Feed aggregator

Cytora’s platform helps insurers digitise their risk data at scale, turning complex documents and unstructured information into structured, decision-ready formats. The acquisition brings together Cytora’s AI-enabled risk digitisation platform with Applied Systems' suite of insurance solutions, enabling greater intelligent automation, connectivity and efficiency across the insurance lifecycle. This combination is expected to unlock increased growth and productivity across the sector.

Cytora was founded in 2012 as a University startup with early support from Cambridge Enterprise, which first invested in the company in 2014. Recognising the potential of its technology to transform risk analytics and insurance workflows, Cambridge Enterprise continued to support Cytora through two subsequent investment rounds, backing its evolution from a geopolitical risk analytics start-up into a global provider of AI-powered solutions for risk digitisation.

Amanda Wooding, Deputy Head of Ventures, Cambridge Enterprise Ventures, said: “We are delighted to see Cytora reach this exciting milestone. The acquisition by Applied Systems is a strong endorsement of the transformative impact of their technology on the insurance industry. Supporting Cytora from its early stages has been a privilege and we are proud to have played a part in their journey from a Cambridge startup to the leading risk digitisation platform in the insurance industry.”

This acquisition marks a significant milestone for Cambridge Enterprise Ventures and its mission to support the commercialisation of University research. It reflects the long-term value of investing in early-stage ventures and the potential of Cambridge-founded companies to shape global industries.

Read more about the acquisition from Cambridge Enterprise and Applied Systems.

Applied Systems, a global provider of insurance software solutions, has acquired Cytora, a University of Cambridge AI spinout that has become the leading digital risk-processing platform for the insurance industry.

Getty Images: Your_photo

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

Cytora’s platform helps insurers digitise their risk data at scale, turning complex documents and unstructured information into structured, decision-ready formats. The acquisition brings together Cytora’s AI-enabled risk digitisation platform with Applied Systems' suite of insurance solutions, enabling greater intelligent automation, connectivity and efficiency across the insurance lifecycle. This combination is expected to unlock increased growth and productivity across the sector.

Cytora was founded in 2012 as a University startup with early support from Cambridge Enterprise, which first invested in the company in 2014. Recognising the potential of its technology to transform risk analytics and insurance workflows, Cambridge Enterprise continued to support Cytora through two subsequent investment rounds, backing its evolution from a geopolitical risk analytics start-up into a global provider of AI-powered solutions for risk digitisation.

Amanda Wooding, Deputy Head of Ventures, Cambridge Enterprise Ventures, said: “We are delighted to see Cytora reach this exciting milestone. The acquisition by Applied Systems is a strong endorsement of the transformative impact of their technology on the insurance industry. Supporting Cytora from its early stages has been a privilege and we are proud to have played a part in their journey from a Cambridge startup to the leading risk digitisation platform in the insurance industry.”

This acquisition marks a significant milestone for Cambridge Enterprise Ventures and its mission to support the commercialisation of University research. It reflects the long-term value of investing in early-stage ventures and the potential of Cambridge-founded companies to shape global industries.

Read more about the acquisition from Cambridge Enterprise and Applied Systems.

Applied Systems, a global provider of insurance software solutions, has acquired Cytora, a University of Cambridge AI spinout that has become the leading digital risk-processing platform for the insurance industry.

Getty Images: Your_photo

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

The Romans have long been credited with bringing industry to Britain involving large-scale lead and iron production. But it has been unclear what happened once the Romans left around 400 AD. It was generally assumed that industrial-scale production declined, as no written evidence for lead exploitation after the 3rd century exists.

To test this assumption, researchers from the Universities of Cambridge and Nottingham examined a five-metre-long sediment core from Aldborough in Yorkshire, the Roman tribal town of the Brigantes and an important centre of metal production. Their findings, published in the journal Antiquity, confirm that metal production did not collapse immediately after the Romans left Britain.

Professor Martin Millett, from Cambridge’s Faculty of Classics and Fitzwilliam College, said: “This collaborative work which forms part of a long-term project at Aldborough adds a new dimension to our understanding of the history of this important Roman town in the immediately post-Roman period. It has significant implications for our wider understanding of the end of Roman Britain.”

The study’s findings indicate that metal production in Britain continued long after the end of the Roman period and did not decline until a sudden crash around 550-600 AD.

The researchers found low levels of lead and iron production in the 4th to the early 5th centuries AD, but a large continuous rise in iron – and to a lesser extent, lead smelting through the 5th to mid-6th centuries – with the same ore sources and use of coal as in the Roman period. This undermines the popular belief that post-Roman Britain was a ‘Dark Age’ in which industrial production regressed to pre-Roman levels.

The cause of the sudden crash remains uncertain, but textual evidence from the Mediterranean and modern-day France (from the mid-late 6th century) shows that this period saw multiple waves of bubonic plague, and perhaps smallpox. These findings combined with DNA evidence from Edix Hill cemetery in Cambridgeshire show that bubonic plague was killing people in eastern England from the 540s, and this period marked the point of transformation at Aldborough.

Lead author, Professor Christopher Loveluck from Nottingham’s Department of Classics and Archaeology, says the Aldborough sediment core “has provided the first unbroken continuous record and timeline of metal pollution and metal economic history in Britain, from the 5th century to the present day.”

The cylinder of slowly accumulated silts was extracted from a paleochannel of the River Ure. Previous metal pollution records have been extracted far from their sources – for instance upland peat cores or mountain and polar glaciers – but this data comes from the very epicentre of production.

The researchers analysed the core alongside excavation evidence and knowledge of landscape changes at Aldborough over the last two millennia. The study benefited from the expertise of Charles French, Emeritus Professor of Geoarchaeology at Cambridge, who applies archaeological techniques and micromorphological analytical techniques to the interpretation of buried landscapes.

The study indicates that lead and iron production was very active again before the Vikings arrived and expanded under their control. Textual and archaeological sources already suggest that there was a growing focus on domestic economies rather than international trade by that time. It has been difficult to prove this at a macro-scale, but the new results show a boom in raw metal production between the end of the 8th century and through to the 10th century, revealing regional-level economic growth, which has never been measured beyond single sites before.

The study goes on to show a decline in metal production through the 11th century with renewed large-scale growth in lead and iron production reflected again from the mid-12th to early 13th centuries. Results corroborate annual-written sources for increased Yorkshire and wider British lead production from the 1160s–1220, and comparable pollution increases attributed to Britain for these decades recovered previously from Swedish lakes and Alpine ice-core research from Switzerland.

Following a decline in the 14th century, the researchers found evidence of another recovery in production which was cut short by Henry VIII’s Dissolution of the Monasteries from 1536-38.

“It became uneconomical to make fresh metal because it was ripped off all the monasteries, abbeys and religious houses,” Professor Loveluck explains. “Large-scale production resumed in the later 16th century to resource Elizabeth I’s Spanish and French wars.”

The Aldborough Roman Town Project, directed by Dr Rose Ferraby – an author of the new study – and Professor Martin Millett, from Cambridge’s Faculty of Classics, has carried out nearly 120 hectares of magnetometry inside the town and beyond, to establish a landscape scale view of the sub-surface archaeological remains of the town, its defences, road system and extra-mural areas. It has also used Ground Penetrating Radar more selectively within the town to reveal details and depths of the Roman buildings. Since 2016, a number of excavations have been carried out, re-examining earlier trenches.

Funding

The research was funded by The British Academy and the University of Cambridge.

Reference

C. P. Loveluck, M. J. Millett, S. Chenery, C. Chenery, R. Ferraby, C. French, ‘Aldborough and the metals economy of northern England, c. AD 345–1700: a new post-Roman narrative’. Antiquity (2025). DOI: 10.15184/aqy.2025.10175 

Britain’s industrial economy did not collapse when the Romans left and went on to enjoy a Viking-age industrial boom, a new study finds, undermining a stubborn ‘Dark Ages’ narrative.

It has significant implications for our wider understanding of the end of Roman BritainProfessor Martin MillettD. Powlesland and V. HerringAerial photograph of Aldborough showing the extent of the walled town and the location of the sediment core

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

The Romans have long been credited with bringing industry to Britain involving large-scale lead and iron production. But it has been unclear what happened once the Romans left around 400 AD. It was generally assumed that industrial-scale production declined, as no written evidence for lead exploitation after the 3rd century exists.

To test this assumption, researchers from the Universities of Cambridge and Nottingham examined a five-metre-long sediment core from Aldborough in Yorkshire, the Roman tribal town of the Brigantes and an important centre of metal production. Their findings, published in the journal Antiquity, confirm that metal production did not collapse immediately after the Romans left Britain.

Professor Martin Millett, from Cambridge’s Faculty of Classics and Fitzwilliam College, said: “This collaborative work which forms part of a long-term project at Aldborough adds a new dimension to our understanding of the history of this important Roman town in the immediately post-Roman period. It has significant implications for our wider understanding of the end of Roman Britain.”

The study’s findings indicate that metal production in Britain continued long after the end of the Roman period and did not decline until a sudden crash around 550-600 AD.

