̽��ֱ�� of Cambridge - Roger Barker

Cambridge researchers developing brain implants for treating Parkinson’s disease

sc604 — Thu, 23 Jan 2025 10:33:21 +0000

As part of a £69 million funding programme supported by the Advanced Research + Invention Agency (ARIA), Professor George Malliaras from Cambridge’s Department of Engineering will co-lead a project that uses small clusters of brain cells called midbrain organoids to develop a new type of brain implant, which will be tested in animal models of Parkinson’s disease.

̽��ֱ��project led by Malliaras and Professor Roger Barker from the Department of Clinical Neurosciences, which involves colleagues from the ̽��ֱ�� of Oxford, the ̽��ֱ�� of Lund and BIOS Health, is one of 18 projects funded by ARIA as part of its Precision Neurotechnologies programme, which is supporting research teams across academia, non-profit R&D organisations, and startups dedicated to advancing brain-computer interface technologies.

̽��ֱ��programme will direct £69 million over four years to unlock new methods for interfacing with the human brain at the neural circuit level, to treat many of the most complex neurological and neuropsychiatric disorders, from Alzheimer’s to epilepsy to depression.

By addressing bottlenecks in funding and the lack of precision offered by current approaches, the outputs of this programme will pave the way for addressing a much broader range of conditions than ever before, significantly reducing the social and economic impact of brain disorders across the UK.

Parkinson’s disease occurs when the brain cells that make dopamine (a chemical that helps control movement) die off, causing movement problems and other symptoms. Current treatments, like dopamine-based drugs, work well early on, but can cause serious side effects over time.

In the UK, 130,000 people have Parkinson’s disease, and it costs affected families about £16,000 per year on average – more than £2 billion in the UK annually. As more people age, the number of cases will grow, and new treatments are urgently needed.

One idea is to replace the lost dopamine cells by transplanting new ones into the brain. But these cells need to connect properly to the brain’s network to fix the problem, and current methods don’t fully achieve that.

In the ARIA-funded project, Malliaras and his colleagues are working on a new approach using small clusters of brain cells called midbrain organoids. These will be placed in the right part of the brain in an animal model of Parkinson’s disease. They’ll also use advanced materials and electrical stimulation to help the new cells connect and rebuild the damaged pathways.

“Our ultimate goal is to create precise brain therapies that can restore normal brain function in people with Parkinson’s,” said Malliaras.

“To date, there’s been little serious investment into methodologies that interface precisely with the human brain, beyond ‘brute force’ approaches or highly invasive implants,” said ARIA Programme Director Jacques Carolan. “We’re showing that it’s possible to develop elegant means of understanding, identifying, and treating many of the most complex and devastating brain disorders. Ultimately, this could deliver transformative impact for people with lived experiences of brain disorders.”

Other teams funded by the programme include one at Imperial College London who is developing an entirely new class of biohybridised technology focused on engineering transplanted neurons with bioelectric components. A Glasgow-led team will build advanced neural robots for closed-loop neuromodulation, specifically targeting epilepsy treatment, while London-based Navira will develop a technology for delivering gene therapies across the blood-brain barrier, a crucial step towards developing safer and more effective treatments.

Adapted from an ARIA media release.

Cambridge researchers are developing implants that could help repair the brain pathways damaged by Parkinson’s disease.

Our ultimate goal is to create precise brain therapies that can restore normal brain function in people with Parkinson’s

George Malliaras

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Substantia nigra in the human brain, illustration

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Clinical trial for new stem cell-based treatment for Parkinson’s disease given go ahead

cjb250 — Thu, 20 Oct 2022 11:29:28 +0000

̽��ֱ��Swedish Medical Products Agency has granted approval for the trial to proceed; ethical approval has already been obtained from the Swedish Ethics Review Authority. ̽��ֱ��team, led from Lund ̽��ֱ�� in Sweden, is poised to begin recruitment.

STEM-PD uses human embryonic stem cells, a type of cell that can turn into almost any type of cell in the body. ̽��ֱ��team has ‘programmed’ the cells to develop into dopamine nerve cell, which will be transplanted into the brains of patients to replace cells that are lost in Parkinson’s disease. ̽��ֱ��product has already been shown to be safe and effective at reverting motor deficits in animal models of Parkinson’s disease.

̽��ֱ��trial is a collaboration with colleagues at Skåne ̽��ֱ�� Hospital, the ̽��ֱ�� of Cambridge, Cambridge ̽��ֱ�� Hospitals NHS Foundation Trust (CUH), and Imperial College London.

