University of Cambridge - Department of Clinical Neurosciences

Deaf opera singer welcomes new Cambridge-led cochlear implant trial

cjb250 — Wed, 06 May 2026 07:34:21 +0000

The UK trial will provide bilateral cochlear implants (cochlear implants on both sides) to some profoundly deaf adults. The results will be used to review NHS guidance for the provision of implants to adults.

Each year over 1,000 adults in the UK receive cochlear implants to restore their hearing. Under NHS guidance, adults currently only receive a single (unilateral) implant, yet evidence suggests having two could offer significant improvements in prospects and quality of life and may now be cost effective.

Janine said: “With bilateral implants, I no longer consider myself to be deaf. They have been utterly life changing and, for me, have broken a generational curse. I am excited that this trial will offer the same opportunity to others.”

Funded by the National Institute for Health and Care Research (NIHR), the trial is being co-led from Addenbrooke’s Hospital and the University of Cambridge. It will run in 14 hospitals and include over 250 adult participants, who will either receive one (unilateral) or two (bilateral) implants. Participants will be monitored for 12 months after surgery to assess the effects of the implants on wellbeing, ability to hear speech in noise, and quality of life. The study will also evaluate the economic benefits and cost of bilateral implants for the NHS.

Called LUCIA, the trial will be co-led by Dr Matthew Smith, an ear, nose and throat (ENT) surgeon at Addenbrooke’s Hospital, and Professor Debi Vickers, a speech and hearing scientist in the Department of Clinical Neurosciences, University of Cambridge, who leads the SOUND Lab.

Professor Debi Vickers, who also co-leads the Devices and Advanced Therapies theme at the NIHR Cambridge Biomedical Research Centre, said: “Children routinely receive bilateral cochlear implants. These can provide 3-dimensional hearing, enabling them to hear more naturally than unilateral, with improved access to sound and better engagement with society.

“Adults tell us, and I agree, that they should be given the same hearing opportunities as children. In turn these will result in reduced social isolation, enriched communication, improved mental health, and better overall quality of life.”

The trial, which is expected to begin recruiting patients in the autumn, has been designed in collaboration with Janine and other patients. By involving individuals with lived experience of cochlear implantation, the researchers aim to measure changes that patients consider to be most important.

The primary trial outcome will reflect participants’ own perceptions of their quality of hearing. The study will also measure common challenges faced by patients, such as listening effort and fatigue, a choice directly based on discussions with patient groups.

Dr Smith, who is also an academic surgeon at the University of Cambridge, said: “We know from giving bilateral implants to children that it can have a transformative effect on their quality of life and interactions with other people. Through this study, we can offer the same opportunity to adults who have become deaf, and understand the potential added value of bilateral cochlear implants, not just in terms of hearing, but also how they enrich quality of life.”

Janine was diagnosed as a teenager with a genetic condition that caused hearing loss and eventually led to her needing hearing aids. For over 30 years she hid her deteriorating hearing and became a well-known mezzo-soprano, performing in operas, operettas and musicals, including at the Royal Opera House in London.

It was only in 2019, after she had retired due to profound hearing loss, that she had cochlear implant surgery, and received bilateral implants partly through personal funding. She said: “Having two implants is lightyears away from just one. Sound quality is so much better, sounds are fuller, clearer, louder and more natural. It’s much easier to tell where sounds are coming from, especially in busy spaces.

“If you’re out in public, it can be hard to follow who is speaking, making joining in with conversations almost impossible. As a result, you have debilitating concentration fatigue at the end of every day.”

Just like at the cinema, multi-directional surround sound is a key part of creating an engaging immersive experience. By comparison, living with one implant can be like listening to life through a single, poor-quality speaker.

She explains: “Struggling to hear can be extremely isolating and many people experience anxiety or depression as a result. The implants are life changing. They reconnect you to the world and most importantly people. Communication is surely the longing of every human heart.

“I also feel safer and more secure having the two implants. I am more aware of and connected to what’s happening in the world around me. And, if anything goes wrong with one of the implants, I’m not suddenly plunged into a world of total silence.”

