<![CDATA[Newsroom University of Manchester]]> /about/news/ en Tue, 22 Oct 2024 23:40:33 +0200 Wed, 26 Jun 2024 12:01:31 +0200 <![CDATA[Newsroom University of Manchester]]> https://content.presspage.com/clients/150_1369.jpg /about/news/ 144 UK’s first centre of excellence for music and dementia hosted by 91ֱ Camerata /about/news/uks-first-centre-of-excellence-for-music-and-dementia-hosted-by-manchester-camerata/ /about/news/uks-first-centre-of-excellence-for-music-and-dementia-hosted-by-manchester-camerata/631132Over £1million of funding has been committed by Andy Burnham (Mayor of Greater 91ֱ), Sir Richard Leese (Chair of the NHS Greater 91ֱ) and the National Academy for Social Prescribing’s Power of Music Fund to enable Greater 91ֱ to become the UK’s first Centre of Excellence for Music and Dementia – hosted by 91ֱ Camerata. The project will also receive in-kind support from the University of Manchester and Alzheimer’s Society.

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Over £1million of funding has been committed by Andy Burnham (Mayor of Greater 91ֱ), Sir Richard Leese (Chair of the NHS Greater 91ֱ) and the National Academy for Social Prescribing’s Power of Music Fund to enable Greater 91ֱ to become the UK’s first Centre of Excellence for Music and Dementia – hosted by 91ֱ Camerata. The project will also receive in-kind support from the University of Manchester and Alzheimer’s Society.

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

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Wed, 08 May 2024 14:57:29 +0100 https://content.presspage.com/uploads/1369/98f74c5a-d716-4843-949b-7a92a0a9512f/500_manchestercamerata039smusiccafeatthemonasteryingortoncopyrightduncanelliott.jpg?10000 https://content.presspage.com/uploads/1369/98f74c5a-d716-4843-949b-7a92a0a9512f/manchestercamerata039smusiccafeatthemonasteryingortoncopyrightduncanelliott.jpg?10000
Antipsychotics for dementia linked to more harms than previously acknowledged /about/news/antipsychotics-for-dementia-linked-to-more-harms-than-previously-acknowledged/ /about/news/antipsychotics-for-dementia-linked-to-more-harms-than-previously-acknowledged/627914Risks highest soon after starting drugs, underscoring need for increased caution in early stages of treatment, say expertsAntipsychotic use in people with dementia is associated with higher risks of a wide range of serious health outcomes compared with non-use, according to a new study from a collaboration across the Universities of Manchester, Nottingham, Edinburgh and Dundee.

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Antipsychotic use in people with dementia is associated with higher risks of a wide range of serious health outcomes compared with non-use, according to a new study from a collaboration across the Universities of Manchester, Nottingham, Edinburgh and Dundee.

Higher rates of stroke, blood clots, heart attack, heart failure, fracture, pneumonia, and acute kidney injury were observed in the study funded by the National Institute for Health and Care Research (NIHR)and published in today (17/04/24)

The findings show a considerably wider range of harms associated with antipsychotic use in people with dementia than previously acknowledged in regulatory alerts, with risks highest soon after starting the drugs, underscoring the need for increased caution in the early stages of treatment.

Despite safety concerns, antipsychotics continue to be widely prescribed for behavioural and psychological symptoms of dementia such as apathy, depression, aggression, anxiety, irritability, delirium, and psychosis.

Previous regulatory warnings when prescribing antipsychotics for these symptoms were based on evidence of increased risks for stroke and death, but evidence of other adverse outcomes was less conclusive amongst people with dementia.

To address this uncertainty, The University of Manchester researchers set out to investigate the risks of several adverse outcomes potentially associated with antipsychotic use in people with dementia.

The outcomes of interest were stroke, major blood clots (venous thromboembolism), heart attack (myocardial infarction), heart failure, irregular heart rhythm (ventricular arrhythmia), fractures, pneumonia, and acute kidney injury.

Using linked primary care, hospital, and mortality data in England, they identified 173,910 people (63% women) diagnosed with dementia at an average age of 82 between January 1998 and May 2018 who had not been prescribed an antipsychotic in the year before their diagnosis.

