced the use of single cell and long-read RNA sequencing to map disease pathways and identify potential targets for new treatments. Her expertise in clinical care and functional genomics has enabled her to bridge the gap between patient experience and scientific discovery.

Professor Andrew Morris CBE FRSE PMedSci, President of the Academy of Medical Sciences, said: “The breadth of disciplines represented in this year’s cohort – from mental health and infectious disease to cancer biology and respiratory medicine – reflects the rich diversity of medical science today. Their election comes at a crucial time when scientific excellence and collaboration across disciplines are essential for addressing global health challenges both now and in the future. We look forward to working with them to advance biomedical research and create an environment where the best science can flourish for the benefit of people everywhere.”

The new Fellows will be formally admitted to the Academy at a ceremony on Wednesday 9 July 2025.

Four Cambridge biomedical and health researchers are among those announced today as newly-elected Fellows of the Academy of Medical Sciences.

Big T Images for Academy of Medical SciencesAcademy of Medical Sciences plaque

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Presented by The Sainsbury Laboratory Cambridge University, the exhibit is part of a brand-new GreenSTEM section that celebrates cutting-edge research and innovation in the world of plant science.

Blooming Numbers takes visitors on an immersive journey through the latest discoveries in quantitative plant biology—starting with the humble flower and diving deep into molecular biology, genetics, imaging technologies, computational modelling, and the often-overlooked mathematical patterns that govern plant development.

“This award is just so exciting,” said Kathy Grube from the Sainsbury Laboratory.

“We came in in the morning to water the plants and turn on the microscopes, and the medal had been laid out by the judges. We were jumping up and down when we found it.”

The eye-catching exhibit was a collaborative effort across multiple Cambridge institutions and partners. The University’s Department of Engineering co-designed the infrastructure, drawing inspiration from the Fibonacci sequence—an iconic numerical pattern found throughout nature. The Pollinator Patch, a lush highlight of the exhibit, was designed and cultivated by Oakington Garden Centre to demonstrate pollinator-friendly planting. Darwin Nurseries added wildlife-friendly hanging baskets that captivated visitors and judges alike.

“One of our fellow exhibitors, who have been coming to Chelsea for years, told us that getting a silver-gilt on your first try is a real achievement,” said Kathy.

“The judges came over and said the design of the stand was fantastic, and they loved the interactive exhibits. We’re just so honoured.”

The RHS Chelsea Flower Show, the world’s most famous horticultural show, runs until the end of the week and attracts horticultural experts, designers, and plant lovers from across the globe.
 

The University of Cambridge has made a dazzling debut at the RHS Chelsea Flower Show, winning a prestigious silver-gilt medal for its interactive plant science exhibit, Blooming Numbers.

The Sainsbury Laboratory Cambridge University

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YesRelated Links: GreenSTEM spotlights horticultural science at RHS Chelsea Flower Show

“It is with great pleasure that I welcome the latest cohort of outstanding researchers into the Fellowship of the Royal Society,” said Sir Adrian Smith, President of the Royal Society. “Their achievements represent the very best of scientific endeavour, from basic discovery to research with real-world impact across health, technology and policy. From tackling global health challenges to reimagining what AI can do for humanity, their work is a testament to the power of curiosity-driven research and innovation.

“The strength of the Fellowship lies not only in individual excellence, but in the diversity of backgrounds, perspectives and experiences each new member brings. This cohort represents the truly global nature of modern science and the importance of collaboration in driving scientific breakthroughs.”

The Fellows and Foreign Members join the ranks of Stephen Hawking, Isaac Newton, Charles Darwin, Albert Einstein, Lise Meitner, Subrahmanyan Chandrasekhar and Dorothy Hodgkin.

The new Cambridge fellows are:

Professor Edward Bullmore FMedSci FRS

Professor Ed Bullmore is Professor of Psychiatry and former Head of the Department of Psychiatry. His research mainly involves the application of brain imaging to psychiatry. He has introduced an entirely original approach to the analysis of human brain anatomy, involving graph theory and its application to small-world networks. This has had an enormous impact on the field, especially in relation to understanding the biological basis of schizophrenia and depression. His work has been key to the understanding of the 'wiring' of the human brain.