The researchers found low levels of lead and iron production in the 4th to the early 5th centuries AD, but a large continuous rise in iron – and to a lesser extent, lead smelting through the 5th to mid-6th centuries – with the same ore sources and use of coal as in the Roman period. This undermines the popular belief that post-Roman Britain was a ‘Dark Age’ in which industrial production regressed to pre-Roman levels.

The cause of the sudden crash remains uncertain, but textual evidence from the Mediterranean and modern-day France (from the mid-late 6th century) shows that this period saw multiple waves of bubonic plague, and perhaps smallpox. These findings combined with DNA evidence from Edix Hill cemetery in Cambridgeshire show that bubonic plague was killing people in eastern England from the 540s, and this period marked the point of transformation at Aldborough.

Lead author, Professor Christopher Loveluck from Nottingham’s Department of Classics and Archaeology, says the Aldborough sediment core “has provided the first unbroken continuous record and timeline of metal pollution and metal economic history in Britain, from the 5th century to the present day.”

The cylinder of slowly accumulated silts was extracted from a paleochannel of the River Ure. Previous metal pollution records have been extracted far from their sources – for instance upland peat cores or mountain and polar glaciers – but this data comes from the very epicentre of production.

The researchers analysed the core alongside excavation evidence and knowledge of landscape changes at Aldborough over the last two millennia. The study benefited from the expertise of Charles French, Emeritus Professor of Geoarchaeology at Cambridge, who applies archaeological techniques and micromorphological analytical techniques to the interpretation of buried landscapes.

The study indicates that lead and iron production was very active again before the Vikings arrived and expanded under their control. Textual and archaeological sources already suggest that there was a growing focus on domestic economies rather than international trade by that time. It has been difficult to prove this at a macro-scale, but the new results show a boom in raw metal production between the end of the 8th century and through to the 10th century, revealing regional-level economic growth, which has never been measured beyond single sites before.

The study goes on to show a decline in metal production through the 11th century with renewed large-scale growth in lead and iron production reflected again from the mid-12th to early 13th centuries. Results corroborate annual-written sources for increased Yorkshire and wider British lead production from the 1160s–1220, and comparable pollution increases attributed to Britain for these decades recovered previously from Swedish lakes and Alpine ice-core research from Switzerland.

Following a decline in the 14th century, the researchers found evidence of another recovery in production which was cut short by Henry VIII’s Dissolution of the Monasteries from 1536-38.

“It became uneconomical to make fresh metal because it was ripped off all the monasteries, abbeys and religious houses,” Professor Loveluck explains. “Large-scale production resumed in the later 16th century to resource Elizabeth I’s Spanish and French wars.”

The Aldborough Roman Town Project, directed by Dr Rose Ferraby – an author of the new study – and Professor Martin Millett, from Cambridge’s Faculty of Classics, has carried out nearly 120 hectares of magnetometry inside the town and beyond, to establish a landscape scale view of the sub-surface archaeological remains of the town, its defences, road system and extra-mural areas. It has also used Ground Penetrating Radar more selectively within the town to reveal details and depths of the Roman buildings. Since 2016, a number of excavations have been carried out, re-examining earlier trenches.

Funding

The research was funded by The British Academy and the University of Cambridge.

Reference

C. P. Loveluck, M. J. Millett, S. Chenery, C. Chenery, R. Ferraby, C. French, ‘Aldborough and the metals economy of northern England, c. AD 345–1700: a new post-Roman narrative’. Antiquity (2025). DOI: 10.15184/aqy.2025.10175 

Britain’s industrial economy did not collapse when the Romans left and went on to enjoy a Viking-age industrial boom, a new study finds, undermining a stubborn ‘Dark Ages’ narrative.

It has significant implications for our wider understanding of the end of Roman BritainProfessor Martin MillettD. Powlesland and V. HerringAerial photograph of Aldborough showing the extent of the walled town and the location of the sediment core

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

In a study in mice, researchers have identified genes associated with the dramatic transformation of the mammary gland in pregnancy, breastfeeding, and after breastfeeding as it returns to its resting state.

Their results form the most detailed atlas of genetic expression ever produced for the adult developmental cycle of the mammary gland. They are published today in the journal Nucleic Acids Research.

The mammary gland is made up of different cell types, each with a different function - such as fat cells that provide structural support, and basal cells that are crucial for milk ejection.

The team analysed the cellular composition of the mammary gland at ten different time-points from before the first pregnancy, during pregnancy, during breastfeeding, and during a process called involution when the breast tissue is remodelled to its resting state. The mix of cell types changes dramatically through this cycle.

By measuring gene expression in the mammary gland over the same time-points, the researchers were able to link specific genes to their functions at different stages of the developmental cycle.

“Our atlas is the most detailed to date, allowing us to see which genes are expressed in which cell types at each stage of the adult mammary gland cycle,” said Dr Geula Hanin, a researcher in the University of Cambridge’s Department of Genetics, first author of the report. 

The team found that genes associated with breastfeeding disorders such as insufficient milk supply are active not only in the breast cells that produce milk, but also in other cells such as basal cells - which squeeze out the milk as the infant is suckling. This suggests that in some instances, a mechanical problem - rather than a milk production problem - could be the cause and provides a new cell target for investigation.

The study also found that genes associated with postpartum breast cancer become active immediately after weaning in various cell types - including in fat cells, which have previously been overlooked as contributors to breast cancer linked to childbirth. This offers a future potential target for early detection or prevention strategies.

Hanin said: “We’ve found that genes associated with problems in milk production, often experienced by breastfeeding mothers, are acting in breast cells that weren’t previously considered relevant for milk production. We’ve found genes associated with postpartum breast cancer acting in cells that have been similarly overlooked.

“This work provides many potential new ways of transforming maternal and infant health, by using genetic information to both predict problems with breastfeeding and breast cancer, and to tackle them further down the line.”

Breastfeeding affects lifelong health, for example breast-fed babies are less likely to become obese and diabetic. Yet one in twenty women have breastfeeding difficulties, and despite its importance this is a greatly understudied area of women’s health.

Postpartum breast cancer occurs within five to ten years of giving birth and is linked to hormonal fluctuations, natural tissue remodelling, and the changing environment of the mammary gland during involution that makes it more susceptible to malignancy.

The researchers also focused on ‘imprinted genes’- that is, genes that are switched on or off depending on whether they are inherited from the mother or the father. Imprinted genes in the placenta are known to regulate growth and development of the baby in the womb.

The team identified 25 imprinted genes that are active in the adult mammary gland at precise times during the development cycle. These appear to orchestrate a tightly controlled system for managing milk production and breast tissue changes during motherhood.

Some functions of the genes themselves have been identified in previous studies. This new work provides a detailed understanding of when, and where, the genes become active to cause changes in mammary gland function during its adult development cycle.

“Breastfeeding is a fundamental process that’s common to all mammals; we wouldn’t have survived without it. I hope this work will lead to new ways to support mothers who have issues with breastfeeding, so they have a better chance of succeeding,” said Hanin.

The research was funded primarily by the Medical Research Council.

Hanin co-leads the Cambridge Lactation Network and is a member of Cambridge Reproduction. 

Reference: Hanin, G. et al: ‘Dynamic Allelic Expression in Mouse Mammary Gland Across the Adult Developmental Cycle.’ Nucleic Acids Research, September 2025. DOI: 10.1093/nar/gkaf804

Learn more about the University's research into Women's Health.

A University of Cambridge study of adult mammary gland development has revealed new genes involved in breastfeeding, and provided insights into how genetic changes may be associated with breastfeeding disorders and postpartum breast cancers.

This work provides many potential new ways of transforming maternal and infant health, by using genetic information to both predict problems...and to tackle them further down the line.Geula HaninAlexandr Kolesnikov, GettyMother breastfeeding her baby

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

In a study in mice, researchers have identified genes associated with the dramatic transformation of the mammary gland in pregnancy, breastfeeding, and after breastfeeding as it returns to its resting state.

Their results form the most detailed atlas of genetic expression ever produced for the adult developmental cycle of the mammary gland. They are published today in the journal Nucleic Acids Research.

The mammary gland is made up of different cell types, each with a different function - such as fat cells that provide structural support, and basal cells that are crucial for milk ejection.

The team analysed the cellular composition of the mammary gland at ten different time-points from before the first pregnancy, during pregnancy, during breastfeeding, and during a process called involution when the breast tissue is remodelled to its resting state. The mix of cell types changes dramatically through this cycle.

By measuring gene expression in the mammary gland over the same time-points, the researchers were able to link specific genes to their functions at different stages of the developmental cycle.

“Our atlas is the most detailed to date, allowing us to see which genes are expressed in which cell types at each stage of the adult mammary gland cycle,” said Dr Geula Hanin, a researcher in the University of Cambridge’s Department of Genetics, first author of the report. 

The team found that genes associated with breastfeeding disorders such as insufficient milk supply are active not only in the breast cells that produce milk, but also in other cells such as basal cells - which squeeze out the milk as the infant is suckling. This suggests that in some instances, a mechanical problem - rather than a milk production problem - could be the cause and provides a new cell target for investigation.