Professor Roger Barker from the Wellcome-MRC Stem Cell Institute at the ̽��ֱ�� of Cambridge and CUH is clinical lead on the project. “ ̽��ֱ��use of stem cells will in theory enable us to make unlimited amounts of dopamine neurons and thus opens the prospect of producing this therapy to a wide patient population. This could transform the way we treat Parkinson’s disease”

This is the first such trial in Europe and the preclinical and clinical studies of STEM-PD have been funded by national and EU funding agencies. In addition, the STEM-PD team has obtained funding and valuable support for the current study from Novo Nordisk; a collaboration which will continue for future product development.

̽��ֱ��cells to be used in the trial have been manufactured under ‘good manufacturing practice’ at the Royal Free Hospital in London and have undergone rigorous testing in the lab.

Professor Malin Parmar who leads the STEM-PD team from Lund ̽��ֱ�� said: “We are looking forward to this clinical study of STEM-PD, hoping that it could potentially help reduce the significant burden of Parkinson’s disease. This has been a massive team effort for over a decade, and the regulatory approval is a major and important milestone.”

̽��ֱ��STEM-PD trial will assess safety and tolerability of the transplanted product one year after transplantation, measuring the effects on Parkinson’s symptoms. ̽��ֱ��trial will enrol eight patients for transplantation, starting with patients from Sweden, and with subsequent plans for enrolment of patients also from Cambridge ̽��ֱ�� Hospitals. All transplantation surgery will be performed at Skåne ̽��ֱ�� Hospital in Lund.

Parkinson’s disease is the second most common neurodegenerative disease worldwide, yet remains without a cure. Typical motor symptoms of Parkinson’s disease are slowness of movement, tremor and stiffness and later also gait difficulties. It is not well known how the disease arises or develops, but the core feature common to all patients is the loss of dopamine neurons in the midbrain.

Suitable patients will be invited to participate in the trial; it is not possible to volunteer to participate.

Adapted from a press statement from Lund ̽��ֱ��

Cambridge researchers will play a key role in clinical trials of a new treatment that involves transplanting healthy nerve cells into the brains of patients with Parkinson’s disease.

This could transform the way we treat Parkinson’s disease

Roger Barker

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Hands of an elderly man with walking stick

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Stimulate your brain with the Cambridge BRAINFest 2017

cjb250 — Mon, 05 Jun 2017 09:14:32 +0000

̽��ֱ��three day event, running from 23-25 June, will allow audiences to quiz more than 130 leading Cambridge neuroscientists on everything from dementia and dyslexia through to memory and mental health.

“We’re all fascinated by the brain – its complexity is what makes us so unique as a species,” says Dr Dervila Glynn, coordinator of Cambridge Neuroscience, who is organising the event. “Cambridge is one of the major centres in the UK, if not the world, for studying how the brain works, and why in many cases it goes wrong, leading to disease. Cambridge BRAINFest is our chance to showcase the brilliant work that is taking place across the city.”

Throughout the weekend, the Cambridge Corn Exchange will be transformed into an interactive tour of the brain, with themes including ‘Development’, ‘Brain & Body’, ‘Pain & Pleasure’, Perception & Imagination’ and ‘Learning & Forgetting’ spanning research from molecules to man. Visitors, adults and children alike, will get the opportunity to take part in experiments across 30 different interactive exhibits and even build their own brain. A ‘Secret Cinema’ will show a series of films that illustrate how Cambridge researchers are tackling conditions such as dementia and OCD. Meanwhile, Café Scientifique will explore the breadth of brain science from body clocks and brain networks to the weird and wonderful world of the naked mole-rat.

On 23 June, the opening night, audiences at the Babbage Lecture Theatre will hear from BBC Horizon presenter Dr Giles Yeo about why we are all getting fatter, from Professor Usha Goswami about how dyslexic brains may be in tune but out of time, and from Professor Roger Barker on how we can repair the degenerating brain. Poet Lavinia Greenlaw will perform a moving poem about dementia, while Cambridgeshire-based Dance Ensemblé will explore the story of Parkinson’s disease through the medium of dance.

̽��ֱ��following night, Professor Sir Simon Wessely, President of the Royal College of Psychiatrists, will chair a panel discussion with mental health experts from the ̽��ֱ�� of Cambridge and from Cambridgeshire & Peterborough NHS Foundation Trust, looking at the ongoing research that will help us better understand and treat mental health disorders and how we can bridge the existing gap between neuroscience research and current practice in the health service. ̽��ֱ��panel will look at issues including how the brain and body interact, the stigma surrounding mental health problems and the transition between child and adult psychiatry.