Each of the 35,339 patients prescribed an antipsychotic on or after the date of their dementia diagnosis was then matched with up to 15 randomly selected patients who had not used antipsychotics.

The most commonly prescribed antipsychotics were risperidone, quetiapine, haloperidol, and olanzapine, which together accounted for almost 80% of all prescriptions.

Potentially influential factors including personal patient characteristics, lifestyle, pre-existing medical conditions, and prescribed drugs were also taken into account.

Compared with non-use, antipsychotics were associated with increased risks for all outcomes, except ventricular arrhythmia. For example, in the first three months of treatment, rates of pneumonia among antipsychotic users were 4.48% vs 1.49% for non-users. At one year, this rose to 10.41% for antipsychotic users vs 5.63% for non-users. 

Risks were also high among antipsychotic users for acute kidney injury (1.7-fold increased risk), as well as stroke and venous thromboembolism (1.6-fold increased risk) compared with non-users.

For almost all outcomes, risks were highest during the first week of antipsychotic treatment, particularly for pneumonia.

The researchers estimate that over the first six months of treatment, antipsychotic use might be associated with one additional case of pneumonia for every 9 patients treated, and one additional heart attack for every 167 patients treated. At two years, there might be one additional case of pneumonia for every 15 patients treated, and one additional heart attack for every 254 patients treated.

This was a large analysis based on reliable health data. However, because it was an observational study, no firm conclusions can be drawn about cause and effect. And although a range of factors have been adjusted for, the possibility that other unmeasured variables may have affected the results can’t be ruled out.

Senior author Prof Darren M Ashcroft, University of Manchester, Director of NIHR Greater 91ֱ Patient Safety Research Collaboration (PSRC), NIHR Senior Investigator said: “In recent years, it has become clear that more people with dementia are being prescribed antipsychotic drugs, despite existing regulatory safety warnings. It is important that any potential benefits of antipsychotic treatment are weighed carefully against the risk of serious harm, and treatment plans need to be regularly reviewed in all health and care settings.” 

Co-investigator Prof Tony Avery, OBE, University of Nottingham, and NIHR Senior Investigator said: “For many years there have been safety concerns about the use of antipsychotics for managing the behavioural and psychological symptoms of dementia, with increased risk of stroke and death being reported. Our study shows that the use of antipsychotics in this group of patients is also associated with other harms including pneumonia, venous thromboembolism, myocardial infarction, heart failure, fracture, and acute kidney injury. This means that it is even more important to take account of risk of harm when considering prescribing these medicines, and to use alternative approaches wherever possible.”

Lead author Dr Pearl Mok, Research Fellow, University of Manchester said: “With the number of people living with dementia forecast to increase greatly in the coming years, further research into safer drug and more efficacious non-drug treatments for behavioural and psychological symptoms of dementia are needed.” 

Multiple adverse outcomes associated with antipsychotic use in people with dementia: population based matched cohort study is published in the doi: 10.1136/bmj-2023-076268

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Care home study highlights poor care for dementia residents with hearing problems /about/news/care-home-study-highlights-poor-care-for-dementia-residents-with-hearing-problems/ /about/news/care-home-study-highlights-poor-care-for-dementia-residents-with-hearing-problems/590347Hard of hearing people with dementia are not receiving the care they desperately need, according to a new study by University of Manchester researchers.

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Hard of hearing people with dementia are not receiving the care they desperately need, according to a new study by University of Manchester researchers.

The anonymised study of 10 staff from 8 different care homes, published in the journal Disability and Rehabilitation, revealed how residents were largely unable to access audiology services.

The problem is particularly relevant in the UK, where around 70% of long-term care home residents have dementia and 85% have hearing loss.

“People with dementia already are some of the most vulnerable people in society,” said Lead author Dr Hannah Cross, “And because hearing loss in these people can exacerbate agitation, confusion, increase loneliness and social withdrawal, the task of providing high quality care is even more important.”

All the participants in the study said audiologists rarely visit care homes compared to other healthcare professionals; two said they had never had seen one at all.

Though most of the staff interviewed by the researchers believed hearing support was beneficial, lack of training meant they did not have the knowledge to implement it effectively.

