The University of Manchester’s leading social prescribing researchers – Dr Luke Mumford and Paul Wilson – will lead on the research across three years. The researchers will work with the Greater 91ֱ�� Secure Data Environment (GM Care Record) which was created by the University of Manchester and NHS GM to access pseudonymised NHS data in a secure environment in order to assess NHS utilisation for people living with dementia benefitting from music support.

This vital funding will enable 91ֱ�� Camerata and Alzheimer’s Society to continue their ground[1]breaking research-based music therapy programmes – Music in Mind (Camerata) and Singing for the Brain (Alzheimer’s Society) to offer more musical support to people living with dementia across all of Greater 91ֱ��.

According to the NHS, there are over 940,000 people in the UK who have dementia with 1 in 11 people over the age of 65 being most affected. Alzheimer’s Society suggests that by 2025 there will be over 1 million people with dementia in the UK, projected to rise to nearly 1.6 million by 2040. Currently, the care of these people in the UK costs over £34billion per year. The long-term goal of this - the UK’s first Centre of Excellence for Music and Dementia - is to use the knowledge and research built up over the next three years to analyse how the implementation of music in dementia care can reduce the need for health and care services whilst simultaneously improving quality of life.

This significant and successful bid will see both organisations run four weekly music cafes (two ‘Music in Mind’ and two ‘Singing for the Brain’) in each of the 10 Greater 91ֱ�� boroughs. Together they will collaborate with the University of Manchester and the NHS to undertake anonymised data-driven research into the impact and power that these music sessions have for people living with dementia and the way in which they can reduce pressure on hard-pressed frontline NHS and social care staff.

91ֱ�� Camerata and Alzheimer’s Society will recruit, nurture and train a volunteer and community workforce of 300 ‘Music Champions’ who will be trained to deliver the Music Cafes, helping to support over 1000 people living with dementia in Greater 91ֱ�� across three years starting from October 2024. The research and data analysed by the University of Manchester will demonstrate the impact of embedding music support as part of dementia care and how this model can be scaled up and rolled out across the UK and result in cost-saving measures for the NHS.

Bob Riley, Chief Executive of Manchester Camerata, said: “This is a colossal moment built on over ten years of work and research in partnership with The University of Manchester. We know it will bring much-needed support for people living with dementia and their carers. It will create new opportunities for our amazing musicians in the UK, and bring about changes in the way we invest in music to bring the widest possible benefits to society.

“Sincere thanks to the leadership and vision of Andy Burnham, Sir Richard Leese and NHS GM, the National Academy of Social Prescribing, The Utley Foundation, Arts Council England and many others. We appreciate their boldness and commitment to the power of music, and in recognising our outstanding musicians whose passion and commitment makes such an incredible impact on and off the stage.”

Mayor of Greater 91ֱ��, Andy Burnham, said: "This is fantastic news for Greater 91ֱ��, and a reminder of the power of music to shape our lives and our communities. 91ֱ�� Camerata have played a key role in our Music Commission, and I’ve seen firsthand the transformational impact of what they do in our city-region. They are the ideal partner to pioneer the UK’s first Centre of Excellence for Music and Dementia, working with the Alzheimer’s Society to unlock the potential of music as therapy.

“This project will provide life-changing support to people with dementia and their carers in our 10 boroughs – support that is grounded in our communities and delivered with a real expert focus. It will also generate groundbreaking research that will influence health and care policy across the country while directly improving lives across Greater 91ֱ��."

Charlotte Osborn-Forde, Chief Executive of the National Academy for Social Prescribing, said: “We worked with the Utley Foundation and Arts Council England to create The Power of Music Fund, to ensure that many more people living with dementia can benefit from musical projects. Through the Centre of Excellence, we aim to demonstrate how prescribing music to people living with dementia can improve quality of life, reduce isolation, and lessen the need for medication, hospital admissions and GP appointments.

“We were delighted to choose Greater 91ֱ�� after an outstanding bid. This project will provide a lifeline to people living with dementia in 91ֱ��, but also provide new evidence and a model that can be replicated across the country.”

91ֱ�� Camerata’s Music in Mind is an internationally renowned programme that uses the principles of music therapy to improve the wellbeing of people living with dementia. The programme was created in collaboration with research partner the University of Manchester and the programme was devised from the foundations of some of the world’s leading dementia experts and their research. The Camerata has established training, delivery and support offers to help partners create Music Cafes and recruit Music Champions, and has worked with partners in Hong Kong, Taiwan, Sweden and Japan to help them set up their own music and dementia programmes.

Alzheimer’s Society’s Singing for the Brain is a programme based on music therapy principles, bringing people living with dementia together to sing a variety of songs they know and love, in a fun and friendly environment. The sessions also include vocal exercises that help improve brain activity and wellbeing whilst also creating an opportunity for people living with dementia and their carers to socialise with others and experience peer support.

The Power of Music Fund was established by the National Academy for Social Prescribing, with generous support from the Utley Foundation, Arts Council England and other partners. It builds on the recommendations of the 2022 Power of Music report. In addition to the Centre of Excellence in Greater 91ֱ��, the Fund is also awarding small grants to 70 grassroots music and dementia projects across the UK and will support more than 5500 people in total

In a study published in eBioMedicine, the elements, including selenium (a metalloid), sodium, potassium, magnesium, calcium, iron, zinc, copper, and manganese, were studied in 11 parts of the brain.

In particular, the scientists found substantial decreases in selenium levels in all 11 regions of the HD brains, calculating there was a high risk of having the disease when levels are low.

Increased sodium and potassium ratios were observed in every region except the substantia nigra, and many of the regions showed increased calcium and/or zinc levels. Localised decreases in iron, copper, and manganese were present in the globus pallidus, cerebellum, and substantia nigra, respectively.

Huntington's disease is a fatal condition that causes nerve cells in parts of the brain to gradually break down and die, resulting in memory lapses, stumbling, involuntary jerking, mood swings and , speaking and breathing.

Caused by a faulty gene inherited from a parent and often occurring between the ages of 30 and 50, its pathogenic mechanisms remain poorly understood.

There is currently no treatment for HD and according to the Alzheimer’s Society it affects around 8 in every 100,000 people in the UK.

The scientists analysed tissue donated by 9 people with HD after they died from the NZ Neurological Foundation Douglas Human Brain Bank at the University of Auckland.

Selenium is known to have an important role in protection against oxidative stress—an imbalance between free radicals and antioxidants which can damage organs and tissues and lead to HD.

It is also implicated in the dysfunction of mitochondria, one of the main powerhouses of human cells, which is also known to occur in the development of HD.

Sodium and potassium play an important role in the central nervous system by regulating the conduction of electrical nerve impulses.

Calcium, zinc, iron copper and manganese are also involved in processes as wide-ranging as gene expression, cell signalling, and cell death.

The areas with different levels of neurodegeneration were studied using cutting edge technology called inductively coupled plasma mass spectrometry.

Lead author Dr Melissa Scholefield said: “This is the first known study which investigated metals simultaneously across many regions of the HD brain in the same cohort.

“We think the changes we found in their levels could contribute to several pathogenic mechanisms, including mitochondrial dysfunction, oxidative stress, and blood–brain barrier dysfunction, as shown by previous studies in mice.

“However, we caution that it is dangerous to self-medicate with supplements; the blood-brain barrier could mean these could elements might build up in someone’s blood stream, with potentially toxic effects.”

Principal Investigator Professor Garth Cooper said: “The most striking finding is the deficiency of selenium in every part of the brain we studied.

“Because selenium was deficient in all regions of the brain, that might mean it could be easier to one day target therapeutically, as it’s very hard to home in on specific brain regions.

“Further studies determining the time course, cause, and downstream effects of selenium alterations in HD may eventually present a potential therapeutic target for the treatment of this disease.

”However, the results from the current human brain study should be treated as preliminary due to the relatively small size of our cohort.”

The study was mainly funded by the Lee Trust.

The paper Widespread selenium deficiency in the brain of cases with Huntington’s disease presents a new potential therapeutic target is available

In the UK, 5-20% of over 60s population experience mild cognitive impairment (MCI), a decline in one cognitive area, such as memory, language, spatial orientation, or forward planning, over time. MCI is confirmed by pen-and-paper testing.