The study also found that genes associated with postpartum breast cancer become active immediately after weaning in various cell types - including in fat cells, which have previously been overlooked as contributors to breast cancer linked to childbirth. This offers a future potential target for early detection or prevention strategies.

Hanin said: “We’ve found that genes associated with problems in milk production, often experienced by breastfeeding mothers, are acting in breast cells that weren’t previously considered relevant for milk production. We’ve found genes associated with postpartum breast cancer acting in cells that have been similarly overlooked.

“This work provides many potential new ways of transforming maternal and infant health, by using genetic information to both predict problems with breastfeeding and breast cancer, and to tackle them further down the line.”

Breastfeeding affects lifelong health, for example breast-fed babies are less likely to become obese and diabetic. Yet one in twenty women have breastfeeding difficulties, and despite its importance this is a greatly understudied area of women’s health.

Postpartum breast cancer occurs within five to ten years of giving birth and is linked to hormonal fluctuations, natural tissue remodelling, and the changing environment of the mammary gland during involution that makes it more susceptible to malignancy.

The researchers also focused on ‘imprinted genes’- that is, genes that are switched on or off depending on whether they are inherited from the mother or the father. Imprinted genes in the placenta are known to regulate growth and development of the baby in the womb.

The team identified 25 imprinted genes that are active in the adult mammary gland at precise times during the development cycle. These appear to orchestrate a tightly controlled system for managing milk production and breast tissue changes during motherhood.

Some functions of the genes themselves have been identified in previous studies. This new work provides a detailed understanding of when, and where, the genes become active to cause changes in mammary gland function during its adult development cycle.

“Breastfeeding is a fundamental process that’s common to all mammals; we wouldn’t have survived without it. I hope this work will lead to new ways to support mothers who have issues with breastfeeding, so they have a better chance of succeeding,” said Hanin.

The research was funded primarily by the Medical Research Council.

Hanin co-leads the Cambridge Lactation Network and is a member of Cambridge Reproduction. 

Reference: Hanin, G. et al: ‘Dynamic Allelic Expression in Mouse Mammary Gland Across the Adult Developmental Cycle.’ Nucleic Acids Research, September 2025. DOI: 10.1093/nar/gkaf804

Learn more about the University's research into Women's Health.

A University of Cambridge study of adult mammary gland development has revealed new genes involved in breastfeeding, and provided insights into how genetic changes may be associated with breastfeeding disorders and postpartum breast cancers.

This work provides many potential new ways of transforming maternal and infant health, by using genetic information to both predict problems...and to tackle them further down the line.Geula HaninAlexandr Kolesnikov, GettyMother breastfeeding her baby

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

YesLicence type: Attribution

The £42.8 million Generation New Era birth cohort study will create a comprehensive picture of early childhood development in all four nations of the UK.

Funded by the UKRI Economic and Social Research Council (ESRC), this is the first new UK-wide longitudinal birth cohort study in 25 years and comes as the government publishes its Giving every child the best start in life policy paper.

Generation New Era will collect data at two key developmental stages – between 9-11 months and again at 3-4 years – providing crucial insights before children enter formal education. The research will examine physical, mental and social development, and explore how technological, environmental and social changes affect early childhood experiences. The intention is that the initiative will track these children and their families throughout their lives.

Generation New Era will be led jointly by Co-Directors Professor Pasco Fearon of the University of Cambridge and Professors Alissa Goodman and Lisa Calderwood of UCL.

Professor Fearon, Director of the Centre for Child, Adolescent and Family Research at Cambridge, said: “Children’s lives have changed dramatically since the last UK birth cohort study was launched at the turn of the century. In the past decade, unprecedented social, technological, political and economic events have taken place that have changed the landscape for families raising children dramatically.

“New UK-wide data are needed urgently to help us understand how these changes impact children as they grow up, and there will be new opportunities and challenges for families coming down the line, like AI, that a study like this can help us to better understand.”

As a four-nations cohort study, the study team will benefit from the expertise of senior academics based at the universities of Swansea, Ulster, and Edinburgh, who will serve as the study's leads in their countries.

It will invite over 60,000 children and their families from across the UK with the aim of recruiting 30,000 to participate in the project. There will be a particular focus on recruiting fathers as well as mothers and including groups previously underrepresented in population research, giving a voice to as many communities in UK society as possible

This comprehensive approach will ensure the findings are representative of the diverse experiences of families across the country and that comparisons can be made to help all areas of the UK to learn what works best to improve lives and livelihoods.

The findings generated by the study will directly inform policy development across government departments, helping to ensure services and support for families are based on robust evidence.

Professor Alissa Goodman from the UCL Centre for Longitudinal Studies said: “Generation New Era is a landmark scientific endeavour which will improve the lives of children and benefit science and society for many years to come.  

“As the government works to give every child the best start in life, the study can help shape vital policies and services for babies and parents across the UK. Thanks to the commitment of our participants, we can support the health and development of this generation - and help future generations thrive.”

Generation New Era is part of a long tradition of research council-funded UK longitudinal birth cohort studies which have followed the lives of tens of thousands of people over the past eight decades.

ESRC executive chair Stian Westlake said: “I am excited to see what Generation New Era will discover about the lives of children born next year and how they differ across the UK. The evidence this study produces can underpin policy that makes the UK a happier, healthier and fairer place, improving lives and livelihoods. It is an investment in the future that we are proud to make.”

The study will begin inviting families to take part in the study from summer 2026.

Adapted from a press release from the ESRC

Cambridge is to co-lead a new UK-wide scientific study that will follow the lives of 30,000 children born in 2026, helping provide evidence to improve the lives of future generations.

In the past decade, unprecedented social, technological, political and economic events have taken place that have changed the landscape for families raising children dramaticallyPasco FearonSolStock (Getty Images)Friends and their children at the beach

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

The £42.8 million Generation New Era birth cohort study will create a comprehensive picture of early childhood development in all four nations of the UK.

Funded by the UKRI Economic and Social Research Council (ESRC), this is the first new UK-wide longitudinal birth cohort study in 25 years and comes as the government publishes its Giving every child the best start in life policy paper.

Generation New Era will collect data at two key developmental stages – between 9-11 months and again at 3-4 years – providing crucial insights before children enter formal education. The research will examine physical, mental and social development, and explore how technological, environmental and social changes affect early childhood experiences. The intention is that the initiative will track these children and their families throughout their lives.

Generation New Era will be led jointly by Co-Directors Professor Pasco Fearon of the University of Cambridge and Professors Alissa Goodman and Lisa Calderwood of UCL.

Professor Fearon, Director of the Centre for Child, Adolescent and Family Research at Cambridge, said: “Children’s lives have changed dramatically since the last UK birth cohort study was launched at the turn of the century. In the past decade, unprecedented social, technological, political and economic events have taken place that have changed the landscape for families raising children dramatically.

“New UK-wide data are needed urgently to help us understand how these changes impact children as they grow up, and there will be new opportunities and challenges for families coming down the line, like AI, that a study like this can help us to better understand.”

As a four-nations cohort study, the study team will benefit from the expertise of senior academics based at the universities of Swansea, Ulster, and Edinburgh, who will serve as the study's leads in their countries.

It will invite over 60,000 children and their families from across the UK with the aim of recruiting 30,000 to participate in the project. There will be a particular focus on recruiting fathers as well as mothers and including groups previously underrepresented in population research, giving a voice to as many communities in UK society as possible

This comprehensive approach will ensure the findings are representative of the diverse experiences of families across the country and that comparisons can be made to help all areas of the UK to learn what works best to improve lives and livelihoods.

The findings generated by the study will directly inform policy development across government departments, helping to ensure services and support for families are based on robust evidence.

Professor Alissa Goodman from the UCL Centre for Longitudinal Studies said: “Generation New Era is a landmark scientific endeavour which will improve the lives of children and benefit science and society for many years to come.  

“As the government works to give every child the best start in life, the study can help shape vital policies and services for babies and parents across the UK. Thanks to the commitment of our participants, we can support the health and development of this generation - and help future generations thrive.”

Generation New Era is part of a long tradition of research council-funded UK longitudinal birth cohort studies which have followed the lives of tens of thousands of people over the past eight decades.

ESRC executive chair Stian Westlake said: “I am excited to see what Generation New Era will discover about the lives of children born next year and how they differ across the UK. The evidence this study produces can underpin policy that makes the UK a happier, healthier and fairer place, improving lives and livelihoods. It is an investment in the future that we are proud to make.”

The study will begin inviting families to take part in the study from summer 2026.

Adapted from a press release from the ESRC

Cambridge is to co-lead a new UK-wide scientific study that will follow the lives of 30,000 children born in 2026, helping provide evidence to improve the lives of future generations.

In the past decade, unprecedented social, technological, political and economic events have taken place that have changed the landscape for families raising children dramaticallyPasco FearonSolStock (Getty Images)Friends and their children at the beach

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

The squishy material can be loaded with anti-inflammatory drugs that are released in response to small changes in pH in the body. During an arthritis flare-up, a joint becomes inflamed and slightly more acidic than the surrounding tissue.