Staff, for example, found it hard to recognise if residents’ communication difficulties are caused by dementia or hearing loss.

Training on hearing loss for care home staff is not mandatory in the UK.

But basic hearing support training, hearing aids, communication techniques and other tools such as flashcards, would make a difference to residents’ quality of life, argue the researchers.

Dr Cross said: “Often residents with dementia are expected to attend audiology clinics outside their care home, mostly in a hospital or clinic. That causes stress and confusion for residents, on the occasions they are able to attend.

“For care home residents with dementia, it is completely up to professional care staff and audiologists to support them and their hearing needs.

“Effectively treating their hearing problems can really improve the quality of life for residents and their carers.”

The study was conducted online at the height of the pandemic, when care homes were largely cut off from public access.

However the problems caused by the pandemic seemed to make little difference to audiology services received by residents-  who were already receiving minimal care.

She added: “We think a radical overhaul of training and service provision is needed if we are to help people living in care homes with dementia and hearing loss.

“Staff Hearing Champions’ have been recommended, though without proper incentivisation it’s not clear how much of an impact they would make for staff who already have a very high workload.

“But without a doubt, greater co-operation between care homes and audiology services is desperately needed, so residents have equitable access to healthcare services, ideally within the care home.

“And training for staff around hearing aid maintenance and communication techniques will also make a difference.”

The paper “We’re just winging it”. Identifying targets for intervention to improve the provision of hearing support for residents living with dementia in long-term care: An interview study with care staff is available

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and social withdrawal, the task of providing high quality care is even more important ]]> Tue, 12 Sep 2023 15:13:00 +0100 https://content.presspage.com/uploads/1369/500_hearing-impaired.jpg?10000 https://content.presspage.com/uploads/1369/hearing-impaired.jpg?10000
People with dementia in care homes aren’t getting enough help with their hearing loss – new survey /about/news/people-with-dementia-in-care-homes-arent-getting-enough-help-with-their-hearing-loss--new-survey/ /about/news/people-with-dementia-in-care-homes-arent-getting-enough-help-with-their-hearing-loss--new-survey/582447Most care home residents have both dementia and hearing loss, which can leave them feeling lonely and depressed.

Hearing loss and dementia both cause difficulties with listening, understanding and communicating. This can lead to breakdowns in relationships because something as simple as a conversation with a loved one can become impossible.

People with dementia often don’t know, or can’t communicate, that they have problems with their hearing. This means that a lot of the time, their carers don’t know either.

Crucially, many people with dementia, and especially those living in care homes, rely on carers to support their hearing needs. This might mean helping with hearing aids or other hearing devices, using communication techniques, writing things down or using flashcards and making sure background noise isn’t too loud.

When hearing care is given properly it can improve residents’ , mood and engagement with peers. Unfortunately, in a new study, my colleagues and I found that only of residents with dementia in UK care homes are given help with their hearing loss.

Poorly supported hearing loss leaves residents at risk of emotional and behavioural problems, worsened confusion and difficulties communicating with important people in their life like family, friends, carers and healthcare professionals. In the same study, just 27% of care staff said that they check that residents’ hearing aids are working properly. This is a huge problem as most residents with dementia aren’t able to do this themselves.

Complicated reasons

The survey results also revealed that the reasons residents with dementia aren’t receiving help with their hearing are complicated. The biggest problem in care homes appears to be access to resources, such as enough time, enough staff or enough things like hearing aid batteries or flashcards. Staff who completed the survey said that not enough resources in the care homes made it difficult to provide hearing-related care to residents with dementia.

Another part of the problem is that care staff don’t always have the relevant knowledge and skills to help residents with their hearing problems. Just under 25% of staff reported having had any training on hearing loss (despite over of residents having hearing loss), but almost all said that they wanted this training to be provided.

Hearing loss isn’t always prioritised in care homes. Compared to dehydration, infections or injuries, hearing and communication problems don’t cause immediate risk or physical harm to residents. So helping residents to hear well isn’t often a priority for staff, who have limited time and a heavy workload. That doesn’t mean that hearing and communicating aren’t essential for a person’s wellbeing and happiness.