While hearing aids help people with mild to moderate hearing loss by making sounds louder, they often provide very little benefit for people with severe or profound hearing loss. Cochlear implants bypass the outer, middle and inner ear and send electrical impulses directly to the hearing nerve which carries signals to the brain.

Participants in the trial will need to have become deaf later in life and cannot already have an implant.

People with cochlear implants will also be involved in delivering the trial. They will be specially trained to participate in interviewing trial participants that will be used to measure the impacts of the trial.

Professor Anthony Gordon, Programme Director for the NIHR Health Technology Assessment Programme, which funded the trial, said: "We fund innovative trials like the LUCIA study which explore how advances in technology can help make a positive difference to the day-to-day lives of those affected. This study offers real hope to people with severe hearing loss and the chance of a significant improvement in their quality of life."

Adapted from a press release from Cambridge University Hospitals NHS Foundation Trust

Janine Roebuck, a formerly deaf opera singer who regained her hearing thanks to cochlear implants, has described as ‘life changing’ an upcoming Cambridge-led trial in hearing loss.

We know from giving bilateral implants to children that it can have a transformative effect on their quality of life and interactions with other people. Through this study, we can offer the same opportunity to adults

Matthew Smith

Janine Roebuck

Janine Roebuck as Flora in La Traviata by Verdi at New Sadler's Wells Opera

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

Study highlights stroke risk linked to recreational drugs, including among young users

cjb250 — Mon, 09 Mar 2026 00:01:00 +0000

Stroke is a major global health challenge – the third leading cause of death and disability combined. But it also a condition that, for the most part, results from modifiable risk factors, such as poor diet, lack of exercise and other lifestyle factors.

In 2024, 8.8% of adults aged 16 to 59 years in England and Wales – around 2.9 million individuals - reported having used a legal or illegal recreational drug in the past year. Recent data from the USA reports that over half of all those aged over 12 have used drugs such as cocaine, cannabis and opiates at least once.

There is increasing evidence that these drugs may increase the risk of stroke, but the evidence is often of differing quality and is observational only, meaning it is impossible to say whether the use of these drugs itself increases the risk of stroke, or whether this is purely a correlation.

To investigate this further, a team from the Department of Clinical Neurosciences at the University of Cambridge first carried out a meta-analysis of studies encompassing more than 100 million people. A meta-analysis is a method for pooling and analysing cohort data from all of the published evidence. This approach allows researchers to bring together studies which, on their own may not provide sufficient evidence and sometimes disagree with each other, to provide more robust conclusions.

In findings published in the International Journal of Stroke, the team found that the use of cocaine and amphetamines was associated with around double the risk of stroke (cocaine increased the risk by 96%, amphetamines by 122%), while cannabis use increased the risk by around 37%. The team found no statistically significant link between opioid use and stroke risk.

When the researchers restricted their analysis to individuals under 55 years, they found that amphetamine use almost tripled the risk of stroke (an increase of 174%); cannabis use increase stroke risk but by a smaller amount (14%), while cocaine use increased the risk by 97%.

To analyse these links further, the researchers used a statistical technique known as Mendelian randomisation, which looks at naturally occurring genetic variants related to risk factors and stroke and uses these to evaluate whether there is evidence to support a causal association with a particular risk factor.

This analysis showed that cocaine use disorders were particularly associated with brain haemorrhage and cardioembolic stroke (where a blood clot forms in the heart and travels to the brain, blocking blood flow and leading to damage of brain tissue). Cannabis use disorders were associated with stroke overall, particularly large artery stroke. This genetic evidence suggests a causal link, rather than just correlation.

Problematic alcohol use was linked to an increased risk of cardioembolic stroke and large artery stroke, while alcohol addiction increased the risk of stroke overall.

The researchers were unable to use Mendelian randomisation to look at associations with amphetamine as there are currently no large genetic datasets available with information on their usage.

The researchers suggest that possible reasons why these drugs are linked to an increased risk of stroke include sudden spikes in blood pressure, blood vessel spasm and constriction, heart rhythm problems, increased blood clotting (especially cannabis), and inflammation or vasculitis (especially amphetamines). These are all well-established pathways known to cause both ischaemic strokes, which result from blood clots, and haemorrhagic strokes.