Though patients exhibiting MCI don't necessarily have dementia they often suffer with conditions linked to dementia like Alzheimer's disease, and have a higher risk of developing dementia in the two years following diagnosis of MCI.

MCI patients who do go onto to exhibit symptoms of dementia experience a very slow progression of symptoms, which may be between five and 10 years. This uncertainty causes stress on patients and their families, as it is difficult to plan ahead for their life and care needs.

It has however, been established that high levels of Tau and altered levels of Amyloid proteins – also indicative of Alzheimer's disease – can predict progression and onset of dementia accurately. Tau and Amyloid can be measured in a number of ways, for example either PET or within the cerebrospinal fluid (CSF) obtained via a lumbar puncture.

Where PET scans are expensive and lumbar punctures largely perceived as risky or dangerous by patients, MRI scans are accessible and affordable. The technology is more readily available than PET scanners or the clinical skills required for a lumbar puncture.

Diffusion MRI, specifically, is used to look at the neuronal architecture of the brain. Researchers are able to see patterns of neuronal connections and their arrangements using this technique and therefore can identify normal and abnormal patterns. What constitutes as healthy ageing in the brain is becoming well established, the neuronal patterns people with dementia develop are also becoming better characterised. The brain looks as if it's aged more, and quicker, in people with dementia.

Hamied Haroon and the team of neuroimaging researchers at the University of Manchester are currently trying to develop new techniques in MRI scanning and image analysis to support this. They’re improving our capacity to measure loss of brain cells as this loss is the root cause of many symptoms of dementia.

Additionally, they’re developing novel methods to measure the changes in blood delivery to the brain, and therefore the availability of oxygen. Lack of oxygen also leads to cell death which may advance vascular dementia.

Hamied Haroon, Research Fellow in Quantitative Biomedical Magnetic Resonance Imaging, University of Manchester, says:

“MR imaging allows us to map the brain non-invasively and repeatability, as there is no ionising radiation involved, providing unique insights on the brain’s organisation and function in health and ageing.

“We are developing exciting analysis methods to detect the earliest signs of such devastating conditions as dementia, when promising new therapies should have better chances of halting the disease in its tracks.”

High blood pressure is the main cause of vascular dementia, a condition characterised by poor blood flow to the brain. The reduced blood supply starves brain cells of nutrients and over time they become damaged and die. Symptoms of vascular dementia include loss of energy, lack of concentration and poor memory.

It's normal for the brain’s arteries to narrow and widen in response to changes in blood pressure. However, consistently high blood pressure causes arteries to stay narrow and restrict the brain’s blood supply. Until now, it was not known why.

The study, from researchers at the Geoffrey Jefferson Brain Research Centre at The University of Manchester, reveals that – in mice – high blood pressure disrupts messaging within artery cells in the brain. Messages that should tell the artery to dilate to allow more blood to flow through aren’t able to reach their target, leaving arteries permanently constricted.

By identifying drugs that could restore this communication, the researchers hope to soon be able to improve blood supply to affected areas of the brain and slow the progression of vascular dementia.

Professor Adam Greenstein, a clinician scientist specialising in high blood pressure at the University of Manchester and one of the leaders of the research, said:

“By uncovering how high blood pressure causes arteries in the brain to remain constricted, our research reveals a new avenue for drug discovery that may help to find the first treatment for vascular dementia. Allowing blood to return as normal to damaged areas of the brain will crucial to stopping this devastating condition in its tracks.

“Any drugs that are discovered to improve brain blood supply may also be able to open a new line of attack in treating Alzheimer’s disease, which causes very similar damage to blood vessels as vascular dementia. Drugs to restore healthy blood flow could make current treatments, which focus on removing harmful amyloid plaques in the brain, more effective.“

91ֱ��ing mice with high blood pressure, researchers identified that a protein called junctophilin-2 was damaged. In healthy mice, junctophilin-2 holds two cells structures closely together, helping to transmit messages that tell arteries to relax. But, when junctophilin-2 is damaged, this signalling is disrupted.

Professor Sir Nilesh Samani, Medical Director at the British Heart Foundation, who funded the research, said: 

“Vascular dementia affects around 150,000 people in the UK, and this number is going up. There are no treatments to slow or stop the disease, but we know that high blood pressure is an important risk factor. The incurable symptoms are hugely distressing for patients and those close to them.  

“This exciting research reveals a specific mechanism by which high blood pressure might increase the risk of vascular dementia. Pinpointing how arteries remain permanently narrowed in vascular dementia could lead to the development of new effective treatments, raising hope that there may soon be a way to prevent this illness from destroying more lives.” 

While the findings are yet to be confirmed in humans, the processes of blood vessel narrowing and widening are very similar in mice and humans. The researchers are now investigating drugs that could restore junctophilin-2 function, which they hope, in future will lead to human studies that aim to restore healthy brain blood flow in vascular dementia.

The agreement will progress a development project for the use of Clickmers for highly selective detection of biomarkers associated with Alzheimer's disease (AD). Clickmers are single-stranded DNA oligonucleotides modified with Nobel prize-winning Click chemistry.

Under the terms of the collaboration, APIS and PharmaKure will advance the development of specific Clickmers targeting biomarkers associated with Alzheimer's disease pathology and their clinical validation for diagnostic purposes. Certain blood biomarkers of amyloid-b (Total, Ab40 and Ab42), aggregated α-synuclein, aggregated Tau (Total and pTAU (181)), NFL and DJ-1 have been associated with Alzheimer’s Disease pathology. The Clickmer technology will be used to sensitively and accurately quantify the levels of these biomarkers in blood.

‘We are excited to collaborate with APIS on the possibility of using Clickmers for advancing increased binding affinity towards Alzheimer's biomarkers such as amyloid-b,’ said Dr Farid Khan, CEO at PharmaKure.  “This is one of the steps to bring to the market effective disease-modifying therapeutics in AD by combining our lead drug candidate PK051 with an early detection of disease-related biomarker assays”.

‘We are very excited to be collaborating with the PharmaKure team. It is a fantastic opportunity to support the development of novel diagnostic tests that detect biomarkers associated with neurodegenerative diseases, such as Alzheimer’s’ said Dr Helen Fielder, Head of Technology at APIS. “Using APIS’ novel Clickmer technology, we aim to deliver highly specific and high affinity detection of Alzheimer’s biomarkers, to support earlier detection of the disease. Earlier detection alongside PharmaKure’s lead drug candidate PK051 has the potential to significantly improve the treatment of AD patients”.

“Our goal is to accurately identify patients that are starting on the road to Alzheimer’s Disease, even before they have any symptoms. The Clickmer Systems technology will allow us to measure the levels of the protein forms that trigger the onset of the disease’ said Professor Andrew Doig from The University of Manchester, Head of Research and Development at PharmaKure. “A combination of new drugs and diagnostics will finally allow us to find the effective treatments for Alzheimer’s Disease that we so desperately need.”

Alzheimer’s disease is a fatal illness that causes progressive decline in memory and other aspects of cognition. Dementia due to Alzheimer’s is the most common form of dementia, accounting for 60 to 80 percent of all cases. Every 3 seconds someone in the world develops dementia. 850,000 (UK) and 44 million (worldwide) are suffering from Alzheimer’s or dementia related illnesses. In 2020, the total cost of cost of care for people with dementia in the UK is £34.7 billion. Globally, the cost was $360 billion and by 2050 the costs could be a $1 trillion (source Alzheimer’s Research UK).  In the US alone, there was an increase of 8 million new caregivers from 2015 to 2020. The current annual societal and economic cost of dementia is estimated as $1 trillion, an amount that is expected to double by 2030 unless we find a way to slow the disease.

The research will focus on the everyday lived experience of veterans with dementia who live in the community, and build an evidence base so that effective support can be provided to veterans and their family members who provide care. The project will also explore perceived links between previous experiences in the Armed Forces and dementia diagnoses.