Hearing loss isn’t always prioritised.

Results from our survey show that people with dementia living in care homes are not getting the care that they need and deserve to help them to hear, understand and communicate. Care home residents are often very vulnerable, and being able to hear well is essential to maintaining a good quality of life and engaging with .The Conversation

, Postdoctoral Research Associate,

This article is republished from under a Creative Commons license. Read the .

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Tue, 25 Jul 2023 22:20:30 +0100 https://content.presspage.com/uploads/1369/500_hearing-impaired.jpg?10000 https://content.presspage.com/uploads/1369/hearing-impaired.jpg?10000
My work investigating the links between viruses and Alzheimer’s disease was dismissed for years – but now the evidence is building /about/news/my-work-investigating-the-links-between-viruses-and-alzheimers-disease-was-dismissed-for-years--but-now-the-evidence-is-building/ /about/news/my-work-investigating-the-links-between-viruses-and-alzheimers-disease-was-dismissed-for-years--but-now-the-evidence-is-building/547789This article is part of the Insights Uncharted Brain series. There are many competing theories about what causes Alzheimer’s disease. Here, Ruth Itzhaki reflects on a career dedicated to one of the more controversial lines of research.

When I was about seven or eight, I asserted that I wanted to be a scientist, or so my parents told me years later, even though I would have had little idea of what that word meant. In my mind, I was perhaps associating it with making momentous discoveries that were immediately recognised and applauded by the whole world. Soon after, I avidly read , the book by Eve Curie about her mother Marie and how she overcame poverty and the many challenges faced by women in the late 19th and early 20th century to become a Nobel prize-winning scientist. Marie Curie became my lodestar for the future and thanks to my parents’ support and self-sacrifice, I did eventually become a scientist.

Marie Curie won two Nobel Prizes in 1903 for Physics and in 1911 for Chemistry.

Many years later, I found myself confronting what seemed like insuperable odds just as Curie did, though in very different circumstances. I have been an independent researcher since the age of 26 when I completed my PhD. My subsequent research in a Cambridge University department on (a complex of DNA and proteins) went well. Then, after eight years, my husband and I moved to 91ֱ where the head of the institute where I worked for 12 years decided to end my contract, leaving me jobless and lab-less.

In the decades that followed, my research into viruses as a possible cause of Alzheimer’s disease was greeted with much hostility, and almost all my funding applications were refused: a hostility that has continued for 25 years and which has only recently abated, thanks to .

 

I, along with my tiny research group, survived only through the award of a few small grants from more open-minded charities and companies interested in new approaches. Once I even managed to swap a business class ticket to the US (that was provided for me to speak at a conference) for economy class, so I could use the several thousand-dollar surplus for my lab instead.

But, after years of struggle, there is finally hope for this line of research. An for Alzheimer’s – the first ever – is now taking place at Columbia University. This study is building on the years of work done by my team. Meanwhile, our is looking into the way infectious illnesses increase the risk of Alzheimer’s.

Dementia brought home

Career and academic challenges can always be balanced with the help of a support network: a family. I was always lucky with mine. During many of these years, my husband, Shaul Itzhaki, a retired academic who had worked on nucleic acid biochemistry, supported my struggles and never once suggested that I change to a safer, more conventional and non-contentious topic. He was always touchingly happy with any successes I had, and I will always remember our celebratory days when I was awarded a for Medical Research, and later a Newnham College Fellowship, during our years in Cambridge.

Sadly, he died in April 2022, after suffering for about ten years from vascular dementia (a dementia distinct from Alzheimer’s disease but with many similar symptoms) and latterly, from a fractured femur that disabled him. The last four or so years were particularly hard to endure as he became increasingly aware of his failing memory. The term “brain fog” is often used in this context, but to me, it seemed more like a mist through which he could very dimly see or perceive what he was struggling to recall; the frustration – desperation, perhaps – that he felt at his inability to grasp, hold, then voice these elusive thoughts was pitiful.