Dr Megan Ritson from the Stroke Research Group at the University of Cambridge said: “This is the most comprehensive analysis ever conducted on recreational drug use and stroke risk and provides compelling evidence that drugs like cocaine, amphetamines, and cannabis are causal risk factors for stroke. These findings give us stronger evidence to guide future research and public health strategies.”

Dr Eric Harshfield, Alzheimer's Society Research Fellow at the Department of Clinical Neurosciences, said: “Our analysis suggests that it is these drugs themselves that increase the risk of stroke, not just other lifestyle factors among users. Taken together, our findings emphasise the importance of public health measures to reduce substance abuse as a way of helping also reduce stroke risk.”

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

Reference

Ritson, M, et al. Does Illicit Drug Use Increase Stroke Risk? A Systematic review, Meta-Analyses and Mendelian Randomization analysis. International Journal of Stroke; 9 March 2026; DOI: 10.1177/17474930261418926

The recreational drugs cannabis, cocaine and amphetamines significantly increase the risk of stroke – including among younger users – Cambridge researchers have concluded after analysing data from more than 100 million people.

Our analysis suggests that it is these drugs themselves that increase the risk of stroke, not just other lifestyle factors among users

Eric Harshfield

Kindel Media (Pexels)

Close-up of a person holding a roll-up

Yes

Licence type:

Public Domain

Dementia linked to problems with brain’s waste clearance system

cjb250 — Thu, 23 Oct 2025 11:00:01 +0000

A study led by researchers at the University of Cambridge found that impaired movement of cerebrospinal fluid (CSF) – the clear liquid that cushions and cleans the brain – predicted risk of dementia later in life among 40,000 adults recruited to UK Biobank. Their findings are published today in Alzheimer's & Dementia: The Journal of the Alzheimer's Association and are being presented at the World Stroke Congress 2025 in Barcelona.

In the healthy brain, the so-called glymphatic system serves to clear out toxins and waste materials, keeping the brain healthy. Only discovered as recently as 2012, this system functions by flushing CSF through the brain along tiny channels around blood vessels known as perivascular spaces. It collects waste then drains out of the brain, helping keep it clean and healthy.

The glymphatic system is thought to be important in protecting against many of the common forms of dementia, which are often characterised by the build-up of toxic substances in the brain – for example, Alzheimer's disease sees amyloid ‘plaques’ and tau ‘tangles accumulate in brain tissue.

One of the most common forms of dementia is vascular dementia, caused by reduced blood flow to the brain. The most common cause of this type of dementia is cerebral small vessel disease, which affects the small blood vessels in the brain. But the impact of cerebral small vessel disease is even greater because it also interacts with other dementias making them worse; for example, a study of nuns in the US found that among those nuns whose brains showed signs of Alzheimer's disease post mortem, only around a half exhibited symptoms of dementia – but this increased to around nine in 10 if they also had cerebral small vessel disease.

Professor Hugh Markus and colleagues at the University of Cambridge wanted to see whether cerebral small vessel disease and other cardiovascular risk factors damage the glymphatic system – and whether this in turn increases the risk of dementia.

Until recently, it has only been possible to study glymphatic function in mice, but recent advances in MRI scanning have made it possible to study it indirectly in humans. Even so, it was only possible to do this practically in relatively small numbers, but Yutong Chen, while a medical student at the University of Cambridge, developed machine learning algorithms capable of assessing glymphatic functions from MRI scans at scale.

The team applied the algorithm to MRI scans taken from around 40,000 adults in UK Biobank. They found three biomarkers – biological signatures – associated with impaired glymphatic function assessed at baseline, predicted the risk of dementia occurring over the subsequent decade. One of these was DTI-ALPS, a measure of the diffusion of water molecules along the perivascular spaces. Another was the size of the choroid plexus, where the CSF is produced. The third measure reflected the flow velocity of CSF into the brain.

Yutong Chen, from the Department of Clinical Neurosciences at Cambridge, said: “Although we have to be cautious about indirect markers, our work provides good evidence in a very large cohort that disruption of the glymphatic system plays a role in dementia. This is exciting because it allows to ask: how can we improve this?”

