Research News from the School

Highlighting the last 10 years of partnership through scientific collaboration, nurturing talent and strengthening our ecosystem

Highlighting the last 10 years of partnership through scientific collaboration, nurturing talent and strengthening our ecosystem

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

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-Noncommerical

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

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-Noncommerical

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

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.

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.

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.

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-Noncommerical

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

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-Noncommerical

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.

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.

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

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-Noncommerical

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

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-Noncommerical

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

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