The author in her laboratory. Author provided

I often took him to talks on topics such as the climate, migration, history and ageing, hoping to keep his mind occupied. He seemed to understand many of them, but afterwards, he was quite unable to discuss them, as his memory and ability to speak were declining inexorably. Communication of any type between us was slowly becoming impossible, although he was the person with whom I had once shared my thoughts and hopes, just as he had done with me, and it became particularly sad and unsettling, as we had had so many interests in common. Eventually came the realisation that I had “lost” him. It was a bereavement – the loss of him as a person, loss of a mind, not the death of a body; he was existing but not really living.

Another common feature of dementia – sudden changes of mood – affected him during these years. He had been a generally gentle, courteous person. But when, at times, the illness overcame his natural traits, he became violently angry, often for no obvious reason. Part of the problem was that his sense of location had faltered and often during the evenings he became convinced that we were about to leave and go “home” to 91ֱ, a place we had left in 2013. He would ask repeatedly and anxiously when we had to leave to catch the train to get there. Television programmes, even those on historical events, which would have been of particular interest to him, had to be vetted as he lost himself within them. So that after watching one that dealt with, say, the horrors of war, he thought that he was actually living in that frightening world.

Of course, there are so many families going through what my family went through. And there will be many more. That fact has provided one of the main motives for my pursuing my research, despite all the difficulties that have come with it.

Early challenges

During the last five years, studies supporting the idea of a viral role in Alzheimer’s disease have . Despite this, there is still much opposition to the concept, while many in the field still ignore it.

I am often asked why there has been such hostility. A charitable explanation is that the possible role of a virus in dementia is difficult for others to assess because it straddles two very different topics: virology and Alzheimer’s disease. Also, many cannot grasp the concept that people can be infected but not affected (asymptomatic, when the virus resides in the brain without causing symptoms) so they dismiss the data. Either way, I have always stressed that many possible factors lead to Alzheimer’s disease – a viral role is just one of them.

My interest in this particular area began, rather unpromisingly, in 1978 when the aforementioned head of institute ended my work contract. The reason he cited was that my research on chromatin, and on the effects of carcinogens on chromatin, was “rather individualistic”. I thought this was an extraordinarily inept criticism, as I had generally been acknowledged as being an innovative researcher, and innovation is surely the key to good research. The funding body offered me a post in Glasgow, but that would have meant leaving my husband and children in 91ֱ.

Luckily, I was immediately given a home in the lab of a medical virologist friend, Richard Sutton. Sutton was an eccentric and pioneering man. He was dogged and wiley, in an endearing way. It was Sutton who first suggested to me the possibility of viral involvement in Alzheimer’s disease.

The argument for the role of the cold sore virus, herpes simplex type 1 (HSV1), in Alzheimer’s disease was first suggested by American neuropathologist in 1984. But he did not pursue the idea in any practical way. Sutton and I carried out what was probably the first convincing experiment seeking the DNA of HSV1 in the human brain. We had predicted that it might be detectable in the brain of immunosuppressed patients because in the absence of an adequate immune system to keep it under control, the virus would be able to multiply. We did indeed find it, and published our in 1986.

The central concept

is mainly transmitted by oral-to-oral contact, causing oral herpes (cold sores). Globally, an estimated 3.7 billion people under age 50 (67%) have HSV1 infection. Most infections are asymptomatic.

Over the years, the supportive data we gathered for the key role of HSV1 in Alzheimer’s led me to propose a central concept: that HSV1 is a major cause of Alzheimer’s disease; that in many people, the virus travels to the brain, probably in middle age, and remains present there in latent (dormant) form, but is frequently activated by episodes of stress, head injury, immuno- suppression and infections. These “reactivations” lead to productive HSV1 infection and inflammation (and consequent damage to the brain) over the years. The accumulated damage leads eventually to the development of the disease.

The possible role of HSV1, specifically, was proposed for three main reasons. The locations of the damage the virus causes in the brain during the rare but extremely serious acute disease herpes simplex encephalitis (HSE) – caused by HSV1 – are precisely the main sites of damage found in the brains of patients with Alzheimer’s disease.

The other reasons for implicating HSV1 were that it is very common, affecting of the population (in earlier decades more probably 90%), and its ability to remain dormant in the body for years.

These features meet two main characteristics of Alzheimer’s disease: that it is all too common, and that it almost always waits until old age to strike its victims. Certain other infectious agents are probably involved too, perhaps individually or in combination, but so far these have been less well studied than HSV1.