Further analysis showed that several cardiovascular risk factors impaired glymphatic function – and hence increased dementia risk, and that this was partly via causing cerebral small vessel disease, which is visible in the MRI scans.

First author Hui Hong, now a radiologist at the Second Affiliated Hospital of Zhejiang University, Hangzhou, China, said: “We already have evidence that small vessel disease in the brain accelerates diseases like Alzheimer's, and now we have a likely explanation why. Disruption to the glymphatic system is likely to impair our ability to clear the brain of the amyloid and tau that causes Alzheimer's disease.”

The research suggests possible approaches for reducing dementia risk. One is to look at strategies for improving glymphatic function. Sleep plays an important role in glymphatic function, and so disrupted sleep patterns are likely to impair its ability to clear toxins. Alternatively, there may be existing medicines that could be repurposed, or new ones that could be developed, to improve glymphatic function.

Another possible approach is to treat vascular risk factors such as high blood pressure. This is supported by recent studies: the SPRINT MIND trial, for example, showed that intensive blood pressure control (maintaining a systolic blood pressure of less than 120 mm Hg) led to a 20% reduction in cognitive decline or dementia compared to participants in the standard treatment group.

Professor Markus, who leads the Stroke Research Group at the University of Cambridge and is a Fellow of Clare Hall, Cambridge, said: “We already know the importance of cardiovascular risk factors when it comes to dementia, and our findings further emphasise this link.

“At least a quarter of all dementia risk is accounted for by common risk factors like blood pressure and smoking. If these impair glymphatic function, then we can intervene. Treating high blood pressure or encouraging people to stop smoking would be an achievable way to helping the glymphatic system work better.”

Professor Bryan Williams, Chief Scientific and Medical Officer at the British Heart Foundation, said: “This study offers us a fascinating glimpse into how problems with the brain's waste clearance system could be quietly increasing the chances of developing dementia later in life. By improving our understanding of the glymphatic system, this study opens exciting new avenues for research to treat and prevent dementia. It also emphasises the importance of managing known cardiovascular risk factors, such as high blood pressure, for reducing dementia risk.”

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

Reference

Hong, H et al. MRI markers of cerebrospinal fluid dynamics predict dementia and mediate the impact of cardiovascular risk. Alz & Dem; 23 Oct 2025; DOI: 10.1002/alz.70699

Problems with the brain’s waste clearance system could underlie many cases of dementia and help explain why poor sleep patterns and cardiovascular risk factors such as high blood pressure increase the risk of dementia.

Treating high blood pressure or encouraging people to stop smoking would be an achievable way to helping the glymphatic system work better

Hugh Markus

Maskot (Getty Images)

Caretaker and senior woman using digital tablet at nursing home - stock photo

Yes

‘Disease in a dish’ study of progressive MS finds critical role for unusual type of brain cell

cjb250 — Fri, 10 Oct 2025 15:00:31 +0000

The discovery, reported today in Neuron, is a significant step towards understanding the complex mechanisms that drive the disease and provides a promising new avenue for research into more effective therapies for this debilitating condition.

MS is a chronic disease in which the immune system mistakenly attacks the brain and spinal cord, disrupting communication between the brain and the body. While many individuals initially experience relapses and remissions, a significant proportion transition to progressive MS, a phase marked by a steady decline in neurological function with limited treatment options.

To model what is happening in the disease, researchers at the University of Cambridge, UK, and National Institute on Aging, US, took skin cells from patients with progressive MS and reprogrammed them into induced neural stem cells (iNSCs), an immature type of cell capable of dividing and differentiating into various types of brain cells.

Using this ‘disease in a dish’ approach, the team observed that a subset of the cultured brain cells was somehow reverting to an earlier developmental stage, transforming into an unusual cell type known as radial glia-like (RG-like) cells. Notably, these cells were highly specific and appeared approximately six times more frequently in iNSC lines derived from individuals with progressive MS compared to controls. As a result, they were designated as disease-associated RG-like cells (DARGs).