The material, developed by researchers at the University of Cambridge, has been designed to respond to this natural change in pH. As acidity increases, the material becomes softer and more jelly-like, triggering the release of drug molecules that can be encapsulated within its structure.

Since the material is designed to respond only within a narrow pH range, the team say that drugs could be released precisely where and when they are needed, potentially reducing side effects.

If used as an artificial cartilage in arthritic joints, this approach could allow for the continuous treatment of arthritis, improving the efficacy of drugs to relieve pain and fight inflammation. Arthritis affects more than 10 million people in the UK, costing the NHS an estimated £10.2 billion annually. Worldwide, it is estimated to affect over 600 million people.

While extensive clinical trials are needed before the material can be used in patients, the researchers say their approach could improve outcomes for people with arthritis, and for those with other conditions including cancer. Their results are reported in the Journal of the American Chemical Society.

The material developed by the Cambridge team uses specially engineered and reversible crosslinks within a polymer network. The sensitivity of these links to changes in acidity levels gives the material highly responsive mechanical properties.

The material was developed in Professor Oren Scherman’s research group in Cambridge’s Yusuf Hamied Department of Chemistry. The group specialises in designing and building these unique materials for a range of potential applications.

“For a while now, we’ve been interested in using these materials in joints, since their properties can mimic those of cartilage,” said Scherman, who is Professor of Supramolecular and Polymer Chemistry and Director of the Melville Laboratory for Polymer Synthesis. “But to combine that with highly targeted drug delivery is a really exciting prospect.”

“These materials can ‘sense’ when something is wrong in the body and respond by delivering treatment right where it’s needed,” said first author Dr Stephen O’Neill. “This could reduce the need for repeated doses of drugs, while improving patient quality of life.”

Unlike many drug delivery systems that require external triggers such as heat or light, this one is powered by the body’s own chemistry. The researchers say this could pave the way for longer-lasting, targeted arthritis treatments that automatically respond to flare-ups, boosting effectiveness while reducing harmful side effects.

In laboratory tests, researchers loaded the material with a fluorescent dye to mimic how a real drug might behave. They found that at acidity levels typical of an arthritic joint, the material released substantially more drug cargo compared with normal, healthy pH levels.

“By tuning the chemistry of these gels, we can make them highly sensitive to the subtle shifts in acidity that occur in inflamed tissue,” said co-author Dr Jade McCune. “That means drugs are released when and where they are needed most.”

The researchers say the approach could be tailored to a range of medical conditions, by fine-tuning the chemistry of the material. “It’s a highly flexible approach, so we could in theory incorporate both fast-acting and slow-acting drugs, and have a single treatment that lasts for days, weeks or even months,” said O’Neill.

The team’s next steps will involve testing the materials in living systems to evaluate their performance and safety in a physiological environment. The team say that if successful, their approach could open the door to a new generation of responsive biomaterials capable of treating chronic diseases with greater precision.

The research was supported by the European Research Council and the Engineering and Physical Sciences Research Council (EPSRC), part of UK Research and Innovation (UKRI). The research is being commercialised with the support of Cambridge Enterprise, the University’s commercialisation arm. Oren Scherman is a Fellow of Jesus College, Cambridge.

 

Reference:
Stephen J.K. O’Neill et al. ‘Kinetic locking of pH-sensitive complexes for mechanically responsive polymer networks.’ Journal of the American Chemical Society (2025). DOI: 10.1021/jacs.5c09897

Researchers have developed a material that can sense tiny changes within the body, such as during an arthritis flare-up, and release drugs exactly where and when they are needed.

Penpak Ngamsathain via Getty ImagesWoman's hand holding a knee

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

The squishy material can be loaded with anti-inflammatory drugs that are released in response to small changes in pH in the body. During an arthritis flare-up, a joint becomes inflamed and slightly more acidic than the surrounding tissue.

The material, developed by researchers at the University of Cambridge, has been designed to respond to this natural change in pH. As acidity increases, the material becomes softer and more jelly-like, triggering the release of drug molecules that can be encapsulated within its structure.

Since the material is designed to respond only within a narrow pH range, the team say that drugs could be released precisely where and when they are needed, potentially reducing side effects.

If used as an artificial cartilage in arthritic joints, this approach could allow for the continuous treatment of arthritis, improving the efficacy of drugs to relieve pain and fight inflammation. Arthritis affects more than 10 million people in the UK, costing the NHS an estimated £10.2 billion annually. Worldwide, it is estimated to affect over 600 million people.

While extensive clinical trials are needed before the material can be used in patients, the researchers say their approach could improve outcomes for people with arthritis, and for those with other conditions including cancer. Their results are reported in the Journal of the American Chemical Society.

The material developed by the Cambridge team uses specially engineered and reversible crosslinks within a polymer network. The sensitivity of these links to changes in acidity levels gives the material highly responsive mechanical properties.

The material was developed in Professor Oren Scherman’s research group in Cambridge’s Yusuf Hamied Department of Chemistry. The group specialises in designing and building these unique materials for a range of potential applications.

“For a while now, we’ve been interested in using these materials in joints, since their properties can mimic those of cartilage,” said Scherman, who is Professor of Supramolecular and Polymer Chemistry and Director of the Melville Laboratory for Polymer Synthesis. “But to combine that with highly targeted drug delivery is a really exciting prospect.”

“These materials can ‘sense’ when something is wrong in the body and respond by delivering treatment right where it’s needed,” said first author Dr Stephen O’Neill. “This could reduce the need for repeated doses of drugs, while improving patient quality of life.”

Unlike many drug delivery systems that require external triggers such as heat or light, this one is powered by the body’s own chemistry. The researchers say this could pave the way for longer-lasting, targeted arthritis treatments that automatically respond to flare-ups, boosting effectiveness while reducing harmful side effects.

In laboratory tests, researchers loaded the material with a fluorescent dye to mimic how a real drug might behave. They found that at acidity levels typical of an arthritic joint, the material released substantially more drug cargo compared with normal, healthy pH levels.

“By tuning the chemistry of these gels, we can make them highly sensitive to the subtle shifts in acidity that occur in inflamed tissue,” said co-author Dr Jade McCune. “That means drugs are released when and where they are needed most.”

The researchers say the approach could be tailored to a range of medical conditions, by fine-tuning the chemistry of the material. “It’s a highly flexible approach, so we could in theory incorporate both fast-acting and slow-acting drugs, and have a single treatment that lasts for days, weeks or even months,” said O’Neill.

The team’s next steps will involve testing the materials in living systems to evaluate their performance and safety in a physiological environment. The team say that if successful, their approach could open the door to a new generation of responsive biomaterials capable of treating chronic diseases with greater precision.

The research was supported by the European Research Council and the Engineering and Physical Sciences Research Council (EPSRC), part of UK Research and Innovation (UKRI). The research is being commercialised with the support of Cambridge Enterprise, the University’s commercialisation arm. Oren Scherman is a Fellow of Jesus College, Cambridge.

 

Reference:
Stephen J.K. O’Neill et al. ‘Kinetic locking of pH-sensitive complexes for mechanically responsive polymer networks.’ Journal of the American Chemical Society (2025). DOI: 10.1021/jacs.5c09897

Researchers have developed a material that can sense tiny changes within the body, such as during an arthritis flare-up, and release drugs exactly where and when they are needed.

Penpak Ngamsathain via Getty ImagesWoman's hand holding a knee

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

When we feel socially isolated, our brain motivates us to seek rewards. Current theory holds that this is a beneficial evolutionary adaptation to help us reconnect with others.

The University of Cambridge-led study found that people in their late teens are very sensitive to the experience of loneliness. After just a few hours without any social interaction, adolescents make significantly more effort to get rewards.  

This increased motivation to seek rewards can help with social reconnection. But when connecting with others is not possible, the behaviour change might be problematic – for example, by making some people more prone to seek out rewards such as alcohol or recreational drugs.

The study found that the effect was stronger in adolescents who reported feeling lonelier while in isolation. When study participants were allowed to interact with others on social media during isolation, they reported feeling less lonely – and their reward-seeking behaviour changed less dramatically as a result.

The report is published today in the journal Communications Psychology.

“Our study demonstrates just how sensitive young people are to very short periods of isolation,” said Dr Livia Tomova, first author of the report, who conducted the study while in the Department of Psychology at the University of Cambridge.

“We found that loneliness significantly increases adolescents’ motivation to seek out rewards – whether that’s more social contact, money, or something else,” added Tomova, who is now based at the University of Cardiff.

Studies suggest that adolescent loneliness has doubled worldwide over the past decade. Social media has been suggested as the culprit, but the researchers say many other changes in society could also be to blame.

“Social media can lead to loneliness in some adolescents, but our study suggests that this relationship is complex,” said Professor Sarah-Jayne Blakemore in the University of Cambridge’s Department of Psychology, senior author of the report.

She added: “Virtual interaction with others seems to make isolated teens less driven to seek external rewards, compared to when they are isolated without access to social media. That suggests social media might reduce some of the negative effects of isolation – but of course we don’t know what potentially harmful effects it might have at the same time.”

While study participants got less bored and lonely in isolation if they had access to social media, they still experienced the same decrease in positive mood as those without access.