Professor Gábor Csányi FRS

Professor Gábor Csányi is Professor of Molecular Modelling in the Department of Engineering, and a Fellow of Pembroke College. His work is in the field of computational chemistry, and is focused on developing algorithms to predict the properties of materials and molecules from first principles. He pioneered the application of machine learning to molecular modelling which lead to enormous gains in the efficiency of molecular dynamics simulation.

Professor Judith Driscoll FRS

Professor Judith Driscoll is Professor of Materials Science in the Department of Materials Science and Metallurgy, and a Fellow of Trinity College. Her research is concerned with the nanoscale design and tuning of functional oxide thin film materials for energy-efficient electronic applications. A particular focus of her research group is oxide thin films, owing to their wide range of functionalities and their stability. However, their compositions tend to be complex, defects are prevalent, and interface effects play a strong role. Also, for many applications device structural dimensions are required down to nanometre length-scales. Together, all these factors produce exciting challenges for the materials scientist.

Professor Marie Edmonds FRS

Professor Marie Edmonds is Head of Department and Professor of Volcanology and Petrology in the Department of Earth Sciences. She is also a Fellow of Queens’ College. Her research focuses on understanding the impact of volcanoes on our environment and on the habitability of our planet. Her research spans the boundaries between traditional disciplines, from deciphering the nature of the interior of the Earth, to magma transport and storage in the crust, to volcano monitoring, understanding ore deposits and the dynamic chemistry of volcanic gases in the atmosphere and climate.

Professor Julian Hibberd FRS

Professor Julian Hibberd is Head of the Department of Plant Sciences and a Fellow of Emmanuel College. His research focuses on guiding optimisation of photosynthesis to improve crop yields. The C4 pathway is a complex form of photosynthesis that evolved around 30 million years ago and is now used by the most productive plants on the planet. Professor Hibberd has provided key insights into the evolution of C4 photosynthesis through analysis of plant physiology, cell specialisation, organelle development, and the control of gene expression.

Dr Gregory Jefferis FRS

Dr Gregory Jefferis is Joint Head of the Neurobiology Division at the MRC Laboratory of Molecular Biology and Director of Research of the Department of Zoology. The broad goal of his research is to understand how smell turns into behaviour in the fruit fly brain. His group is particularly interested in how odour information is processed by the higher olfactory centres that mediate innate and learned behaviour.

Professor Jason Miller FRS

Professor Jason Miller is a Professor in the Department of Pure Mathematics and Mathematical Statistics and a Fellow of Trinity College. His research interests are in probability, in particular stochastic interface models, random walk, mixing times for Markov chains, and interacting particle systems.

Professor Andrew Pitts FRS

Professor Andrew Pitts is Emeritus Professor of Theoretical Computer Science in the Department of Computer Science and Technology and an Emeritus Fellow of Darwin College. His research makes use of techniques from category theory, mathematical logic and type theory to advance the foundations of programming language semantics and theorem proving systems. His aim is to develop mathematical models and methods that aid language design and the development of formal logics for specifying and reasoning about programs. He is particularly interested in higher-order typed programming languages and in dependently typed logics.

Dr Marta Zlatic FRS

Dr Marta Zlatic is Programme Leader at the MRC Laboratory of Molecular Biology, and Director of Research in the Department of Zoology. She is also a Fellow of Trinity College. Her research aims to understand the relationship between the structure of the nervous system and its function and to discover the basic principles by which neural circuits implement fundamental computations. A major focus of her research is the circuit implementation of learning and decision-making.

Nine outstanding Cambridge scientists have been elected as Fellows of the Royal Society, the UK’s national academy of sciences and the oldest science academy in continuous existence.

Tom MorrisEntrance to the Royal Society

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What is a memory?