Anthea Innes, Professor of Health Aging and Society at McMaster University said: “This project was developed because veterans and their family members have told us that it is needed. It began by listening to those with lived experience, and hearing about their experiences of feeling overlooked and lacking appropriate support. As such, the research will focus on listening to these people, and the gap they have identified in the evidence which policymakers and practitioners have available to them.”

Dr Lydia Morris, a Clinical Psychologist and Clinical Lecturer at The University of Manchester said: “I am very pleased to be involved in this research because veterans living with dementia and their families have told us how much it is needed. It seems that these individuals can ‘fall through gaps’ in service provision and so be left unsupported.  We are keen to understand the issues and improve service provision.”

Tom McBarnet, Chief Executive of Forces in Mind Trust, said “Forces in Mind Trust exists to support those transitioning from the Armed Forces to civilian life and their families. Little evidence exists on veterans’ experiences of living with dementia and the support they receive or would like to receive. This will be the first empirical research focussing on the everyday experience of this community and their families. We are pleased to be funding this important community-focussed research, which will give a voice to those living with this complex condition and their families.”

For anyone who supports veterans with dementia living in their communities in the Greater 91ֱ�� area who is interested in taking part in the research, please contact Dr Lydia Morris by emailing lydia.morris@manchester.ac.uk.

Image contains public sector information licensed under the Open Government Licence v3.0.

Spotlight on Dementia challenges researchers funded by the charity to showcase their vital work through creative images and video. Entries explored diverse topics such as detecting dementia using virtual reality, the impact of young-onset dementia on people’s careers, and the potential involvement of the brain’s immune system in the processes behind dementia.

Dr Emma Ferguson-Coleman is a Research Fellow at the University of Manchester and is being funded by Alzheimer’s Society for her current research study into the support needs of Deaf carers who care for people with dementia.

Emma won the Research in Motion category for her video called Losing my Language, which is about Deaf man who has been living with dementia for a few years. In this video, which is composed from qualitative research data after she interviewed a native BSL Deaf man and his family members, the actor representing the Deaf man shares his perception of living with dementia and what the future might mean for him. This is portrayed in a moment where he uses one sign (rather than a few full sentences in BSL) to describe his in-depth emotions about the possibility of fading away as a person and losing his language, BSL.

Emma said about winning the Research in Motion category: “It’s an absolute honour for me to see the story of Harold and his family represented in the wider mainstream – it is amazing.

‘As a Deaf BSL user myself, I am privileged to represent the stories of Deaf people living with dementia and their carers

‘This video took about three months to develop. I contacted Ilan (ILAN) Dwek (a famous Deaf actor) and discussed this conversation with him; sharing a video of myself mimicking Harold’s signs (for the purpose of research confidentiality) and Ilan filmed himself at home representing Harold’s story. Ilan did an amazing job in reflecting Harold’s emotions. 

‘It was critical that Ilan was able to represent Harold’s position in all its’ entirety. If Ilan had just signed the one sign, there would be no context and no appreciation of the many layers of emotion that Harold was portraying in that moment.

‘I hope that from seeing this brief film, that the wider mainstream community come to understand and appreciate the rich complexities of communicating in BSL, especially with a Deaf BSL user living with dementia. This film will raise awareness of this minority community that use BSL as their first or preferred language and hopefully remove barriers in learning how to communicate either in BSL, or with a BSL interpreter to assist with two-way conversations.”

Emma entered academia as a research assistant in 2010 and studied for her PhD between 2010-2016. Her PhD was focussed on Deaf British Sign Language (BSL) users’ understanding and knowledge of dementia, as well as interviewing, for the first time, Deaf BSL users living with dementia with their carers about their everyday experiences.

Emma also has a personal link to dementia as her grandmother lived with vascular dementia after having had a stroke.

Dr Richard Oakley, Associate Director of Research at Alzheimer’s Society, said:

“Spotlight on Dementia brings together science and art to reveal the wonder and variety of the research we fund. Each breath-taking entry tells a different story about the drive and enthusiasm of our stellar researchers working across dementia diagnosis, treatment and care.

“Alzheimer’s Society is a vital source of support and a powerful force for change for people with dementia. The charity only funds the most cutting-edge dementia research and currently we fund over 155 projects worth over £29.5m. We do this because we know research will beat dementia and improve the lives of people affected by the condition.

“Times are hard at the moment, but more funding is desperately needed to help us find breakthroughs and a cure. Decades of underfunding mean dementia research lags about twenty years behind the progress we’ve made in cancer, and we’re still waiting for the Government to act on its commitment over two years ago to double dementia research funding.”

17 hi-res photos from the overall winners and Emma’s video is available *

The £255,000 scheme run by dementia communications specialists at The University of Manchester, Greater 91ֱ�� Mental Health NHS Foundation Trust, Age UK and  the University of Salford aims to improve relationships between people living with dementia and their carers.

Called ‘ and funded by the National Institute of Health Research, carers are invited to sign up for the 6 online sessions, held over 2 hours in groups of up to 12 people.

The course is delivered by specially trained facilitators who have themselves cared for someone with dementia.

They train carers in using a conversational style of communication, rather than direct questioning, encouraging the carer and person with dementia to respond to cues.

The groups give carers opportunity to reflect on how they communicate, share their experiences with each other, and learn techniques to help them manage their stress levels.

A first research study into a face-to-face version of Empowered Conversations-  carried out before the pandemic -  showed it reduced carer stress and improved communication.

Now a second investigation is looking at how well it works when used online.

The level of existing support for carers depends on where you live, though the team are not aware of any other specialist communications support of this kind in the UK.

Lead researcher Dr Lydia Morris, a psychologist from the University of Manchester said: “It can be bewildering for a carer faced with trying to communicate with someone with dementia.

“This intervention aims to give them confidence, reduce their stress and help them realise they are not alone.

“Most of the existing support for carers deals with practical questions, such as finances and tips for dealing with memory problems, which is of course extremely important.

“But good communication techniques are not addressed in detail anywhere in the UK- certainly not in a group or online format- as far as we know.”

Cassie Eastham, research associate on the study and an Occupational Therapist at Greater 91ֱ�� Mental Health NHS Foundation Trust, who specializes in working with people with dementia said: “This communication course offers carers a space to pause, reflect and re-connect with family members living with dementia.

“It has been designed to enable carers to establish and maintain good communication and relationships with those they support.

”Hundreds of carers have already benefited from Empowered Conversations. Our aim is to run a larger, national trial of the course in the future.”

The report launch comes days after the government launched the White Paper detailing a wide ranging 10-year vision for Social Care with a recurring phrase, ‘Make every decision about care a decision about housing’.  

Housing and Living Well with Dementia: from Policy to Practice in Greater 91ֱ��, has been produced by the Greater 91ֱ�� Health and Social Care Partnership and The University of Manchester (Healthy Ageing Research Group and the 91ֱ�� Institute for Collaborative Research on Ageing).

The report examines the existing health, social care, and housing options available to people living with dementia - focusing on how to provide housing within community settings.

Dementia is a syndrome (a group of related symptoms) associated with an ongoing decline of brain functioning. There are many different causes of dementia, and many different types.

In 2019, at least 21,851 Greater 91ֱ�� residents were living with dementia, 1 in 25 of this number diagnosed with younger onset dementia (people under the age of 65).

The report calls for all services that support people living with dementia, carers and loved ones to work more closely together. It makes clear recommendations on how the diverse needs of housing for people living with dementia must be taken into greater consideration, and how people’s specific circumstances - such as ethnicity, age, and sexual identity - must be at the centre of future planning and developments.

The report has been shaped by the views of people with lived experience of dementia, carers and loved ones, as well as professionals from across Greater 91ֱ��’s housing, health and care sector that provide support to those living the condition.

Warren Heppolette, Greater 91ֱ�� Health and Social Care Partnership’s executive lead for strategy & system development said:

“Dementia can affect anyone - and as such, people have very different needs if they are to continue to live as fulfilling a life as possible.

“More needs to be done to treat people as individuals, so we can make sure they can get the type of support that is right for them – including housing. This report shows how that can be achieved through making information more accessible and being more aware of the changing demographic of Greater 91ֱ��.