These DARGs exhibit characteristic features of radial glia—specialized cells that serve as scaffolding during brain development and possess the capacity to differentiate into various neural cell types. Essentially, they function both as structural support and as fundamental building blocks, making them critical for proper brain development. Unexpectedly, DARGs not only revert to an ‘infant’ state but also display hallmark features of premature aging, or senescence.

These newly identified DARGs possess a distinctive epigenetic profile—patterns of chemical modifications that regulate gene activity—although the factors influencing this epigenetic landscape remain unclear. These modifications contribute to an exaggerated response to interferons, the immune system’s ‘alarm signals,’ which may help explain the high levels of inflammation observed in MS.

Professor Stefano Pluchino from the Department of Clinical Neurosciences at the University of Cambridge, joint senior author, said: “Progressive MS is a truly devastating condition, and effective treatments remain elusive. Our research has revealed a previously unappreciated cellular mechanism that appears central to the chronic inflammation and neurodegeneration driving the progressive phase of the disease.

“Essentially, what we’ve discovered are glial cells that don’t just malfunction – they actively spread damage. They release inflammatory signals that push nearby brain cells to age prematurely, fuelling a toxic environment that accelerates neurodegeneration.”

The team validated their findings by cross-referencing with human data from individuals with progressive MS. By analysing gene expression patterns at the single-cell level—including new data exploring the spatial context of RNA within post-mortem MS brain tissue—they confirmed that DARGs are specifically localised within chronically active lesions, the regions of the brain that sustain the most significant damage. Importantly, DARGs were found near inflammatory immune cells, supporting their role in orchestrating the damaging inflammatory environment characteristic of progressive MS.

By isolating and studying these disease-driving cells in vitro, the researchers aim to explore their complex interactions with other brain cell types, such as neurons and immune cells. This approach will help to explain the cellular crosstalk that contributes to disease progression in progressive MS, providing deeper insights into underlying pathogenic mechanisms.

Dr Alexandra Nicaise, co-lead author of the study from the Department of Clinical Neurosciences at Cambridge, added: “We’re now working to explore the molecular machinery behind DARGs, and test potential treatments. Our goal is to develop therapies that either correct DARG dysfunction or eliminate them entirely.

“If we’re successful, this could lead to the first truly disease-modifying therapies for progressive MS, offering hope to thousands living with this debilitating condition.”

To date, DARGs have only ever been seen in a handful of diseases, such as glioblastoma and cerebral cavernomas, clusters of abnormal blood vessels. However, this may be because scientists have until now lacked the tools to find them. Professor Pluchino and colleagues believe their approach is likely to reveal that DARGs play an important role in other forms of neurodegeneration.

This work received funding from the Medical Research Council, the Wellcome Trust, the National MS Society, FISM - Fondazione Italiana Sclerosi Multipla, the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), the National Institute on Aging, the UK Dementia Research Institute, the Austrian Science Fund FWF, the UK MS Society Centre of Excellence, the Bascule Charitable Trust, and the Ferblanc Foundation, with support from the National Institute for Health and Care Research Cambridge Biomedical Research Centre.

Reference

Park, B, Nicaise AM & Tsitsipatis D et al. Integrated Multi-Omics Reveals Disease-Associated Radial Glia-like Cells with Epigenetically Dysregulated Interferon Response in Progressive Multiple Sclerosis. Neuron; 10 Oct 2025; DOI: 10.1016/j.neuron.2025.09.022

Scientists have identified an unusual type of brain cell that may play a vital role in progressive multiple sclerosis (MS), likely contributing to the persistent inflammation characteristic of the disease.

Progressive MS is a truly devastating condition, and effective treatments remain elusive

Stefano Pluchino

Mark Hunt (Getty Images)

Woman with multiple sclerosis in a wheelchair putting on her coat with service dog watching her

Yes

Diabetes drug and antihistamine could together repair multiple sclerosis damage, trial finds

fpjl2 — Fri, 26 Sep 2025 12:05:54 +0000

A combination of metformin, a common diabetes drug, and clemastine, an antihistamine, can help repair myelin – the protective coating around nerves, which gets damaged in multiple sclerosis (MS) causing symptoms like fatigue, pain, spasms and problems with walking.