Is it a distinct pattern of brain activity, a blueprint for future behaviour, or a skill that we can improve with a little training? Probably all these things and more, argues Jon Simons, Professor of Cognitive Neuroscience in the Department of Psychology and Head of the School of the Biological Sciences.

Jon’s Memory Lab studies all aspects of memory. They invite volunteers to complete memory tasks online, in the laboratory, or sometimes while lying in an MRI machine while the team scans their brains. 

If memory serves

The biochemical changes that represent memories range across the brain’s real estate. A long list of factors determine which brain areas light up during the experience: whether a memory is being encoded or reconstructed, whether it's an old or a new pattern, and what kind of information it deals with.

“We know that the hippocampus is crucial for forming new memories, but it’s not necessarily the permanent storage site," Jon says. "For long-term storage, we also recruit cortical areas – the frontal lobes, temporal lobes, parietal lobes and more.”

To plot a route through tangled terrain, researchers divide memory into different types. Short-term memory lasts a minute at most and has a limited capacity – around 7 items give-or-take, according to Harvard’s George Miller in the 1950s. Think of repeating numbers to yourself while jotting down someone’s phone number. If we don’t record those numbers fast enough, they’ll fade quickly. 

But even short-term memory isn’t unitary. Alan Baddeley (Churchill 1959), former director of Cambridge’s Medical Research Council (MRC) Applied Psychology Unit (now called the MRC Cognition and Brain Sciences Unit), coined a new way of understanding how short-term memories are stored and manipulated. His 'working memory' model proposes that separate brain systems deal with different kinds of inputs. One part rehearses and replays sounds, for instance, while another holds visual information like a ‘mental canvas’. 

the_working_memory_model.svg_.png

This is different yet again from our long-term memories. These deeper experiences can stay with us for a lifetime. Recalling them can be thought of as a kind of ‘mental time-travel’, allowing us to subjectively relive past events complete with the sights, smells and sounds of cherished scenes.

Researchers now believe that we reconstruct our memories each time we experience them. From scant traces, we extrapolate the narrative of what happened. In this way, memory is a creative act, not a simple recap. One classic Cambridge study revealed how our memories are morphed by bias, beliefs, feelings and expectations.
 

Cambridge’s long memory

Enter the elegant study of Sir Frederic Bartlett, Cambridge’s first Psychology professor. 

Bartlett’s book ‘Remembering’ (1932) made use of a now famous story: the war of the ghosts. 

In this Native American folk tale, a man meets warriors paddling their canoes downriver, who invite him to join a war party. He later realises the men are ghosts, waging war on the living. 

Bartlett taught his Edwardian undergraduates this tale, then asked them to retell it in their own words. Over several retellings, his students altered key elements of the story so that it sounded more like the world they knew. ‘Canoes’ became ‘boats’, while mentions of ‘spirits’ were dropped altogether.

canoe.jpg

Bartlett's study showed the effects of culture on recall, and how the changes we make to our memories aren’t random. Even if we’re not conscious of doing so, we prefer to change story elements so that they align with our expectations, biases and cultural norms.

This feature of memory has massive implications for how we remember the past. Eye-witness testimony will be prey to the same biases. Unintentional errors, made in favour of what is familiar to us, are very difficult to avoid.

Another titan of memory research was an undergraduate while Bartlett was teaching. During World War II, Brenda Milner (Newnham 1936) helped the Psychology department repurpose itself for the war effort. After this, Milner moved to Canada to analyse patient Henry Molaison (formerly known as H M). Molaison would become one of the most famous patients in all of psychology. 

Molaison had profound amnesia. This was due to experimental surgery, where doctors removed his hippocampus to try and improve his epilepsy. Milner meticulously documented how Molaison’s memory functioned after surgery. She showed how he was unable to form new memories or remember events from the years leading up to his surgery, but that his memories from earlier in life remained intact. This work transformed our understanding of the hippocampus’ role in memory.

Psychologists like Milner and Bartlett showed us the primacy of the hippocampus and highlighted the creative nature of memory. Modern Cambridge researchers can take our investigations even further.
 