Social interaction is a basic human need, and lack of it leads to loneliness. Until now there has been very limited understanding of how loneliness affects adolescent behaviour, with most scientific experiments carried out in animal models.

HOW WAS THE STUDY DONE?

Researchers recruited young people from the local area in Cambridge, UK, conducting extensive screening to gather a group of 40 adolescents aged 16-19 who had good social connections, no history of mental health problems, and average levels of loneliness for their age group.

Participants were given initial tests to establish their baseline score for each task. Then on two different days, they were asked to spend between three and four hours alone in a room before completing the same computer-based tasks again.

On one of the isolation days participants had no social interaction at all, but on the other they had access to virtual social interactions through their phone or laptop.

The study found that when virtual interactions were available, almost half the participants spent over half their time online – predominantly using Snapchat, Instagram and WhatsApp to message their friends.

Overall, the study found that participants became more motivated to look at images of positive social interactions, and to play games where they could win money, after being in isolation for around four hours. They were also better at learning how to get these rewards in ‘fruit machine’-type games.

If they could interact virtually with others while in isolation, they reported feeling less lonely. They were also less inclined to make an effort in the tasks than when they didn’t have virtual social interaction during their isolation.

This research was funded by a Henslow Research Fellowship from the Cambridge Philosophical Society, Wellcome, Jacobs Foundation, and Cambridge Biomedical Research Centre.

Reference: Tomova, L. et al: ‘Acute isolation is associated with increased reward seeking and reward learning in human adolescents.’ Communications Psychology, September 2025. DOI: 10.1038/s44271-025-00306-6

A study has found that adolescents become highly motivated to seek rewards after just a few hours of social isolation. This may be beneficial in driving them towards social interaction, but when opportunities for connection are limited could lead them to pursue less healthy rewards like alcohol or drugs.

Our study demonstrates just how sensitive young people are to very short periods of isolationLivia TomovaSDI Productions, GettyTeenage girl sitting on sofa

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

When we feel socially isolated, our brain motivates us to seek rewards. Current theory holds that this is a beneficial evolutionary adaptation to help us reconnect with others.

The University of Cambridge-led study found that people in their late teens are very sensitive to the experience of loneliness. After just a few hours without any social interaction, adolescents make significantly more effort to get rewards.  

This increased motivation to seek rewards can help with social reconnection. But when connecting with others is not possible, the behaviour change might be problematic – for example, by making some people more prone to seek out rewards such as alcohol or recreational drugs.

The study found that the effect was stronger in adolescents who reported feeling lonelier while in isolation. When study participants were allowed to interact with others on social media during isolation, they reported feeling less lonely – and their reward-seeking behaviour changed less dramatically as a result.

The report is published today in the journal Communications Psychology.

“Our study demonstrates just how sensitive young people are to very short periods of isolation,” said Dr Livia Tomova, first author of the report, who conducted the study while in the Department of Psychology at the University of Cambridge.

“We found that loneliness significantly increases adolescents’ motivation to seek out rewards – whether that’s more social contact, money, or something else,” added Tomova, who is now based at the University of Cardiff.

Studies suggest that adolescent loneliness has doubled worldwide over the past decade. Social media has been suggested as the culprit, but the researchers say many other changes in society could also be to blame.

“Social media can lead to loneliness in some adolescents, but our study suggests that this relationship is complex,” said Professor Sarah-Jayne Blakemore in the University of Cambridge’s Department of Psychology, senior author of the report.

She added: “Virtual interaction with others seems to make isolated teens less driven to seek external rewards, compared to when they are isolated without access to social media. That suggests social media might reduce some of the negative effects of isolation – but of course we don’t know what potentially harmful effects it might have at the same time.”

While study participants got less bored and lonely in isolation if they had access to social media, they still experienced the same decrease in positive mood as those without access.

Social interaction is a basic human need, and lack of it leads to loneliness. Until now there has been very limited understanding of how loneliness affects adolescent behaviour, with most scientific experiments carried out in animal models.

HOW WAS THE STUDY DONE?

Researchers recruited young people from the local area in Cambridge, UK, conducting extensive screening to gather a group of 40 adolescents aged 16-19 who had good social connections, no history of mental health problems, and average levels of loneliness for their age group.

Participants were given initial tests to establish their baseline score for each task. Then on two different days, they were asked to spend between three and four hours alone in a room before completing the same computer-based tasks again.

On one of the isolation days participants had no social interaction at all, but on the other they had access to virtual social interactions through their phone or laptop.

The study found that when virtual interactions were available, almost half the participants spent over half their time online – predominantly using Snapchat, Instagram and WhatsApp to message their friends.

Overall, the study found that participants became more motivated to look at images of positive social interactions, and to play games where they could win money, after being in isolation for around four hours. They were also better at learning how to get these rewards in ‘fruit machine’-type games.

If they could interact virtually with others while in isolation, they reported feeling less lonely. They were also less inclined to make an effort in the tasks than when they didn’t have virtual social interaction during their isolation.

This research was funded by a Henslow Research Fellowship from the Cambridge Philosophical Society, Wellcome, Jacobs Foundation, and Cambridge Biomedical Research Centre.

Reference: Tomova, L. et al: ‘Acute isolation is associated with increased reward seeking and reward learning in human adolescents.’ Communications Psychology, September 2025. DOI: 10.1038/s44271-025-00306-6

A study has found that adolescents become highly motivated to seek rewards after just a few hours of social isolation. This may be beneficial in driving them towards social interaction, but when opportunities for connection are limited could lead them to pursue less healthy rewards like alcohol or drugs.

Our study demonstrates just how sensitive young people are to very short periods of isolationLivia TomovaSDI Productions, GettyTeenage girl sitting on sofa

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

The finding could pave the way for a new type of treatment for glioblastoma, the most aggressive form of brain cancer, although extensive testing will be required before it can be trialled in patients. Glioblastoma is the most common type of brain cancer, with a five-year survival rate of just 15%.

The researchers, from the University of Cambridge, found that cancer cells rely on the flexibility of hyaluronic acid (HA) — a sugar-like polymer that makes up much of the brain’s supporting structure — to latch onto receptors on the surface of cancer cells to trigger their spread throughout the brain.

By locking HA molecules in place so that they lose this flexibility, the researchers were able to ‘reprogramme’ glioblastoma cells so they stopped moving and were unable to invade surrounding tissue. Their results are reported in the journal Royal Society Open Science.

“Fundamentally, hyaluronic acid molecules need to be flexible to bind to cancer cell receptors,” said Professor Melinda Duer from Cambridge’s Yusuf Hamied Department of Chemistry, who led the research. “If you can stop hyaluronic acid being flexible, you can stop cancer cells from spreading. The remarkable thing is that we didn’t have to kill the cells — we simply changed their environment, and they gave up trying to escape and invade neighbouring tissue.”

Glioblastoma, like all brain cancers, is difficult to treat. Even when tumours are surgically removed, cancer cells that have already infiltrated the brain often cause regrowth within months. Current drug treatments struggle to penetrate the tumour mass, and radiotherapy can only delay, not prevent, recurrence of the cancer.

However, the approach developed by the Cambridge team does not target tumour cells directly, but instead attempts to change the tumour’s surrounding environment – the extracellular matrix – to stop its spread.

“Nobody has ever tried to change cancer outcomes by changing the matrix around the tumour,” said Duer. “This is the first example where a matrix-based therapy could be used to reprogramme cancer cells.”

Using nuclear magnetic resonance (NMR) spectroscopy, the team showed that HA molecules twist into shapes that allow them to bind strongly to CD44 — a receptor on cancer cells that drives invasion. When HA was cross-linked and ‘frozen’ into place, those signals were shut down.

The effect was seen even at low concentrations of HA, suggesting the cells were not being physically trapped but instead reprogrammed into a dormant state.

The study may also explain why glioblastoma often returns at the site of surgery. A build-up of fluid, or oedema, at the surgical site dilutes HA, making it more flexible and potentially encouraging cell invasion. By freezing HA in place, it could be possible to prevent recurrence.

“This could be a real opportunity to slow glioblastoma progression,” said Duer. “And because our approach doesn’t require drugs to enter every single cancer cell, it could in principle work for many solid tumours where the surrounding matrix drives invasion.

“Cancer cells behave the way they do in part because of their environment. If you change their environment, you can change the cells.”

The researchers are hoping to conduct further testing in animal models, which could lead to clinical trials in patients.

The research was supported in part by the European Research Council and the Engineering and Physical Sciences Research Council (EPSRC), part of UK Research and Innovation (UKRI). Melinda Duer is a Fellow of Robinson College, Cambridge.

Melinda Duer will be discussing her research on Saturday, 27 September, as part of the Cambridge Alumni Festival 2025. 

Reference:
Uliana Bashtanova, Agne Kuraite, Rakesh Rajan, Melinda J Duer. ‘Molecular flexibility of hyaluronic acid has a profound effect on invasion of cancer cells.’ Royal Society Open Science (2025). DOI: 10.1098/rsos.251036

Scientists have found a way to stop brain cancer cells spreading by essentially ‘freezing’ a key molecule in the brain.