This is according to early findings from the phase two clinical trial, CCMR-Two, carried out by researchers at the University of Cambridge’s Department of Clinical Neurosciences, and funded by the MS Society.

The scientists say the results take us another step closer to finally being able to stop disease progression in MS. However, they stress that people should not attempt to acquire the drugs outside a clinical trial, as further research is needed to fully understand their efficacy and safety in MS.

Previous evidence from animal studies showed that metformin enhances the effect of clemastine on myelin repair, but until now the two drugs had never been tested together in people. News of the latest trial was presented today at this year’s European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) – one of the world’s biggest MS research conferences.

“I am increasingly sure that remyelination is part of the solution to stopping progressive disability in MS,” said Dr Nick Cunniffe, a clinical lecturer in Neurology at Cambridge, who led the CCMR-Two trial.

“We still need to research the long-term benefits and side effects before people with MS consider taking these drugs. But my instinct is that we are on the brink of a new class of treatments to stop MS progression, and within the next decade we could see the first licensed treatment that repairs myelin and improves the lives of people living with MS.”

Over 150,000 people live with MS in the UK. While there are around 20 disease-modifying therapies for people with relapsing MS, and some emerging for active progressive MS, tens of thousands of people remain without effective treatment.

Those drugs that do exist only work on one aspect of the condition – the immune system. They don’t stop the gradual nerve damage that leads to long-term disability. Scientists say that protecting nerves from damage by boosting the body's natural ability to put myelin back onto nerves could offer a way forward.

“We desperately need ways to protect nerves from damage and repair lost myelin, and this research gives us real hope that myelin repair drugs will be part of the armoury of MS treatments in the future,” said Dr Emma Gray, Director of Research at the MS Society. “These results are truly exciting, and could represent a turning point in the way MS is treated.”

Some 70 people with relapsing MS took part in the trials for six months, half of whom took the drug combination and half took a placebo. The primary outcome used to gauge the effectiveness of the drug was a ‘visual evoked potential’ test, which measures how quickly signals travel between the eyes and the brain. The speed of signals slowed down in the placebo group over the course of six months, but remained constant in the drug group.

While the primary outcome was positive, scientists point out that people did not feel better on the drugs. The benefit from myelin repair is to insulate and protect damaged nerves, preventing them from degenerating over years. Researchers believe that drugs that promote remyelination will have an effect on disability in the long term, which will be the subject of further research.

Researchers argue that MS is just the beginning. Finding ways to protect the brain before irreversible damage sets in is vital across all neurodegenerative conditions, from Alzheimer’s to Parkinson’s. These diseases collectively cost the UK hundreds of billions and place an enormous burden on the NHS and carers.

Hannah Threlfell, 43, from Abington was diagnosed with relapsing MS in 2019 after experiencing optic neuritis. She joined the CCMR-Two trial in the hope she could help future generations.

“Before I was diagnosed, I sat through a talk from MS specialist Professor Alasdair Coles about groundbreaking MS research. Even though I didn’t know I had it then, I remember thinking how incredible it was that so much had been achieved. And now I have MS, joining the trial was a no brainer,” said Threlfall, a former teacher who has recently become a curate.

“I love helping and I know being on this trial will make a difference to someone else in the future – even small ripples have long-lasting effects! This research gives me even more reason to believe that in my lifetime everyone with MS will have treatments that work for them.”

CCMR-Two is being funded by donations to the MS Society’s Stop MS Appeal. The appeal hopes to raise £100 million by the end of 2025 to help find treatments that could slow or stop the build-up of disability for everyone with MS.

Scientists behind the trial say they are “on the brink of a new class of treatments” and that the findings take us another step closer to stopping disease progression in MS.

My instinct is that we are on the brink of a new class of treatments to stop MS progression

Dr Nick Cunniffe

MS Society

Dr Nick Cunniffe running a 'visual evoked potential' test with a trial participant in the Cambridge Clinical Vision Laboratory.