For those wishing to take advantage of the sights around Cambridge, a historical self-guided ‘Neurotrail’ will lead explorers around the places, people, and discoveries that have put our city at the heart of our understanding of the brain. Maps will be available at the Corn Exchange on the weekend.

̽��ֱ��foyer of the Corn Exchange will be transformed by BRAINArt, an exhibition of brain-inspired art by local school children. In the lead up to Cambridge BRAINFest, Dr Glynn visited 1,400 pupils, talked about the brain and enthused her audiences about the body’s most complex organ.

“As a researcher, it can be thrilling to discuss our work with the public,” says Professor Angela Roberts, chair of the organising committee. “It’s an opportunity for us to share some of the excitement that comes from working at the cutting-edge of research. But equally, it’s a chance for us to hear the public’s views about our work. We expect some fascinating – and potentially challenging – discussions will arise.”

Cambridge BRAINFest 2017 builds on the success of major public engagement events organised by the ̽��ֱ�� of Cambridge, including the Cambridge Science Festival in spring and the Festival of Ideas in autumn.

All events are free, but booking is recommended for the evening events at the Babbage Lecture Theatre. Further details, including how to book, can be found on the Cambridge BRAINFest 2017 website.

Join the #CambridgeBRAINfest conversation on Twitter @CamNeuro and on Facebook.

Why are we getting so fat? Why do teenagers really need to lie-in? And can we fix a broken brain? These are just some of the questions that will be answered at Cambridge BRAINFest 2017, a free public festival celebrating the most complex organ in the body.

Cambridge is one of the major centres in the UK, if not the world, for studying how the brain works, and why in many cases it goes wrong, leading to disease. Cambridge BRAINFest is our chance to showcase the brilliant work that is taking place across the city

Dervila Glynn

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̽��ֱ��Academy of Medical Sciences announces new Fellows for 2015

jeh98 — Mon, 11 May 2015 09:38:09 +0000

Forty-eight researchers from across the UK, including five Cambridge ̽��ֱ�� academics, have been recognised for their contribution to the advancement of medical science by election to the Fellowship of the Academy of Medical Sciences.

Academy Fellows are elected for excellence in medical research, for innovative application of scientific knowledge or for their conspicuous service to healthcare. ̽��ֱ��expertise of the new Fellows includes addictions, anaesthesia, age-related diseases and animal biology.

̽��ֱ��Fellows elected from the ̽��ֱ�� of Cambridge are:

Professor Roger Barker – Professor of Clinical Neuroscience and Honorary Consultant Neurologist, Addenbrooke’s Hospital and Department of Clinical Neurosciences

Professor Sarah Bray – Professor of Developmental Biology, Department of Physiology, Development and Neuroscience

Professor John Danesh – BHF Professor of Epidemiology and Medicine and Head of the Department of Public Health and Primary Care

Professor Fiona Gribble – Professor of Endocrine Physiology, Department of Clinical Biochemistry

Professor David Klenerman – Professor of Biophysical Chemistry, Department of Chemistry

Professor Sir John Tooke PMedSci, President of the Academy of Medical Sciences said: “ ̽��ֱ��Academy of Medical Sciences champions the excellence and diversity of medical science in the UK, and this is clearly demonstrated in this year’s cohort of new Fellows. Their broad range of expertise and fantastic achievements to date shows just how strong the Fellowship is – from the NHS knowledge of Sir Andrew Dillon to the policy experience of Professor Christl Donnelly. Their election is a much deserved honour, and I know they will contribute greatly to the Academy. I am delighted to welcome them all to the Fellowship, and look forward to working with them in the future.”

̽��ֱ��independent Academy of Medical Sciences promotes advances in medical science and campaigns to ensure these are translated into benefits for patients. ̽��ֱ��Academy’s Fellows are the United Kingdom’s leading medical scientists from hospitals, academia, industry and the public service.

View the full list of new Fellows.

̽��ֱ��Academy of Medical Sciences has announced the election of its new Fellows, including five Cambridge ̽��ֱ�� academics.

̽��ֱ��Academy of Medical Sciences

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Search and rescue: scientists identify a novel therapy with potential for treating Parkinson’s disease

ns480 — Thu, 22 Dec 2011 11:29:41 +0000

Scientists at the ̽��ֱ�� of Cambridge have made a significant step in the development of a novel therapy that could one day help to slow down, or even halt, the damage caused by Parkinson’s disease (PD), one of the most common neurodegenerative disorders. ̽��ֱ��therapy, which has been shown to be effective in rat models of the condition, involves exploiting the natural process by which common viruses protect mitochondria (the energy-producing power house of cells) in order to keep cells alive while they replicate.