The laboratory work

I was offered a more long-term prospect for my research in a department of the University of Manchester’s Institute of Science and Technology. The head of the department, John Cronley Dillon, was a larger-than-life character, a bon viveur and art lover, full of novel ideas and wild enthusiasm. He encouraged me to build up a research group (minuscule though it was) and eventually we started the research on HSV1 and Alzheimer’s.

It was known that when a person is infected with HSV1, the virus resides lifelong in the peripheral nervous system (PNS) – the part of the nervous system that doesn’t include the brain and the spinal cord — in a latent state. It is dormant until it is activated by events such as stress. In 1989 we decided to look for HSV1 in the brain, using the technique of polymerase chain reaction, or PCR. We used to examine DNA extracted from autopsy specimens of Alzheimer’s disease patients.

This was the first time PCR, then a new technique, had been used for this purpose. The principle of PCR is to detect a specific sequence in the target DNA by chemically amplifying it, thereby making it vastly more sensitive than the methods used in the previous few studies seeking HSV1 DNA in the brain. However, this method was prone to contamination and could produce spurious data. This meant that my poor PhD student, Gordon Jamieson, spent many frustrating months trying to get it to work satisfactorily. So we were overjoyed when , unambiguously, the DNA of the virus in the brain in 1991.

This was the first microbe to be detected in the human brain (in controls, in the absence of a disease). We were puzzled, though, as to why the virus was present in a high proportion of brains – both control brain specimens (people who had not been diagnosed with Alzheimer’s) as well as the brains of patients who had died with the disease. This near equality of prevalence does not undermine the role of HSV1 in Alzheimer’s, as some in the field have asserted. Many of the control brains were, in fact, infected with HSV1 but were asymptomatic.

So people can be infected but be asymptomatic, indicating that infection alone is not sufficient to cause disease. A very relevant example is that of cold sores which afflict only a proportion (ranging from 20-40%) of those infected with HSV1. The other 60-80% are asymptomatic. Clearly, another factor determines the degree of damage caused by the virus.

Other supporting factors

That was something we identified in 1997 when that the virus confers a high risk of Alzheimer’s disease when in the brains of people who carry a specific genetic factor. We were extremely excited by this finding, but also apprehensive about adverse reactions of some in the field, as had occurred before when we discovered HSV1 DNA in elderly brains.

So we were even more excited when, after I’d suggested examining cold sore sufferers (via a small blood sample), to find what variant of the specific genetic factor they carried, we discovered that it was the same variant as for Alzheimer’s. In other words, the same variant of the genetic factor conferred a risk of damage in the peripheral nervous system, as well as the central nervous system.

Of course, the question arose as to what it is doing, if anything, in the brain. Is it residing there merely as a passenger, doing little or nothing, or does it cause damage?

We by examining cerebrospinal fluid (the liquid that bathes the brain) looking for antibodies to the virus. We detected these antibodies in most samples of cerebrospinal fluid, again, consistently, in both Alzheimer’s patients and those in the age-matched control groups. This showed that indeed the virus was not just a passive fellow traveller.

We then decided to find if there were direct links between the effects of HSV1 infection and Alzheimer’s. Very hesitantly, like explorers in a new continent, we infected human brain cells with HSV1, then stained the cells with antibodies to the specific abnormal proteins seen in Alzheimer’s brains – and .

To our surprise and delight we saw accumulations of both types of protein. Also, we found amyloid deposition in the brains of infected mice. However, getting the results published was a Sisyphean task and journal reviewers’ comments were often incredulous.

We subsequently used a very complex technique (in-situ PCR) which revealed that in tissue sections of brain, most of the viral DNA was located very specifically within amyloid plaques. This suggested that amyloid might act to cage the virus, thereby inactivating it. All this work provided strong support for a major role of HSV1 in Alzheimer’s, and much has since been extended by .

that anti-herpes treatment was protective because it substantially reduced the damage level in the cell cultures we were testing. This further supported a role for the virus in the disease – and pointed to a potential treatment.