“The Greater 91ֱ�� Health and Social Care Partnership is in a unique position to lead the way in addressing the challenges identified by this report, as we seek to build on the city-region’s position as the first in the UK to join the WHO Global Network of Age Friendly Cities.”

Alistair Burns, Professor of Old Age Psychiatry, University of Manchester, said: “The University of Manchester is a global leader in the fields of ageing research, working to improve policy and practice through providing evidence that promotes health, wellbeing and equity in later life.

“Our work to ensure the lives of those living with dementia, their loved ones and carers is critical, especially as we look towards integration of our care systems and the re-imagining of social care with the role of the home as a central tenet for enabling someone to live well and with dignity in their home for as long as they wish.” 

The recommendations of the report will be used to develop a three-year plan (2022-2025) implemented through the forthcoming Greater 91ֱ��’s Integrated Care System.

High blood pressure is known to be the main risk factor in developing vascular dementia. However, the way that high blood pressure damages the small blood vessels, causing them to narrow and restrict blood flow to specific areas of the brain, has been unknown. The effectiveness of different types of blood pressure medication on these arteries has also never been directly tested.

Now, researchers at the University of Manchester working with colleagues in the USA have discovered that the blood pressure drug amlodipine could help treat vascular dementia or stop it in the early stages.

They looked at blood flow in the brains of mice with high blood pressure and vascular damage in the brain. Mice treated with amlodipine had better blood flow to more active areas of the brain. Their arteries were able to widen, allowing more oxygen and nutrients to reach the parts of the brain that needed it most.

The team also discovered for the first time that high blood pressure decreases the activity of a protein called Kir2.1 that is present in cells lining the blood vessels and increases blood flow to active areas of the brain.

Amlodipine was found to restore the activity of Kir2.1 and protect the brain from the harmful effects of high blood pressure. Researchers say that this protein could also be targeted by other drugs in the future, presenting a potential additional way to help fight the disease.

The team now hope to trial amlodipine as an effective treatment for vascular dementia in humans. If successful, it would be the first clinically proven treatment for vascular dementia as a result of small vessel disease and could be used in those with early signs of the condition to prevent further progression.

This research has opened up the field of vascular dementia to not only one but two possible treatment options, and gives hope to those diagnosed with this incurable disease.

Dr Adam Greenstein, Clinical Senior Lecturer in Cardiovascular Sciences at the University of Manchester, who led the 91ֱ�� team, said: 

“The way vascular dementia develops has remained a mystery until now, and there are currently no clinically proven treatments. Patients are presenting with symptoms of vascular dementia earlier than ever before, and with further research we could potentially offer those patients hope to prevent the progression of this life-changing disease.”

 Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation said:

“The way to better understand this devastating disease and find new treatments is through research. This study is a vital step forward towards finding new ways of stopping vascular dementia from progressing.

“These new discoveries highlight the major role that high blood pressure plays in developing the disease and shed light on how this occurs and might be prevented in the future. At present, the most important thing you can do to lower your risk of the disease is to keep your blood pressure within the healthy range. You can get your blood pressure checked for free at your GP or local pharmacy.” 

New guidance has been published to support people with dementia and their carers facing isolation and reduced services as a result of COVID-19.

The features five simple tips, developed using the latest research and with the input of people affected by dementia and be distributed across Greater 91ֱ�� via the Adult Social Care team and Dementia United.

It is part-funded by the National Institute for Health Research (NIHR), in a project led by the University of Exeter and the NIHR Older People and Frailty Policy Research Unit

Partners include The University of Manchester, Alzheimer’s Society, Bradford University and Brunel University London.

People with dementia, say the team, are particularly vulnerable to the psychological and social impacts of isolation and lockdown.

Worries expressed by people affected by dementia include maintaining supplies of food and medication, anxiety about hospital admission, lack of confidence, feeling of loss and grief, agitation, and rapid decline in cognitive and functional ability.

And carers say they feel more captive in their role and lack respite opportunities. Many find it difficult to explain the current restrictions to a person with dementia and worry about their safety and well-being.

Alistair Burns, professor of old age psychiatry at The University of Manchester said: “People with dementia are more likely to develop a confusional state and have other physical illnesses which can make them vulnerable to developing severe symptoms and complications.

“Those with more advanced dementia may also have difficulty understanding the need for self-isolation or hand washing techniques. And they may not be able to describe their symptoms so clinicians may have to rely on observations about the signs of COVID-19. That is why as doctors, we should look beyond words. During this crisis, the carers of people with dementia can feel particularly isolated and so support for them and their families is also essential.”

Professor Linda Clare, of the University of Exeter Medical School, who led the project, said: “While not currently classed as “vulnerable” on health grounds, people with dementia and their family carers are disproportionately affected by social distancing, isolation and lockdown. Our research tells us that many people living with dementia and carers felt isolated and lonely before COVID-19, and now these feelings will be amplified. They can feel overwhelmed by the volume of generic advice and guidance available, and may be unsure how to select information that is relevant to them and their families and what information to trust. This project aims to provide robust information, developed with the crucial input of people affected by dementia, to offer support through this crisis.”

The leaflet, available , gives practical and self-help tips, as well as signposting sources of support, on five key points:

• Staying safe and well
• Staying connected
• Keeping a sense of purpose
• Staying active
• Staying positive

It is being distributed online through a network of organisations who support people affected by dementia and will form part of Alzheimer’s Society’s support package via helplines and frontline staff.

Relative and friends are urged to print the leaflet and give a physical copy to people affected who do not have access to the internet.

A hypothesis which has been the standard way of explaining how the body develops Alzheimer’s Disease for almost 30 years is flawed, according to a University of Manchester biologist.

The ‘Amyloid Cascade’ argues that a series of stages, starting from the deposition of a starch-like protein called amyloid and ending with dementia, should be reassessed.

Prof Andrew Doig’s review of 120 scientific papers finds that the stages were not linked together in a cascade and the progression to dementia was not linear.

His review is published in the Journal of Alzheimer’s Disease.

“It’s wrong to use a series of waterfalls as an analogy for how dementia develops, as water cannot flow uphill”, said Prof Doig.

“My review shows the system is actually cyclical and does not flow one way – but is a series of feedback loops. Progress in recent years shows some of the elements go back and forth- both upstream and downstream.

”Most research has been at the top of the cascade. But we need to consider other drug targets too.”

According to the cascade, enzymes cut the amyloid into fragments which form plaques that damage cells.

Calcium rises in cells, followed by inflammation and then oxidative stress - an imbalance between certain molecules containing oxygen and antioxidants - and then cell death which causes dementia.

However, according to the research reviewed by Prof Doig, inflammation can either lead to enhanced amyloid deposition or oxidative stress.

Prof Doig added: “The fact that this process is cyclical has important implications as we’re missing opportunities for drug discovery.

“So for example, we need to take a closer look at inflammation and oxidative stress and their relation to amyloid plaques. If we use the Amyloid Cascade hypothesis, that would be less likely to happen.”

“Over the 26 years since the cascade was first described, hundreds of drugs based on this hypothesis have been trialled in people but none of them have worked.

“But if you realise the cyclical nature of this, then combinations of therapies could have a part to play.”

Positive Feedback Loops in Alzheimer’s Disease – The Alzheimer’s Feedback Hypothesis is published in the 

Hearing aids and cataract surgery are strongly linked to a slower rate of age-related cognitive decline, according to new research by University of Manchester academics.

According to and , cognitive decline- which affects memory and thinking skills- is slowed after patient’s hearing and sight are improved.

The rate of decline was halved following cataract surgery and was 75% less following the adoption of hearing aids.

The research on cataract surgery - which is published in  today– was carried out using 2,068 individuals who underwent cataract surgery between Wave 2 and Wave 6 of the English Longitudinal 91ֱ�� of Ageing survey from between 2002 to 2014.

They were compared with 3,636 individuals with no cataract surgery.

And the research on hearing aids, published in the Journal of the American Geriatrics Society in July, was carried out using 2040 participants in the American Health and Retirement survey from 1996 to 2014

Both surveys assess cognitive decline by testing memory, asking participants to recall 10 words immediately and then at the end of the cognitive function module.