This could be a real opportunity to slow glioblastoma progressionMelinda DuerKATERYNA KON/SCIENCE PHOTO LIBRARY via Getty ImagesComputer illustration of a brain tumour

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

The finding could pave the way for a new type of treatment for glioblastoma, the most aggressive form of brain cancer, although extensive testing will be required before it can be trialled in patients. Glioblastoma is the most common type of brain cancer, with a five-year survival rate of just 15%.

The researchers, from the University of Cambridge, found that cancer cells rely on the flexibility of hyaluronic acid (HA) — a sugar-like polymer that makes up much of the brain’s supporting structure — to latch onto receptors on the surface of cancer cells to trigger their spread throughout the brain.

By locking HA molecules in place so that they lose this flexibility, the researchers were able to ‘reprogramme’ glioblastoma cells so they stopped moving and were unable to invade surrounding tissue. Their results are reported in the journal Royal Society Open Science.

“Fundamentally, hyaluronic acid molecules need to be flexible to bind to cancer cell receptors,” said Professor Melinda Duer from Cambridge’s Yusuf Hamied Department of Chemistry, who led the research. “If you can stop hyaluronic acid being flexible, you can stop cancer cells from spreading. The remarkable thing is that we didn’t have to kill the cells — we simply changed their environment, and they gave up trying to escape and invade neighbouring tissue.”

Glioblastoma, like all brain cancers, is difficult to treat. Even when tumours are surgically removed, cancer cells that have already infiltrated the brain often cause regrowth within months. Current drug treatments struggle to penetrate the tumour mass, and radiotherapy can only delay, not prevent, recurrence of the cancer.

However, the approach developed by the Cambridge team does not target tumour cells directly, but instead attempts to change the tumour’s surrounding environment – the extracellular matrix – to stop its spread.

“Nobody has ever tried to change cancer outcomes by changing the matrix around the tumour,” said Duer. “This is the first example where a matrix-based therapy could be used to reprogramme cancer cells.”

Using nuclear magnetic resonance (NMR) spectroscopy, the team showed that HA molecules twist into shapes that allow them to bind strongly to CD44 — a receptor on cancer cells that drives invasion. When HA was cross-linked and ‘frozen’ into place, those signals were shut down.

The effect was seen even at low concentrations of HA, suggesting the cells were not being physically trapped but instead reprogrammed into a dormant state.

The study may also explain why glioblastoma often returns at the site of surgery. A build-up of fluid, or oedema, at the surgical site dilutes HA, making it more flexible and potentially encouraging cell invasion. By freezing HA in place, it could be possible to prevent recurrence.

“This could be a real opportunity to slow glioblastoma progression,” said Duer. “And because our approach doesn’t require drugs to enter every single cancer cell, it could in principle work for many solid tumours where the surrounding matrix drives invasion.

“Cancer cells behave the way they do in part because of their environment. If you change their environment, you can change the cells.”

The researchers are hoping to conduct further testing in animal models, which could lead to clinical trials in patients.

The research was supported in part by the European Research Council and the Engineering and Physical Sciences Research Council (EPSRC), part of UK Research and Innovation (UKRI). Melinda Duer is a Fellow of Robinson College, Cambridge.

Melinda Duer will be discussing her research on Saturday, 27 September, as part of the Cambridge Alumni Festival 2025. 

Reference:
Uliana Bashtanova, Agne Kuraite, Rakesh Rajan, Melinda J Duer. ‘Molecular flexibility of hyaluronic acid has a profound effect on invasion of cancer cells.’ Royal Society Open Science (2025). DOI: 10.1098/rsos.251036

Scientists have found a way to stop brain cancer cells spreading by essentially ‘freezing’ a key molecule in the brain.

This could be a real opportunity to slow glioblastoma progressionMelinda DuerKATERYNA KON/SCIENCE PHOTO LIBRARY via Getty ImagesComputer illustration of a brain tumour

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

The visit brought together fundamental plant science research with crop and Agri-Tech researchers from across the University for a series of research demonstrations and a roundtable discussion. 

Mr Zeichner toured the award-winning facility, meeting researchers in the open-plan office and lab spaces, which foster collaboration and advances in multi-disciplinary research. 

The Minister saw exciting examples of foundational research, which have the potential to transform agriculture and ensure long term sustainability.  

The first demonstration was led by Dr Sebastian Schornack and PhD student Nicolas Hernandez, who are investigating the plant developmental processes. The Minister saw through the microscope how they are using beetroot pigments to enable us to see how fungi is colonising living plant roots. This research allows us to track and measure in real time how chemicals, soil tillage and environmental conditions impact this beneficial plant-microbe relationship.  

Mr Zeichner then visited the Lab’s microscopy room, and met with Dr Madelaine Bartlett and her colleague Terice Kelly. Dr Madelaine Bartlett's team researches the development of maize flowers (among other grass and cereal species) with a particular focus on the genetics behind these specialised flowers and future crop improvement. The team demonstrated how they image a maize flower on the Lab’s desktop scanning electron microscope. 

The Sainsbury Laboratory boasts its own Bee Room, where Dr Edwige Moyroud demonstrated how bumble bees are helping to reveal the characteristics of petal patterns that are most important for attracting pollinators. Dr Moyroud and her team are identifying the genes that plants use to produce patterns that attract pollinators by combining various research techniques, including experiments, modelling, microscopy and bee behaviour. 

Finally, overlooking Cambridge’ Botanic Gardens, academics from the Department of Plant Sciences and the Crop Science Centre presented on research into regenerative agriculture and using AI to measure and prevent crop disease.  

Professor Lynn Dicks presented on the latest findings of the H3 research on regenerative agriculture. Professor Dicks and colleagues, during this ongoing five-year project, have worked collaboratively with farming clusters in the UK to study the impacts of a transition on regenerative agriculture, which has so far has been shown to improve soil health and reduce the use of chemicals. 

Professor Eves-van Den Akker and his team, based at the University’s Crop Science Centre, have combined low-cost 3D printing of custom imaging machines with state-of-the-art deep-learning algorithms to make millions of measurements, of tens of thousands of parasites across hundreds of genotypes. They are now working with companies to translate this fundamental research, with the aim of accelerating their breeding programs for crop resistance to pests and disease. 

The visit concluded with a discussion of the UK’s leading strengths in Agri-Tech and crop science, and how the UK and Cambridge are an attractive place for researchers from around the world to work, and make exciting advances, with global impact. 

The University of Cambridge hosted a visit from local MP, and Farming Minister Daniel Zeichner MP, at the Sainsbury Laboratory.

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

The visit brought together fundamental plant science research with crop and Agri-Tech researchers from across the University for a series of research demonstrations and a roundtable discussion. 

Mr Zeichner toured the award-winning facility, meeting researchers in the open-plan office and lab spaces, which foster collaboration and advances in multi-disciplinary research. 

The Minister saw exciting examples of foundational research, which have the potential to transform agriculture and ensure long term sustainability.  

The first demonstration was led by Dr Sebastian Schornack and PhD student Nicolas Hernandez, who are investigating the plant developmental processes. The Minister saw through the microscope how they are using beetroot pigments to enable us to see how fungi is colonising living plant roots. This research allows us to track and measure in real time how chemicals, soil tillage and environmental conditions impact this beneficial plant-microbe relationship.  

Mr Zeichner then visited the Lab’s microscopy room, and met with Dr Madelaine Bartlett and her colleague Terice Kelly. Dr Madelaine Bartlett's team researches the development of maize flowers (among other grass and cereal species) with a particular focus on the genetics behind these specialised flowers and future crop improvement. The team demonstrated how they image a maize flower on the Lab’s desktop scanning electron microscope. 

The Sainsbury Laboratory boasts its own Bee Room, where Dr Edwige Moyroud demonstrated how bumble bees are helping to reveal the characteristics of petal patterns that are most important for attracting pollinators. Dr Moyroud and her team are identifying the genes that plants use to produce patterns that attract pollinators by combining various research techniques, including experiments, modelling, microscopy and bee behaviour. 

Finally, overlooking Cambridge’ Botanic Gardens, academics from the Department of Plant Sciences and the Crop Science Centre presented on research into regenerative agriculture and using AI to measure and prevent crop disease.  

Professor Lynn Dicks presented on the latest findings of the H3 research on regenerative agriculture. Professor Dicks and colleagues, during this ongoing five-year project, have worked collaboratively with farming clusters in the UK to study the impacts of a transition on regenerative agriculture, which has so far has been shown to improve soil health and reduce the use of chemicals. 

Professor Eves-van Den Akker and his team, based at the University’s Crop Science Centre, have combined low-cost 3D printing of custom imaging machines with state-of-the-art deep-learning algorithms to make millions of measurements, of tens of thousands of parasites across hundreds of genotypes. They are now working with companies to translate this fundamental research, with the aim of accelerating their breeding programs for crop resistance to pests and disease. 

The visit concluded with a discussion of the UK’s leading strengths in Agri-Tech and crop science, and how the UK and Cambridge are an attractive place for researchers from around the world to work, and make exciting advances, with global impact. 