Yes

Cambridge researchers awarded UKRI Future Leader Fellowships

Anonymous — Tue, 16 Sep 2025 08:03:24 +0000

Cambridge researchers Dr Claudia Bonfio, Dr Akshay Deshmukh and Dr Elizabeth Radford have been awarded UKRI Future Leader Fellowships, which provides up to seven years of support to enable them to tackle ambitious programmes or multidisciplinary questions, and new or emerging research and innovation areas and partnerships.

Dr Claudia Bonfio’s lab in the Department of Biochemistry studies how life emerges from non-living matter and tries to answer this question by designing and building active primitive cells. Her Future Leader Fellowship project addresses this evolutionary question through an approach that bridges chemistry and biophysics, by investigating how the synergy between primitive lipids and peptides led to the emergence of membrane proteins – a hallmark of living cells.

Dr Akshay Deshmukh is returning to Cambridge’s Department of Chemical Engineering and Biotechnology from MIT to take up his Future Leader Fellowship. To reach net zero by 2050, we will require seven times more critical metals than we produce today. Current extraction methods use large amounts of energy, water, chemicals, and land. During his Fellowship, Deshmukh will develop new processes to recover metals from sources like brines and recycling streams. His research combines experiments, spectroscopy, and mechanistic studies to create a framework for designing next-generation membranes, and aims to speed up the development of cheaper, more sustainable separation technologies.

Dr Elizabeth Radford is a paediatric neurologist whose Fellowship will be based in the Department of Clinical Neurosciences. Her research is working to accelerate diagnosis and expand the treatment options for children affected by neurodevelopmental genetic conditions. Everyone carries small genetic changes, and while most are harmless, some disrupt how the proteins in our cells work and can affect a child’s development. However, it isn’t always clear which changes cause problems, making diagnosis slow and uncertain. During her Fellowship, Radford will study thousands of genetic changes by recreating them in human cells grown in the lab. This will show which changes damage proteins, helping doctors interpret genetic tests and provide earlier diagnoses, and paving the way for future treatments.

UK Research and Innovation’s (UKRI) Future Leaders Fellowships fund allows universities and businesses to develop talented early career researchers and innovators and attract new people to their organisations, including from overseas.

Out of the successful applications, thirteen projects are led by businesses and funded by Innovate UK.

To support excellent research and innovation wherever it arises and to facilitate movement of people and projects between sectors, FLF fellows are based in the most appropriate environment for their projects, be that universities, businesses, charities, or other independent research organisations.

The Fellowship allows the individual to devote their time to tackle challenging research and innovation problems and to develop their careers as they become the next wave of world-class research and innovation leaders.

The Fellowship also allows recipients access to the FLF Development Network, which provides specialised leadership training, access to networks, workshops, mentors, one-to-one coaching, and opportunities for additional seed-funding for collaborative projects.

“UKRI’s Future Leaders Fellowships provide researchers and innovators with long-term support and training to embark on large and complex research programmes, to address key national and global challenges,” said Frances Burstow, Director of Talent and Skills at UKRI. “The programme supports the research and innovation leaders of the future to transcend disciplinary and sector boundaries, bridging the gap between academia and business. UKRI supports excellence across the entire breadth of its remit, supporting early-career researchers to lessen the distance from discovery to real world impact.”

“UKRI’s Future Leaders Fellowships offer long-term support to outstanding researchers, helping them turn bold ideas into innovations that improve lives and livelihoods in the UK and beyond,” said UKRI Chief Executive, Professor Sir Ian Chapman. “These fellowships continue to drive excellence and accelerate the journey from discovery to public benefit. I wish them every success.”

Three Cambridge researchers are among 77 early-career researchers who have been awarded a total of £120 million to lead vital research, collaborate with innovators and develop their careers as the research and innovation leaders of the future.

University of Cambridge

(L-R) Dr Claudia Bonfio, Dr Akshay Deshmukh and Dr Elizabeth Radford

Yes

Cambridge researchers play key role in evidence leading to approval of new treatment for hereditary blindness

cjb250 — Thu, 07 Aug 2025 15:10:05 +0000

Leber hereditary optic neuropathy (LHON) affects around 2,500 people in the United Kingdom. It causes rapidly progressive loss of vision in both eyes. Within weeks of onset, an affected individual reaches the legal threshold to be considered as severely sight impaired (blind).