The researchers compared the rates of decline before and after the patients had surgery or started wearing a hearing aid.

Dr Dawes said: “These studies underline just how important it is to overcome the barriers which deny people from accessing hearing and visual aids.

“It’s not really certain why hearing and visual problems have an impact on cognitive decline, but I’d guess that isolation, stigma and the resultant lack of physical activity that are linked to hearing and vision problems might have something to do with it.

“And there are barriers to overcome: people might not want to wear hearing aids because of stigma attached to wearing them, or they feel the amplification is not good enough or they’re not comfortable.

“Perhaps a way forward is adult screening to better identify hearing and vision problems and in the case of hearing loss, demedicalising the whole process so treatment is done outside the clinical setting. That could reduce stigma.

“Wearable hearing devices are coming on stream nowadays which might also be helpful. They not only assist your hearing, but give you access to the internet and other services

Dr Maharani said: “Age is one of the most important factors implicated in cognitive decline. We find that hearing and vision interventions may slow it down and perhaps prevent some cases of dementia, which is exciting- though we can’t say yet that this is a causal relationship.

“Other studies have attempted to look at rates of cognitive decline- but have not really succeeded as it’s hard to take into account demographic factors.

“But the beauty of this study is that we’re comparing the progress of the same individuals over time.”

‘’ is published in Plos One.

‘’ is published in the Journal of the American Geriatrics Society

This research is funded by the European Commission’s Horizon 2020 Framework

A new commentary by scientists at the Universities of Manchester and Edinburgh on a study by Taiwanese epidemiologists supports the viability of a potential way to reduce the risk of Alzheimer’s disease.

When the Taiwanese authors looked at subjects who suffered severe herpes infection and who were treated aggressively with antiviral drugs, the relative risk of dementia was reduced by a factor of 10.

91ֱ��’s Professor and Edinburgh’s Professor Richard Lathe say the paper, by Tzeng et al. and published in Neurotherapeutics in February 2018, also shows that herpes simplex virus type 1 (HSV1) leads to an increased risk of developing the disease.

“This article and two others by different research groups in Taiwan provide the first population evidence for a causal link between herpes virus infection and Alzheimer’s disease, a hugely important finding,” said Professor Itzhaki.

They publish a commentary in the Journal of Alzheimer’s Disease on the three articles, arguing that they provide the strongest evidence yet for a causal link between herpes infection and Alzheimer’s disease, backing 30 years of research by Professor Itzhaki.

Professor Itzhaki said: “I believe we are the first to realise the implications of these striking data on this devastating condition which principally affects the elderly. No effective treatments are yet available.

“Almost 30 million people worldwide suffer from it and sadly, this figure will rise as longevity increases.

“But we believe that these safe and easily available antivirals may have a strong part to play in combating the disease in these patients.

“It also raises the future possibility of preventing the disease by vaccination against the virus in infancy.

”Successful treatment by a specific drug, or successful vaccination against the putative microbe, are the only ways to prove that a microbe is the cause of a non- infectious human disease.”

Most Alzheimer’s disease researchers investigate its main characteristics – amyloid plaques and neurofibrillary tangles; however, despite the vast amount of research, the causes of their formation are unknown.

HSV1 infects most humans in youth or later and remains lifelong in the body in dormant form within the peripheral nervous system.

From time to time the virus becomes activated and in some people it then causes visible damage in the form of cold sores.

The Taiwanese study identified 8,362 subjects aged 50 or more during the period January to December 2000 who were newly diagnosed with severe HSV infection.

The study group was compared to a control group of 25,086 people with no evidence of HSV infection.

The authors then monitored the development of dementia in these individuals over a follow-up period of 10 years between 2001 and 2010.

The risk of developing dementia in the HSV group was increased by a factor of 2.542. But, when the authors compared those among the HSV cohort who were treated with antiviral therapy versus those who did not receive it, there was a dramatic tenfold reduction in the later incidence of dementia over 10 years.

Professor Richard Lathe added: “Not only is the magnitude of the antiviral effect remarkable, but also the fact that—despite the relatively brief duration and the timing of treatment—in most patients severely affected by HSV1 it appeared to prevent the long-term damage in brain that results in Alzheimer’s.

Professor Itzhaki said: “It was as long ago as 1991 when we discovered that, in many elderly people infected with HSV1, the virus is present also in the brain, and then in 1997 that it confers a strong risk of Alzheimer’s disease in the brain of people who have a specific genetic factor.

“In 2009, we went on to show that HSV DNA is inside amyloid plaques in Alzheimer’s patients’ brains.

“We suggested that the virus in brain is reactivated by certain events such as stress, immunosuppression, and infection/inflammation elsewhere.

“So we believe the cycle of HSV1 reactivation in the brain eventually causes Alzheimer’s in at least some patients.”

The study by Tzeng et al. investigated only people with severe HSV and cannot be generalised to healthy populations.

The paper: ‘’ is published in the Journal of Alzheimer's Disease

An international team of scientists have confirmed the discovery of a major cause of dementia, with important implications for possible treatment and diagnosis.

from The University of Manchester, who leads the 91ֱ�� team, says the build-up of urea in the brain to toxic levels can cause brain damage – and eventually dementia.

The work follows on from Professor Cooper’s earlier studies, which identified metabolic linkages between Huntington’s, other neurodegenerative diseases and type-2 diabetes.

The team consists of scientists from The University of Manchester, the University of Auckland, AgResearch New Zealand, the South Australian Research and Development Institute, Massachusetts General Hospital and Harvard University.

The latest paper by the scientists, published today in the , shows that Huntington’s Disease - one of seven major types of age-related dementia - is directly linked to brain urea levels and metabolic processes.

Their 2016 study revealing that urea is similarly linked to Alzheimer’s, shows, according to Professor Cooper, that the discovery could be relevant to all types of age-related dementias.

The Huntington’s study also showed that the high urea levels occurred before dementia sets in, which could help doctors to one day diagnose and even treat dementia, well in advance of its onset.

Urea and ammonia in the brain are metabolic breakdown products of protein. Urea is more commonly known as a compound which is excreted from the body in urine. If urea and ammonia build up in the body because the kidneys are unable to eliminate them, for example, serious symptoms can result.

Professor Cooper, who is based at The University of Manchester’s , said: “This study on Huntington’s Disease is the final piece of the jigsaw which leads us to conclude that high brain urea plays a pivotal role in dementia.

“Alzheimer’s and Huntington’s are at opposite ends of the dementia spectrum – so if this holds true for these types, then I believe it is highly likely it will hold true for all the major age-related dementias.

“More research, however, is needed to discover the source of the elevated urea in HD, particularly concerning the potential involvement of ammonia and a systemic metabolic defect.

“This could have profound implications for our fundamental understanding of the molecular basis of dementia, and its treatability, including the potential use of therapies already in use for disorders with systemic urea phenotypes.”

Dementia results in a progressive and irreversible loss of nerve cells and brain functioning, causing loss of memory and cognitive impairments affecting the ability to learn. Currently, there is no cure.

The team used human brains, donated by families for medical research, as well as transgenic sheep in Australia.

91ֱ�� members of the team used cutting-edge gas chromatography mass spectrometry to measure brain urea levels. For levels to be toxic urea must rise 4-fold or higher than in the normal brain says Professor Cooper.

He added: “We already know Huntington’s Disease is an illness caused by a faulty gene in our DNA - but until now we didn’t understand how that causes brain damage – so we feel this is an important milestone.

“Doctors already use medicines to tackle high levels of ammonia in other parts of the body Lactulose - a commonly used laxative, for example, traps ammonia in the gut. So it is conceivable that one day, a commonly used drug may be able to stop dementia from progressing. It might even be shown that treating this metabolic state in the brain may help in the regeneration of tissue, thus giving a tantalising hint that reversal of dementia may one day be possible.”

Professor Cooper expresses his thanks to all the families of patients with Huntington's disease in New Zealand who so generously supported this research through the donation of brain tissue to the Neurological Foundation of New Zealand Douglas Human Brain Bank in the Centre for Brain Research.