The University of Cambridge hosted a visit from local MP, and Farming Minister Daniel Zeichner MP, at the Sainsbury Laboratory.

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

The discovery – found in a study in mice – sheds light on the role that inflammation can play in mood disorders and could help in the search for new treatments, in particular for those individuals for whom current treatments are ineffective.

Around 1 billion people will be diagnosed with a mood disorder such as depression or anxiety at some point in their life. While there may be many underlying causes, chronic inflammation – when the body’s immune system stays active for a long time, even when there is no infection or injury to fight – has been linked to depression. This suggests that the immune system may play an important role in the development of mood disorders.

Previous studies have highlighted how high levels of an immune cell known as a neutrophil, a type of white blood cell, are linked to the severity of depression. But how neutrophils contribute to symptoms of depression is currently unclear.

In research published today in Nature Communications, a team led by scientists at the University of Cambridge, UK, and the National Institute of Mental Health, USA, tested a hypothesis that chronic stress can lead to the release of neutrophils from bone marrow in the skull. These cells then collect in the meninges – membranes that cover and protect your brain and spinal cord – and contribute to symptoms of depression.

As it is not possible to test this hypothesis in humans, the team used mice exposed to chronic social stress. In this experiment, an ‘intruder’ mouse is introduced into the home cage of an aggressive resident mouse. The two have brief daily physical interactions and can otherwise see, smell, and hear each other.

The researchers found that prolonged exposure to this stressful environment led to a noticeable increase in levels of neutrophils in the meninges, and that this was linked to signs of depressive behaviour in the mice. Even after the stress ended, the neutrophils lasted longer in the meninges than they did in the blood. Analysis confirmed the researchers’ hypothesis that the meningeal neutrophils – which appeared subtly different from those found in the blood – originated in the skull.

Further analysis suggested that long-term stress triggered a type of immune system ‘alarm warning’ known as type I interferon signalling in the neutrophils. Blocking this pathway – in effect, switching off the alarm – reduced the number of neutrophils in the meninges and improved behaviour in the depressed mice. This pathway has previously been linked to depression – type 1 interferons are used to treat patients with hepatitis C, for example, but a known side effect of the medication is that it can cause severe depression during treatment.

Dr Stacey Kigar from the Department of Medicine at the University of Cambridge said: “Our work helps explain how chronic stress can lead to lasting changes in the brain’s immune environment, potentially contributing to depression. It also opens the door to possible new treatments that target the immune system rather than just brain chemistry.

“There’s a significant proportion of people for whom antidepressants don’t work, possibly as many as one in three patients. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptoms.”

The reason why there are high levels of neutrophils in the meninges is unclear. One explanation could be that they are recruited by microglia, a type of immune cell unique to the brain. Another possible explanation is that chronic stress may cause microhaemorrhages, tiny leaks in brain blood vessels, and that neutrophils – the body’s ‘first responders’ – arrive to fix the damage and prevent any further damage. These neutrophils then become more rigid, possibly getting stuck in brain capillaries and causing further inflammation in the brain.

Dr Mary-Ellen Lynall from the Department of Psychiatry at the University of Cambridge said: “We’ve long known that something is different about how neutrophils behave after stressful events, or during depression, but we didn’t know what these neutrophils were doing, where they were going, or how they might be affecting the brain and mind. Our findings show that these ‘first responder’ immune cells leave the skull bone marrow and travel to the brain, where they can influence mood and behaviour.

“Most people will have experienced how our immune systems can drive short-lived depression-like symptoms. When we are sick, for example with a cold or flu, we often lack energy and appetite, sleep more and withdraw from social contact. If the immune system is always in a heightened, pro-inflammatory state, it shouldn’t be too surprising if we experience longer-term problems with our mood.”

The findings could provide a useful signature, or ‘biomarker’, to help identify those patients whose mood disorders are related to inflammation. This could help in the search for better treatments. For example, a clinical trial of a potential new drug that targets inflammation of the brain in depression might appear to fail if trialled on a general cohort of people with depression, whereas using the biomarker to identify individuals whose depression is linked to inflammation could increase the likelihood of the trial succeeding.

The findings may also help explain why depression is a symptom common in other neurological disorders such as stroke and Alzheimer’s disease, as it may be the case that neutrophils are being released in response to the damage to the brain seen in these conditions. But it may also explain why depression is itself a risk factor for dementia in later life, if neutrophils can themselves trigger damage to brain cells.

The research was funded by the National Institute of Mental Health, Medical Research Council and National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Reference
Kigar, SL et al. Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling in male mice. Nat Comms; 1 Sept 2025; DOI: 10.1038/s41467-025-62840-5

Immune cells released from bone marrow in the skull in response to chronic stress and adversity could play a key role in symptoms of depression and anxiety, say researchers.

There’s a significant proportion of people for whom antidepressants don’t work. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptomsStacey KigarGift Habeshaw (Unsplash)Silhouette photography of man

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: Public Domain

The discovery – found in a study in mice – sheds light on the role that inflammation can play in mood disorders and could help in the search for new treatments, in particular for those individuals for whom current treatments are ineffective.

Around 1 billion people will be diagnosed with a mood disorder such as depression or anxiety at some point in their life. While there may be many underlying causes, chronic inflammation – when the body’s immune system stays active for a long time, even when there is no infection or injury to fight – has been linked to depression. This suggests that the immune system may play an important role in the development of mood disorders.

Previous studies have highlighted how high levels of an immune cell known as a neutrophil, a type of white blood cell, are linked to the severity of depression. But how neutrophils contribute to symptoms of depression is currently unclear.

In research published today in Nature Communications, a team led by scientists at the University of Cambridge, UK, and the National Institute of Mental Health, USA, tested a hypothesis that chronic stress can lead to the release of neutrophils from bone marrow in the skull. These cells then collect in the meninges – membranes that cover and protect your brain and spinal cord – and contribute to symptoms of depression.

As it is not possible to test this hypothesis in humans, the team used mice exposed to chronic social stress. In this experiment, an ‘intruder’ mouse is introduced into the home cage of an aggressive resident mouse. The two have brief daily physical interactions and can otherwise see, smell, and hear each other.

The researchers found that prolonged exposure to this stressful environment led to a noticeable increase in levels of neutrophils in the meninges, and that this was linked to signs of depressive behaviour in the mice. Even after the stress ended, the neutrophils lasted longer in the meninges than they did in the blood. Analysis confirmed the researchers’ hypothesis that the meningeal neutrophils – which appeared subtly different from those found in the blood – originated in the skull.

Further analysis suggested that long-term stress triggered a type of immune system ‘alarm warning’ known as type I interferon signalling in the neutrophils. Blocking this pathway – in effect, switching off the alarm – reduced the number of neutrophils in the meninges and improved behaviour in the depressed mice. This pathway has previously been linked to depression – type 1 interferons are used to treat patients with hepatitis C, for example, but a known side effect of the medication is that it can cause severe depression during treatment.

Dr Stacey Kigar from the Department of Medicine at the University of Cambridge said: “Our work helps explain how chronic stress can lead to lasting changes in the brain’s immune environment, potentially contributing to depression. It also opens the door to possible new treatments that target the immune system rather than just brain chemistry.

“There’s a significant proportion of people for whom antidepressants don’t work, possibly as many as one in three patients. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptoms.”

The reason why there are high levels of neutrophils in the meninges is unclear. One explanation could be that they are recruited by microglia, a type of immune cell unique to the brain. Another possible explanation is that chronic stress may cause microhaemorrhages, tiny leaks in brain blood vessels, and that neutrophils – the body’s ‘first responders’ – arrive to fix the damage and prevent any further damage. These neutrophils then become more rigid, possibly getting stuck in brain capillaries and causing further inflammation in the brain.

Dr Mary-Ellen Lynall from the Department of Psychiatry at the University of Cambridge said: “We’ve long known that something is different about how neutrophils behave after stressful events, or during depression, but we didn’t know what these neutrophils were doing, where they were going, or how they might be affecting the brain and mind. Our findings show that these ‘first responder’ immune cells leave the skull bone marrow and travel to the brain, where they can influence mood and behaviour.

“Most people will have experienced how our immune systems can drive short-lived depression-like symptoms. When we are sick, for example with a cold or flu, we often lack energy and appetite, sleep more and withdraw from social contact. If the immune system is always in a heightened, pro-inflammatory state, it shouldn’t be too surprising if we experience longer-term problems with our mood.”

The findings could provide a useful signature, or ‘biomarker’, to help identify those patients whose mood disorders are related to inflammation. This could help in the search for better treatments. For example, a clinical trial of a potential new drug that targets inflammation of the brain in depression might appear to fail if trialled on a general cohort of people with depression, whereas using the biomarker to identify individuals whose depression is linked to inflammation could increase the likelihood of the trial succeeding.

The findings may also help explain why depression is a symptom common in other neurological disorders such as stroke and Alzheimer’s disease, as it may be the case that neutrophils are being released in response to the damage to the brain seen in these conditions. But it may also explain why depression is itself a risk factor for dementia in later life, if neutrophils can themselves trigger damage to brain cells.