Peak performance

With all we now know about memory, can we understand what makes for better performance?

Together with Professor Simon Baron-Cohen and his team at the Autism Research Centre, Jon is currently studying thousands of the UK’s best memorisers to find the keys to their prowess. Volunteers completed a battery of memory tests online – the best performers then came for brain scans and further testing in the lab.

Their early results suggest some interesting traits, as well as the strategies people use to enhance their abilities. 

“There's a psychological trait called ‘systemising’,” says Jon. “It's found in people who have a drive to analyse and construct rule-based ways of thinking. Those kinds of people seem to be more likely to have exceptional memories.”

Simon Baron-Cohen was the first to define this trait. He did so in relation to people on the autism spectrum, for whom ‘systemising’ is set very high. 

So if you happen to think like a ‘systemiser’, you may have a better memory. If you don’t, there are also concrete strategies to boost your memory capacities.

“Mnemonics are an evidence-based technique that can improve our memories,” Jon explains. “They often involve thinking spatially. Start by visualising somewhere you know well, then mentally ‘place’ important information in that map. You can then 'travel through' that map when recalling.”

Think Sherlock’s ‘mind palace’ from the BBC adaptation of Arthur Conan Doyle’s books. Jon points out that pre-BBC, this strategy was familiar to ancient Greek and Roman orators. They called it the method of loci, using it as a way to remember extremely long speeches. It can also be helpful for everyday tasks, like remembering a shopping list.

gettyimages-1270935214.jpg

Jon’s tip for this method is to make the memory triggers striking. Associate the eggs on your shopping list with a fire-breathing dragon guarding its young, for example, and the sensory impression might be distinct enough to stand out from the background noise. 

“The more bizarre the better! Our memories have a big job in trying to differentiate one memory from another. We can help it out by making key information more distinctive. This helps our brains to distinguish memories from one another, and stop irrelevant ones from overlapping or interfering.”

Indeed, one of the functions of the hippocampus is to perform pattern separation – trying to make our memories distinct. If memories are too similar, we find it harder to recall specific experiences. 

This might go some way to explaining the ‘brain fog’ many experienced during COVID-19 lockdowns. With days inside tending to repeat familiar routines, we had less distinct and varied experiences. Our brains were less able to create rich, meaningful memories. Looking back on 2020 and 2021, people find it hard to separate what happened when.

There’s a lesson for non-lockdown living here too. If we want a rich life that feels like it lasts longer and is full of accessible, interesting memories, we should prioritise variety in our experience.

To further improve memory function, we should strive to decrease stress, fear and anxiety (where possible). These emotional states increase our cognitive load and reduce our memory abilities.

“When anxious thoughts flood our minds, they compete for space in our working memory and impair our ability to recall long-term memories. They pull attention and resources away from the things we’d like to focus on. If we can find ways to reduce stress and anxiety, our memory can often bounce back.”

While this might be easier said than done, science has concrete recommendations for reducing stress and anxiety. Done consistently, a healthy diet, regular exercise and a good sleep schedule, as well as techniques like mindfulness practice, can have transformative effects. 

Researchers like Jon are deepening our understanding of what memories are. The Memory Lab follows an illustrious line of Cambridge psychologists who identified key pieces of memory’s endless puzzle. Wherever the next steps lead, they will affirm a wonder of nature: the intricate patterns our mind weaves to make sense of the world outside.

For a handy guide to building mental resilience, check out Brain Boost by Dr Barbara Sahakian and Dr Christelle Langley. To focus on fighting anxiety with scientific techniques, try Dr Olivia Remes.

To find out how you can participate in Memory Lab studies, get in touch.

By tying together more than a century of memory research at Cambridge, the Memory Lab gives us tangible ways to improve, preserve and understand our memory.

When anxious thoughts flood our minds, they compete for space in our working memory and impair our ability to recall long-term memories. If we can find ways to reduce stress and anxiety, our memory can often bounce back.Jon SimonsSusana CamachoJon Simons, by Susana Camacho

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