This work was supported by the CHDI Foundation (A-8247) and Brain Research New Zealand.

The paper ‘Brain urea increase is an early Huntington’s disease pathogenic event observed in a prodromal transgenic sheep model and HD cases’ is available on request

Other 91ֱ��-based scientists who made important contributions are Dr Stefano Patassini and Dr Jingshu Xu.

Relevant papers include:

• . Biochimica et Biophysica Acta (2016)
• . Biochemical and Biophysical Research Communications (2015)
• . Biochimica et Biophysica Acta (2016)
• . Scientific Reports (2016)
• . Metallomics. (2017)
• . Journal of Huntington’s Disease (2013)
• . Proteomics (2001)

Anyone with queries about Alzheimers should contact The Alzheimer’s Research Society on 0300 111 5555 or visit 

Anyone with queries about Huntington’s Disease should contact The Huntington’s Disease Association on 0151 331 5444 or visit 

New research is showing how being connected with their local community has reaped enormous benefits for people with dementia.

Research Associate Sarah Campbell, from The University of Manchester, says familiarity with people in local shops, cafes and even on the street, was crucial to the participants of the study.

Acts of kindness by neighbours like taking the bins out each week, she said had a huge effect on their wellbeing.

The researchers also found that some people with dementia still had a valuable role in their neighbourhoods by ‘keeping an eye’ out, collecting newspapers and caring for grandchildren.

The research is part of a funded by theand the 

It is one of the first and largest studies to investigate how people living with dementia, and their partners, experience their local neighbourhoods.

56 people -29 with dementia and 27 Family carers - from across Greater 91ֱ�� were interviewed about their experience for the study.

The research team say their findings will encourage others to think about people living with dementia currently thought to be 850,000 people Alzheimer’s Research UK.

The figure worldwide is 44 million people, which is set to treble to 135 million by 2050, Alzheimer’s Research UK.

She said: “These findings together indicate how the neighbourhood operates through a series of links between people and place from the dementia café, to the local newsagents, and the neighbour two doors down.

“Many people with dementia will be living independently in neighbourhoods and communities, with the support of family, friends, neighbours and formal and informal service provides.

“But understanding the nature of support available in neighbourhood settings is crucial to ensuring everyone affected by dementia is able to live life as best they can.

‘Routines and habit’ are also an essential part of everyday life in connecting people to their neighbourhoods and to others. Such as using the same routes to walk the dog, or visiting the same café or attending dementia peer support groups.”

She added: “We would also encourage the public to come along to our drop-in event on 8 November and record their own experiences and thoughts about neighbouring, neighbourhoods and day-to-day life in relation to dementia.

“We’d like the public to also think about how they might be able to help people living with dementia in their own neighbourhoods and reflect on what it might be like to live in their own neighbourhoods with a diagnosis of dementia.”

A free drop in interactive event at the aims to inform the public on how people living with dementia experience everyday life in local places.

Location: 91ֱ�� Central Library on Wed 8 November between 11am and 3pm. The drop-in event is jointly organised by University of Manchester and University of Salford academics.

People with dementia or memory problems, their carers, and anyone who is interested, can sign up to Join - an NIHR scheme designed to recruit participants for clinical research studies that can that can help us understand what causes the disease, develop effective treatments, improve care and hopefully one day find a cure. 

The  research project is led by Dr  from The Universityof Salford. Professor John Keady from The University of Manchester is the Chief Investigator for the wider programme of research.

Disabling a part of brain cells that acts as a tap to regulate the flow of proteins has been shown to cause neurodegeneration, a new study from The University of Manchester has found.

The research, which was carried out in mice, focused on the Golgi apparatus - a compartment inside all cells in the body that controls the processing and transport of proteins. It is fundamental for the growth of the cell membrane and also for the release of many types of proteins such as hormones, neurotransmitters and the proteins that make up our skeletons.

Working with Chinese colleagues, the 91ֱ�� researchers examined the role of the Golgi apparatus in neurons, or brain cells, and found that mice in which the apparatus was disabled suffered from developmental delay, severe ataxia, and postnatal death.

Ataxia is a term for a group of disorders that affect co-ordination, balance and speech. Any part of the body can be affected, but people with ataxia often have difficulties with balance and walking, speaking, swallowing, tasks such as writing and eating, and vision. It can be inherited, brought on through incidents such as a stroke, or through old age.

Although the function of the Golgi apparatus, named after its Italian discoverer, is well understood, it has not been previously been shown to have a role in neurodegeneration. With these results the scientists think they may have found a new avenue to explore in the search for the causes of some neurodegenerative diseases.

, the lead researcher, said: “Our results, combined with previous work, suggest that during the cellular changes that occur, loss of the Golgi function could be an important intermediary step that contributes to cell death.”

How much the Golgi apparatus contributes to the major neurodegenerative diseases such as Alzheimer’s or Parkinson’s is something that is currently unclear, though other studies have made this link.

Professor Lowe added: “Together with other published work our findings suggest that in certain neurodegenerative diseases the loss of function of the Golgi apparatus may contribute to the pathology that is occurring.”

The paper, ‘’, was published in PNAS. doi: 10.1073/pnas.1608576114

The study was carried out by The University of Manchester and the Shilai Bao lab at in Beijing. Funding was provided by a joint grant between The University of Manchester and the Chinese Academy of Science at Beijing, as well as separate funding to both institutions, from and the .

A team led by from The University of Manchester found that the anti-inflammatory drug completely reversed memory loss and brain inflammation in mice.

Nearly everybody will at some point in their lives take non-steroidal anti-inflammatory drugs; mefenamic acid, a common Non-Steroidal Anti Inflammatory Drug (NSAID), is routinely used for period pain.

The findings are published today in a paper authored by Dr Brough and colleagues, in the respected journal Nature Communications. Dr Brough and supervised PhD student Mike Daniels, and postdoc Dr Jack Rivers-Auty who conducted most of the experiments.

Though this is the first time a drug has been shown to target this inflammatory pathway, highlighting its importance in the disease model, Dr Brough cautions that more research is needed to identify its impact on humans, and the long-term implications of its use.

The research, funded by the Medical Research Council and the Alzheimer’s Society, paves the way for human trials which the team hope to conduct in the future.

Around 500,000 people in the UK have Alzheimer’s disease which gets worse over time, affecting many aspects of their lives, including the ability to remember, think and make decisions.

In the study transgenic mice that develop symptoms of Alzheimer's disease were used. One group of 10 mice was treated with mefenamic acid, and 10 mice were treated in the same way with a placebo.

The mice were treated at a time when they had developed memory problems and the drug was given to them by a mini-pump implanted under the skin for one month.

Memory loss was completely reversed back to the levels seen in mice without the disease.

Dr Brough said: “There is experimental evidence now to strongly suggest that inflammation in the brain makes Alzheimer’s disease worse.

“Our research shows for the first time that mefenamic acid, a simple Non-Steroidal Anti Inflammatory Drug can target an important inflammatory pathway called the NLRP3 inflammasome , which damages brain cells.”

He added: “Until now, no drug has been available to target this pathway, so we are very excited by this result.

“However, much more work needs to be done until we can say with certainty that it will tackle the disease in humans as mouse models don’t always faithfully replicate the human disease.

“Because this drug is already available and the toxicity and pharmacokinetics of the drug is known, the time for it to reach patients should, in theory, be shorter than if we were developing completely new drugs.

“We are now preparing applications to perform early phase II trials to determine a proof-of-concept that the molecules have an effect on neuroinflammation in humans.”

Dr Doug Brown, Director of Research and Development at , said: “Testing drugs already in use for other conditions is a priority for Alzheimer’s Society - it could allow us to shortcut the fifteen years or so needed to develop a new dementia drug from scratch.

“These promising lab results identify a class of existing drugs that have potential to treat Alzheimer’s disease by blocking a particular part of the immune response. However, these drugs are not without side effects and should not be taken for Alzheimer’s disease at this stage – studies in people are needed first.”