The research was funded by the National Institute of Mental Health, Medical Research Council and National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Reference
Kigar, SL et al. Chronic social defeat stress induces meningeal neutrophilia via type I interferon signaling in male mice. Nat Comms; 1 Sept 2025; DOI: 10.1038/s41467-025-62840-5

Immune cells released from bone marrow in the skull in response to chronic stress and adversity could play a key role in symptoms of depression and anxiety, say researchers.

There’s a significant proportion of people for whom antidepressants don’t work. If we can figure out what's happening with the immune system, we may be able to alleviate or reduce depressive symptomsStacey KigarGift Habeshaw (Unsplash)Silhouette photography of man

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: Public Domain

While previous research shows outrage and division drive engagement on social media, a new study of digital behaviour during the 2024 US election finds that this effect flips during a major crisis – when “ingroup solidarity” becomes the engine of online virality.

Psychologists say the findings show positive emotions such as unity can cut through the hostility on social media, but it takes a shock to the system that threatens a community.  

In a little over a week during the summer of 2024, the attempted assassination of Donald Trump at a rally (July 13) and Joe Biden’s suspension of his re-election campaign (21 July) completely reshaped the presidential race.

The University of Cambridge’s Social Decision-Making Lab collected over 62,000 public posts from the Facebook accounts of hundreds of US politicians, commentators and media outlets before and after these events to see how they affected online behaviour.*

“We wanted to understand the kinds of content that went viral among Republicans and Democrats during this period of high tension for both groups,” said Malia Marks, PhD candidate in Cambridge’s Department of Psychology and lead author of the study, published in the journal Proceedings of the National Academy of Sciences.

“Negative emotions such as anger and outrage along with hostility towards opposing political groups are usually rocket fuel for social media engagement. You might expect this to go into hyperdrive during times of crisis and external threat.”

“However, we found the opposite. It appears that political crises evoke not so much outgroup hate but rather ingroup love,” said Marks.

Just after the Trump assassination attempt, Republican-aligned posts signalling unity and shared identity received 53% more engagement than those that did not – an increase of 17 percentage points compared to just before the shooting.

These included posts such as evangelist Franklin Graham thanking God that Donald Trump is alive, and Fox News commentator Laura Ingraham posting: “Bleeding and unbowed, Trump faces relentless attacks yet stands strong for America. This is why his followers remain passionately loyal.”

At the same time, engagement levels for Republican posts attacking the Democrats saw a decrease of 23 percentage points from just a few days earlier.

After Biden suspended his re-election campaign, Democrat-aligned posts expressing solidarity received 91% more engagement than those that did not – a major increase of 71 percentage points over the period shortly before his withdrawal.

Posts included former US Secretary of Labor Robert Reich calling Biden “one of our most pro-worker presidents”, and former House Speaker Nancy Pelosi posting that Biden’s “legacy of vision, values and leadership make him one of the most consequential Presidents in American history.”

Biden’s withdrawal saw the continuation of a gradual rise in engagement for Democrat posts attacking Republicans – although over the 25 July days covered by the analysis almost a quarter of all conservative posts displayed “outgroup hostility” compared to just 5% of liberal posts.

Research led by the same Cambridge Lab, published in 2021, showed how social media posts criticizing or mocking those on the rival side of an ideological divide typically receive twice as many shares as posts that champion one’s own side.

“Social media platforms such as Twitter and Facebook are increasingly seen as creating toxic information environments that intensify social and political divisions, and there is plenty of research now to support this,” said Yara Kyrychenko, study co-author and PhD candidate in Cambridge’s Social Decision-Making Lab.

“Yet we see that social media can produce a rally-round-the-flag effect at moments of crisis, when the emotional and psychological preference for one’s own group takes over as the dominant driver of online behaviour.”

Last year, the Cambridge team (led by Kyrychenko) published a study of 1.6 million Ukrainian social media posts in the months before and after Russia’s full-scale invasion in February of 2022.

Following the invasion they found a similar spike for “ingroup solidarity” posts, which got 92% more engagement on Facebook and 68% more on Twitter, while posts hostile to Russia received little extra engagement. 

Researchers argue that the findings from the latest study are even more surprising, given the gravity of the threat to Ukraine and the nature of its population.

“We didn’t know whether moments of political rather than existential crisis would trigger solidarity in a country as deeply polarised as the United States. But even here, group unity surged when leadership was threatened,” said Dr Jon Roozenbeek, Lecturer in Psychology at Cambridge University and senior author of the study.

“In times of crisis, ingroup love may matter more to us than outgroup hate on social media.”

* The study used 62,118 public posts from 484 Facebook accounts run by US politicians and partisan commentators or media sources from 5-29 July 2024.

Research reveals how political crises cause a shift in the force behind viral online content ‘from outgroup hate to ingroup love’.

It appears that political crises evoke not so much outgroup hate but rather ingroup loveMalia Marksconceptphoto.info via FlickrThe Trump assassination attempt on the front page of German newspaper Bild.

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

While previous research shows outrage and division drive engagement on social media, a new study of digital behaviour during the 2024 US election finds that this effect flips during a major crisis – when “ingroup solidarity” becomes the engine of online virality.

Psychologists say the findings show positive emotions such as unity can cut through the hostility on social media, but it takes a shock to the system that threatens a community.  

In a little over a week during the summer of 2024, the attempted assassination of Donald Trump at a rally (July 13) and Joe Biden’s suspension of his re-election campaign (21 July) completely reshaped the presidential race.

The University of Cambridge’s Social Decision-Making Lab collected over 62,000 public posts from the Facebook accounts of hundreds of US politicians, commentators and media outlets before and after these events to see how they affected online behaviour.*

“We wanted to understand the kinds of content that went viral among Republicans and Democrats during this period of high tension for both groups,” said Malia Marks, PhD candidate in Cambridge’s Department of Psychology and lead author of the study, published in the journal Proceedings of the National Academy of Sciences.

“Negative emotions such as anger and outrage along with hostility towards opposing political groups are usually rocket fuel for social media engagement. You might expect this to go into hyperdrive during times of crisis and external threat.”

“However, we found the opposite. It appears that political crises evoke not so much outgroup hate but rather ingroup love,” said Marks.

Just after the Trump assassination attempt, Republican-aligned posts signalling unity and shared identity received 53% more engagement than those that did not – an increase of 17 percentage points compared to just before the shooting.

These included posts such as evangelist Franklin Graham thanking God that Donald Trump is alive, and Fox News commentator Laura Ingraham posting: “Bleeding and unbowed, Trump faces relentless attacks yet stands strong for America. This is why his followers remain passionately loyal.”

At the same time, engagement levels for Republican posts attacking the Democrats saw a decrease of 23 percentage points from just a few days earlier.

After Biden suspended his re-election campaign, Democrat-aligned posts expressing solidarity received 91% more engagement than those that did not – a major increase of 71 percentage points over the period shortly before his withdrawal.

Posts included former US Secretary of Labor Robert Reich calling Biden “one of our most pro-worker presidents”, and former House Speaker Nancy Pelosi posting that Biden’s “legacy of vision, values and leadership make him one of the most consequential Presidents in American history.”

Biden’s withdrawal saw the continuation of a gradual rise in engagement for Democrat posts attacking Republicans – although over the 25 July days covered by the analysis almost a quarter of all conservative posts displayed “outgroup hostility” compared to just 5% of liberal posts.

Research led by the same Cambridge Lab, published in 2021, showed how social media posts criticizing or mocking those on the rival side of an ideological divide typically receive twice as many shares as posts that champion one’s own side.

“Social media platforms such as Twitter and Facebook are increasingly seen as creating toxic information environments that intensify social and political divisions, and there is plenty of research now to support this,” said Yara Kyrychenko, study co-author and PhD candidate in Cambridge’s Social Decision-Making Lab.

“Yet we see that social media can produce a rally-round-the-flag effect at moments of crisis, when the emotional and psychological preference for one’s own group takes over as the dominant driver of online behaviour.”

Last year, the Cambridge team (led by Kyrychenko) published a study of 1.6 million Ukrainian social media posts in the months before and after Russia’s full-scale invasion in February of 2022.

Following the invasion they found a similar spike for “ingroup solidarity” posts, which got 92% more engagement on Facebook and 68% more on Twitter, while posts hostile to Russia received little extra engagement. 

Researchers argue that the findings from the latest study are even more surprising, given the gravity of the threat to Ukraine and the nature of its population.

“We didn’t know whether moments of political rather than existential crisis would trigger solidarity in a country as deeply polarised as the United States. But even here, group unity surged when leadership was threatened,” said Dr Jon Roozenbeek, Lecturer in Psychology at Cambridge University and senior author of the study.

“In times of crisis, ingroup love may matter more to us than outgroup hate on social media.”

* The study used 62,118 public posts from 484 Facebook accounts run by US politicians and partisan commentators or media sources from 5-29 July 2024.

Research reveals how political crises cause a shift in the force behind viral online content ‘from outgroup hate to ingroup love’.

It appears that political crises evoke not so much outgroup hate but rather ingroup loveMalia Marksconceptphoto.info via FlickrThe Trump assassination attempt on the front page of German newspaper Bild.

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