̽��ֱ��research, published this week in the Journal of Experimental Medicine, involved molecular virologists working in collaboration with neuroscientists to share their expertise across disciplines. Building on an earlier study published in 2007, the researchers have now shown proof of principle for their methodology which offers a potential novel disease -modifying approach to treating PD. ̽��ֱ��researchers’ work in harnessing the behaviour of viruses may have wider applications for the treatment of other neurodegenerative diseases - including Alzheimer’s and Huntington’s disease.

Although the age of onset varies considerably, PD is strongly associated with the elderly, with an average age of onset of around 70 years. Around 120,000 people in the UK are directly affected by the disorder with the numbers diagnosed likely to rise as the average age of the population increases. ̽��ֱ��disease results from a loss of many different types of nerve cells in the brain but especially a population that produces dopamine, a chemical that relays signals from one neuron to another. It is not known why these cells die, but when they do the people affected experience problems with walking and moving quickly.

Current treatments for PD centre on symptomatic drugs which, though they help treat some of the motor features of PD, are not able to stop the disease from progressing. Indeed, over time these drugs can produce their own side-effects.

̽��ֱ��novel methodology developed by the Cambridge researchers stemmed from the work of Professor John Sinclair and colleagues at the Department of Medicine in studying the ways in which common viruses – such as herpes - seek to survive and replicate in cells in the body. When these viruses invade a cell, a tiny component of the virus called the Beta2.7 gene guards the mitochondria from damage for an interval of time – typically five days - so that the virus can replicate and spread from cell to cell.

In looking at how the virus gene functions, Professor Sinclair spotted the potential for harnessing this protective function to help cells survive attack by neurological disorders such as PD. ̽��ֱ��component of the virus that protects the cells’ mitochondria is a section of RNA (ribonucleic acid) which, like DNA, is essential for life. ̽��ֱ��molecular virologists led by Professor Sinclair used a method of complexing (mixing) the RNA derived from a human cytomegalovirus to a protein of a rabies virus. This protein was selected as it enables the beta2.7 to cross into the brain when the whole complex is given into the circulation, and, as only of a portion of the rabies and herpes viruses are used, there is no danger of contracting any disease from either virus.

Having identified the potential offered by the virus as an agent for ‘search and rescue’, Professor Sinclair collaborated with Professor Roger Barker and colleagues at the Cambridge Centre for Brain Repair to see whether this novel protein/RNA complex could protect neurons from cell death associated with PD. Using rat models, the results have been promising and resulted in a further tranche of research funding from the Michael J Fox Foundation to take work in the laboratory forward to help develop the novel therapeutic for eventual clinical use.

̽��ֱ��researchers emphasise that much work remains to be done in taking the therapy to the point at which clinical trials can be undertaken. “Our results with rat models are tremendously encouraging, but we need to do a lot more in terms of refining and optimising the therapy before it could be used in patients. For example, we don’t know what the dosages or frequency of treatment might need to be in treating humans,” said Professor Sinclair.

“What we have established is proof of principle – essentially showing that this is a truly novel and highly promising pathway for treating not just the dopamine cell loss in Parkinson’s but also all cell losses in this condition, as well as other chronic neurodegenerative disorders.”

̽��ֱ��novel therapy offers a number of significant advantages over all currently used surgical and drug therapies. Professor Barker explained: “In many ways the therapy we’ve developed is a beautiful treatment. It can be delivered through an injection direct into the bloodstream, for example into the arm of the patient. This makes it much easier to use than many other putative disease-modifying therapies such as growth factors which have to be injected directly into the brain. This new agent also appears to be non-immunogenic – in other words it does not trigger an immune response so it can be used repeatedly and should still maintain its potency. Finally, it appears to go only into the brain and nowhere else in the body and then to target only cells that are unwell.”

̽��ֱ��next stage of the research will be to test the novel therapy in other models of PD to help define the dosage and time course of delivery.

A collaboration between virologists and neuroscientists at Cambridge ̽��ֱ�� has demonstrated how viruses that cross the blood/brain barrier could be exploited to slow down, or even halt, the progress of Parkinson’s and other neurodegenerative diseases.

What we have established is proof of principle – essentially showing that this is a truly novel and highly promising pathway for treating not just the dopamine cell loss in Parkinson’s but also all cell losses in this condition, as well as other chronic neurodegenerative disorders.

Professor John Sinclair

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