, published in the journal . DOI: 10.1038/NCOMMS12504

Please note, this study is experimental and doctors do not prescribe Mefenamic Acid as a treatment for Alzheimer’s Disease. For queries about treatment and care, please contact Alzheimer’s Society on 0330 333 0804. or email enquiries@alzheimers.org.uk

The University of Manchester has opened the multi-million pound Stoller Biomarker Discovery Centre (14 June), which will identify the unique markers of diseases such as cancer or arthritis. These markers will be developed to ensure the right treatment for the right patient as early as possible.

The Stoller Biomarker Discovery Centre, which is funded by a philanthropic gift from the Stoller Charitable Trust, and in partnership with , will help to industrialise the process of identifying biomarkers – the molecular clues that indicate the presence of a disease or other condition.

By detecting these on a scale never seen before in Europe, University scientists and clinicians will be able to work with health companies and the NHS to produce a greater number of tests and develop new treatments to accelerate the process of curing many of the most serious illnesses faced today.

Medicines have historically been developed for whole populations, but biomarkers help to stratify patients so they get the right treatment for them – not one size fits all. In cancer work already ongoing in the Centre has identified possible tests to detect ovarian cancer earlier, gaining valuable advantage by being able to treat this disease earlier and therefore more effectively.

is the Director of the new Centre. He said: “The Centre is a major step forward in precision medicine. Essentially this is the future of healthcare – getting the right treatment to the right person at the right time and in the right dose.

“Without the knowledge of biomarkers we won’t be able to identify which people need treatment or who will benefit from certain medicines, so this new centre underpins everything we’re doing in precision medicine in 91ֱ�� and beyond.”

The Stoller Biomarker Centre is located at , in the midst of biotechnology companies, t and The University of Manchester.

The new Centre is stocked with a large suite of high-end SCIEX mass spectrometers, including TripleTOF^® 6600 Systems with SWATH Acquisition, QTRAP^® 6500+ Systems, and the SCIEX Lipidyzer Platform, for measuring molecules in proteins (proteomics). The University of Manchester has also invested in a number of liquid chromatography and automated sample preparation components for the Centre, from SCIEX and other life science companies.

“SCIEX’s mission of innovating integrated, reliable analytical tools to gain scientific understandings that lead to better health, enables our customers to advance precision medicine with scale and speed like never before,” said Jean-Paul Mangeolle, President of SCIEX.

“And it takes more than providing great instruments to be part of a movement as important as precision medicine; it takes strong collaborations with customers, partnerships with industry leaders and teamwork with our colleagues at other the Danaher Corporation life companies, to establish and deploy the most comprehensive proteomics solutions.”

The Centre was officially opened during a special two day conference (14-15 June), which attracted some of the biggest names in medical research such as Dr Leroy Hood, Dr Leigh Anderson, and Professor Jennifer Van Eyk.

The Centre will build on research carried out at 91ֱ�� including discovering new markers for the earlier detection of cancers – crucial in starting early treatment to save lives. Work to identify new biomarkers for diseases such as arthritis, cardiovascular, Alzheimer’s and psoriasis will also be enhanced.

The Centre will work in the newly devolved healthcare system in Greater 91ֱ��, as the city-region and major bodies and companies operating within it work to remove bottlenecks such as making the transition from lab to bedside with new tests and drugs.

President and Vice-Chancellor of The University of Manchester, said: “91ֱ�� has become a major hub for precision medicine and proteomics we are very grateful to the funders who have backed the cutting-edge work that is carried out by our scientists.

“As a result of their generosity, The Stoller Biomarker Discovery Centre will start work on addressing some of the biggest issues in medicine in an environment where these discoveries can move quickly to improve people’s lives.”

91ֱ��, Salford and 91ֱ�� Metropolitan Universities are teaming up in a new initiative to combat dementia in the region and beyond.

To mark Dementia Awareness Week (May 15-21), leading researchers from the three institutions met today at The University of Manchester’s to open a series of collaborations around a range of dementia issues – from biology to social care.

It comes as the Greater 91ֱ�� region begins to synchronise its health and social care provision under the so-called DevoManc agenda, enabling the NHS, local authorities and research institutions to work together on more co-ordinated approaches to improving the health and wellbeing of local people.

, The University of Manchester’s lead for dementia research said: “Together the three universities in the region are much stronger than the sum of their parts. The highest rates of dementia in the country are in North West England, so working together like this on dementia brings different experts, networks and resources to bear on making a positive difference to those living with dementia, their carers and families.”

At The University of Manchester this includes projects to identify new targets in the brain for drug development. Researchers also work on the crucial issue of early diagnosis by looking for molecular clues – known as biomarkers – in the body that warn of the early stages of dementia.

Developing strategies to live well with dementia is a particular focus of interest with projects providing music therapy and researchers working with carers. All of this is underpinned by the use of ‘big data’ to gather insight and test the effectiveness of research.

At Salford, research includes projects on artificial intelligence that supports people in their own homes, the most effective forms of support for BME communities and a project aimed at better meeting the day-to-day needs of people living with young onset dementia.

Tony Warne, Professor in Mental Health Care at , said: “Dementia is one of the greatest public health challenges of our times and currently too little is known about best practice in care and design for living well with dementia.”

will be researching new ways to protect the brain against stroke-associated dementia by stopping harmful post-stroke proteins. There is also a keen focus on promoting independent living in people with dementia. This week, the University launches a new project analysing GPS-enabled wristbands that can cut social isolation.

Professor Mark Slevin, Director of Manchester Met’s Healthcare Science Research Centre, said: “Dementia is one of the biggest health and wellbeing challenges we face in society. By combining our knowledge, experience and disciplines, we’re able to call upon a powerful research resource that will ensure we’re among the best equipped regions worldwide to tackle dementia.”

To be known as the Greater 91ֱ�� Dementia Consortium, the new memorandum of understanding will run for an initial two years.

More about

The combined impact of dementia, age-related hearing and vision impairment is to be investigated by a new multi-million European research consortium led by The University of Manchester.

Seven in ten Europeans over the age of 65 suffer from either sight or hearing problems and over two thirds suffer from depression or dementia. When combined together the cumulative impact of these dual or triple impairments is far greater than the individual conditions. The scale of combined sensory and cognitive problems is substantial but poorly understood.

The five year project, led by The University of Manchester, has been funded with €6.5m from the European Commission’s research programme. The project aims to investigate this combined impact and develop new tools that could improve quality of life and optimise health and social care budgets across Europe.

, an academic psychiatrist from The University of Manchester, who is the lead researcher on the project, said: “In combination these problems have a much greater effect than each one individually. Imagine if you have dementia which affects your memory or interferes with your recognition of familiar people. When you add visual impairment to that, you can understand why those affected may experience even greater cognitive difficulty or even experience altered behaviour such as agitation or hallucinations.

“The burden on carers – often family members – is also increased as they are required to do much more on a daily basis and we see a greater number of these suffering from burn-out.”

The project seeks to define the scale of the challenges so that authorities across the continent can allocate resources more optimally. At the same time, researchers will also develop online tests, guides and multi-lingual training manuals to help medical professionals diagnose and treat the combined problems more effectively.

Minority groups are particularly disadvantaged with respect to diagnosis and treatment of mental and sensory problems, so researchers will be seeking out people from these groups to participate in the research.

The programme will also trial an intervention of at-home support for people with dual- and triple-impairments. This will be supported by specialist sensory therapists based at and will focus around pragmatic solutions to support both the affected person and their carer.

, a University of Manchester audiologist and co-lead of the SENSE-Cog project said: “Millions of people in the UK and wider EU are affected by this combination of problems and it’s only going to get more prevalent as the population ages. That’s why we have to understand the scale of the problem and then equip the public, carers and health care workers with the tools they need to deal with it. If we could reduce disability due to hearing and vision impairment, there is huge potential to improve mental well-being and even delay the deterioration of dementia.”

The University of Manchester has been awarded £5.3m to buy and install a leading-edge scanner for studying the molecular processes in the brain that cause dementia.

The funding from the Medical Research Council will allow the SIGNA PET/MR scanner, made by , to be installed in .  Currently there are only two of these scanners in the UK, but following the 91ֱ�� funding and money to other university centres in the UK, this number will increase to seven, from a number of manufacturers.