The condition tends to affect young men, with a peak age of onset between the ages of 15 and 35 years old, but women can also be affected and the loss of vision can occur at any age. The prognosis is poor, with only around one in 10 affected individuals experiencing some spontaneous visual improvement, which is invariably partial.

LHON is caused by the loss of retinal ganglion cells, specialised nerve cells in the innermost layer of the retina. The projections, or ‘axons’, from these cells converge to form the optic nerve, the cable that transmits visual information from the eye to the brain. Once these retinal ganglion cells are lost, the damage becomes irreversible. LHON is primarily caused by genetic defects within the mitochondrial genome, which is transmitted down the maternal line.

In 2011, the journal Brain published the results of a landmark randomised placebo-controlled trial of the drug idebenone to treat LHON. The RHODOS trial was led by Patrick Chinnery, at the time a researcher at Newcastle University and now Professor of Neurology at the University of Cambridge. It found some potential benefit in a subgroup of patients. However, treatment with idebenone was only given for six months, and it was not clear whether there was any benefit in treating individuals who had been affected for more than one year.

“At the time, we had only anecdotal evidence that idebenone would work for patients with LHON,” said Professor Chinnery. “Our clinical trial was the first strong evidence that it could help stabilise vision in some patients. It was an important step towards providing a new treatment.”

One of Professor Chinnery’s collaborators on the RHODOS trial was Patrick Yu-Wai-Man, Professor of Ophthalmology at the University of Cambridge, who led the follow-up LEROS trial. This assessed the efficacy and safety of idebenone treatment in patients with LHON up to five years after symptom onset and over a treatment period of 24 months. This second trial found that the drug can help stabilise vision in some patients and, in certain cases, may even lead to improvement when treatment is provided within five years of vision being affected.

These studies provided crucial evidence to support the use of idebenone to treat LHON patients. The drug was licensed for limited use by patients in Scotland, Wales and Northern Ireland and it has now been approved by NICE for use in patients aged 12 years and over in England.

Professor Yu-Wai-Man said: “LHON causes devastating visual loss and it is a life-changing diagnosis for the affected individual and their family. England is now in line with the rest of the United Kingdom with idebenone now available through the NHS. This will come as a great relief to the LHON community in this country bringing hope to those who have experienced significant visual loss from this mitochondrial genetic disorder.”

The development has been welcomed by charities that have been arguing for idebenone to be made available across the UK. A LHON Society spokesperson said: “This is a critical step towards full access to idebenone for patients, that may alleviate some of the impacts of LHON.”

Katie Waller, Head of Patient Programmes at The Lily Foundation, a charity that supports patients affected by mitochondrial diseases, said: “This is a huge win for the mito community and we’re proud to have been a key stakeholder throughout the process. While it isn’t a cure, this treatment offers real potential for patients to preserve or improve vision, giving the chance to regain independence, confidence and a better quality of life.”

Idebenone will not work for everyone, and responses vary from person to person. LHON patients are encouraged to speak with the healthcare professional responsible for their care to understand whether idebenone is the right treatment for them.

The National Institute for Health and Care Excellence (NICE) has today announced the approval of a new treatment for a form of hereditary blindness for use on the NHS in England. Cambridge researchers played a pivotal role in providing the evidence that led to this important development.

This will bring hope to those who have experienced significant visual loss from this mitochondrial genetic disorder

Patrick Yu-Wai-Man

PeopleImages (Getty)

Man undergoing an eye examination

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Cambridge researchers named as 2025 Academy of Medical Sciences Fellows

cjb250 — Wed, 21 May 2025 23:01:41 +0000

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

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

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

Also elected to the Academy of Medical Sciences Fellowship are:

Professor Clare Bryant, Departments of Medicine and Veterinary Medicine

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

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

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

Professor Mina Ryten, UK Dementia Research Institute

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

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

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

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

Big T Images for Academy of Medical Sciences

Academy of Medical Sciences plaque

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