The new scanner will help scientists and clinicians understand the causes and progression of dementia, and provide ways to test the effects of new treatments.  Molecular changes in the brain are believed to be responsible for dementia and the scanners have the potential to link these with the brain changes that they cause – leading to new understanding and new treatments.

is the University’s Director for Dementia Research.  He said: “Dementia is a condition that is poorly understood and difficult to treat effectively.  It’s going to become more of a problem in the coming decades, so our research response needs to pick up as well.

“This scanner and the wider network will give us that ability to understand dementia better and to develop more treatments.”

The scanner is expected to be operational from July 2016 and work is currently underway to refurbish a shelled space adjacent to the Nuclear Medicine Centre to house the scanner suite which will have three treatment rooms, a research office and a radiopharmacy room. CMFT was chosen as the ideal location for the scanner due to its central 91ֱ�� location and close proximity to the main University campus, the co-location of the suite adjacent to the clinical PET/CT scanner at CMFT and the opportunity to take research into clinical practice.

Christine Tonge, the Director of Medical Physics at Central 91ֱ�� said: “We are excited by this opportunity to contribute to this important area of research. This scanner will put 91ֱ�� at the forefront of dementia research and we look forward to collaborating not only with our colleagues from the University, but also  from other hospitals in Greater 91ֱ�� and beyond.”

The scanner is being funded as part of the Dementias Platform UK – a multi-million pound public-private partnership, developed by , to accelerate progress in dementias research. DPUK’s aims are early detection, improved treatment and, ultimately, prevention of dementias. It is the world’s largest study group for use in dementias research, pulling together two million well-characterised participants from over 30 national population studies.

The 91ֱ�� scanner will be supervised by , who is the director of the University’s , which hosts two PET scanners and one MR scanner and produces radiotracers for use in PET scanning.  He said: “91ֱ�� now has a range of scanning facilities which mean that clinicians and scientists can produce high quality research across a range of conditions.

“With the growing urgency of developing treatments for dementia, this new equipment is vital in addressing a major growing health concern.

“Most importantly, being linked with the other four universities which are also purchasing PET-MR scanners will mean 91ֱ�� has the ability to become involved in multi-centre trials and research grants and contracts – increasing the effectiveness of the UK’s research in this area.”

More information on the national announcement can be found .

People with young onset dementia and their carers came together to provide a moving musical and artistic performance that concluded a series of weekly sessions.

Service users from Young Onset Dementia Service teamed up with an artist, composer and musician from to work on songs and artwork in weekly sessions held throughout July and August.

The project, Portraits of a Place, received funding from The University of Manchester as a unique arts and science collaboration. The aim is to use the learning from this pilot project to develop similar activity with others who have young onset dementia locally, regionally and nationally.

The resulting pieces based on the themes of identity, belonging and living in the community were performed for those assembled and included four songs written by the group themselves during the sessions and artwork in the form of sketches, collages, booklets that formed the starting point for music making and informed the lyrical content of the songs.

Mel Brown, Team Manager of the Trust’s Young Onset Dementia Service praised the service users for their enthusiasm in the project: “This has been a groundbreaking project and we’re all proud of their hard work. The artwork, songs and performance were fantastic.  People with dementia often find an increasing sense of isolation from relatives and their wider community.  In addition, younger people with dementia are a group sometimes overlooked by researchers and clinicians. I look forward to reading the research of this project.”

The project brought together 91ֱ�� Camerata, one of the UK’s leading chamber orchestras, the Dementia and Ageing Research team in (SNMS) and the Trust’s Young Onset Dementia Team. 

Lucy Geddes, Learning Officer from 91ֱ�� Camerata, who lead the project said: “This has been an incredibly positive experience for everyone involved. Each week the group has inspired each other, the staff and the team with their creativity, elegance and beauty. Their connection with the project themes has generated fantastically creative, emotional and fun song-writing and their transformation from service user to artist has been a privilege to be part of.”

“We’re very proud to have been able to collaborate further with our colleagues at The University of Manchester’s School of Nursing, Midwifery and Social Work and really look forward to reading the report,” added Lucy. “The film of this project will be shown at 91ֱ�� Camerata’s season opening concert at The Bridgewater Hall on the 26 September so that the audience can also see a small part of the amazing group.” 

The finished work will be shared with friends and family and subsequently throughout 91ֱ�� and beyond. The project journey was documented on film and will be disseminated to raise awareness.  The impact and experience of participants will be evaluated by the Dementia and Ageing Research Team in the SNMS.

The team has experience of working alongside the Camerata and the project will be completed, and evaluated, over a period of 12 months from commencement. 

The musicians, clinicians and people with dementia who will deliver this project will directly share this experience with undergraduate and postgraduate students at the SNMS (including those attending ) through their input into the curricula and through a standalone seminar for the wider University.

Antiviral drugs used to target the herpes virus could be effective at slowing the progression of Alzheimer’s disease (AD), a new study shows.

The University of Manchester scientists have previously shown that the herpes simplex virus type 1 (HSV1) is a risk factor for Alzheimer’s when it is present in the brains of people who have a specific genetic risk to the disease.

AD is an incurable neurodegenerative condition affecting about 18 million people worldwide. The causes of the disease or of the abnormal protein structures seen in AD brains – amyloid plaques and neurofibrillary tangles – are completely unknown.

The 91ֱ�� team has established that the herpes virus causes accumulation of two key AD proteins – β-amyloid (Aβ) and abnormally phosphorylated tau (P-tau) – known to be the main components of plaques and tangles respectively. Both proteins are thought by many scientists to be involved in the development of the disease.

“We have found that the viral DNA in AD brains is very specifically located within amyloid plaques,” said Professor Ruth Itzhaki, who led the team in the University’s Faculty of Life Sciences. “This, together with the production of amyloid that the virus induces, suggests that HSV1 is a cause of toxic amyloid products and of plaques.

“Our results suggest that HSV1, together with the host genetic factor, is a major risk for AD, and that antiviral agents might be used for treating patients to slow disease progression.”

Currently available antiviral agents act by targeting replication of HSV1 DNA, and so the researchers considered that they might be successful in treating AD only if the accumulation of β-amyloid and P-tau accumulation caused by the virus occurs at or after the stage at which viral DNA replication occurs.

“If these proteins are produced independently of HSV1 replication, antivirals might not be effective,” said Professor Itzhaki. “We investigated this and found that treatment of HSV1-infected cells with acyclovir, the most commonly used antiviral agent, and also with two other antivirals, did indeed decrease the accumulation of β-amyloid and P-tau, as well as decreasing HSV1 replication as we would expect.

“This is the first study investigating antiviral effects on AD-like changes and we conclude that since antiviral agents reduce greatly β-amyloid and P-tau levels in HSV1-infected cells, they would be suitable for treating Alzheimer’s disease. The great advantage over current AD therapies is that acyclovir would target only the virus, not the host cell or normal uninfected cells. Further, these agents are very safe and are relatively inexpensive.

“Also, by targeting a cause of Alzheimer’s disease, other viral damage, besides β-amyloid and P-tau, which might be involved in the disease’s pathogenesis, would also be inhibited.

“The next stage of our research – subject to funding – will focus on finding the most suitable antiviral agent – or combination of two agents that operate via different mechanisms – for use as treatment. We then need to investigate the way in which the virus and the genetic risk factor interact to cause the disease, as that might lead to further novel treatments.

“Eventually, we hope to begin clinical trials in humans but this is still some way off yet and again will require new funding.”

The study, carried out with Dr Matthew Wozniak and other colleagues in the Faculty of Life Sciences, is published in the Public Library of Science (PLoS) One journal.

Ends

Notes for editors

A copy of the paper, ‘Antivirals Reduce the Formation of Key Alzheimer’s Disease Molecules in Cell Cultures Acutely Infected with Herpes Simplex Virus Type 1,’ by Wozniak, M., et al, published in PLoS One, is available on request.

For further information contact:

Aeron Haworth
Media Relations
Faculty of Life Sciences
The University of Manchester

Tel: 0161 275 8383
Mob: 07717 881563
Email: aeron.haworth@manchester.ac.uk