A heretic shunned

But a viral role in the development of Alzheimer’s was still seen as heretical by many researchers, so our papers continued to be rejected by one journal after another.

For academics, having research published in top journals is often central to keeping your job and career progression because of the perceived value to universities (related to university league table rankings, supposed research quality and performance management).

Similarly, almost all of our grant applications over that 25 years were refused, too, which was even more serious as without funding, the people in my lab couldn’t be paid nor materials bought. I was very fortunate in having three successive post-doctoral researchers, Woan-Ru Lin, Curtis Dobson, and especially Matthew Wozniak, who were so dedicated that they were willing to continue to work even when on repeated short-term contracts (sometimes for less than 12 months).

So most of my time was taken up in writing research proposals and filling in application forms, interspersed with writing and submitting articles to journals, and when rejected, trying another. I had to face derision and hostile rants unaccompanied by any meaningful, scientific criticism from reviewers. A typical example was: “This grant essentially centres on a question of belief; are viruses important in Alzheimer’s disease, in my view they are not.”

Each rejection seemed like the end of the world. It was a heart-stopping moment when opening the envelope or email from the funding body and scanning the lines in the hope of finding the words, “I’m pleased to tell you …” – though all too often, I found the words, “I regret to tell you”. I hid, weeping tears of despair, while a part of my brain questioned whether the work really was nonsensical and whether the ideas were just wild fantasies.

At conferences, I was often shunned by prominent people in the field. My poster presentations were too (posters were the poor man’s alternative to giving a talk, a privilege I was rarely given). Although, hearteningly, I found that younger people were interested and excited by the research.

Later, I benefited from the generosity of a colleague, . Kulikowski was another eccentric who lived an upside-down life, working at night and either sleeping during the day or else amusing himself by lobbing provocative remarks at colleagues. He was really interested in our research, despite working in the totally different field of vision research.

I do realise of course that many others have suffered refusals of grant applications, and I understand how especially heartbreaking it is for those at the start of their career, as it usually means the end of all their hopes and dreams of becoming a scientist. I realise too that I had been exceptionally lucky in being able to do such utterly engrossing work – a continuous, totally fascinating puzzle and challenge – and in having a loving family.

But after each rejection my fear that the work would end was overwhelming. When I did get a grant – any grant – I was elated: the world sparkled. I was so happy and exuberant, not just with the funding but with the fact that some people in the field were supportive of, or at least willing to consider, a possible role for HSV1. I felt so encouraged, vindicated and ready to face any challenge in my work or from fellow scientists, and brimming over with ideas for new approaches.

Quite often in the later years, some strongly supported our central concept. But there was a huge divide between them and its opponents. And the hostility continues to this day. In 2019, an application by a colleague to a US funding body for a clinical trial of an antiviral for Alzheimer’s was refused. I was involved as an adviser because it was based on my lab’s research, though I was not an applicant.

One reviewer said: “This application is peripherally related to the idea that Human Herpes Virus (HHV) infection could play a role in Alzheimer’s disease pathogenesis … the evidence is weak, the supporting data are weak.” The second reviewer proclaimed: “The novelty of this approach appears to be quite lacking. The suggestion of latent microbe-based activation by (unknown) factors coincident with a ‘deteriorating immune system’ as the cause for Alzheimer’s seems like hand waving”: poetic perhaps, but hardly a brilliant display of scientific disputation. In fact, no adverse comments had ever been supported by any scientific argument, despite a public assertion once by a senior government official that the HSV1/Alzheimer’s work had been refuted (though when challenged, he was unable to cite any such article).

Most researchers acknowledge that new, surprising and challenging ideas should be viewed with caution. But ideas should not be dismissed without any deliberation. Perhaps another major reason for the hostility is that many people in the field have been working for several decades on amyloid as a cause, and so are understandably distressed on learning that it might not be a direct cause, except in rare familial cases. This occurs despite our repeatedly stressing that numerous factors contribute to Alzheimer’s and amyloid is clearly an important feature.

Exciting developments

But, as the Columbia University study shows, attitudes to the topic of Alzheimer’s and HSV1 are slowly, but steadily, improving. Of course, I am very happy about this, for the sake of patients and their carers. And I have to admit that recognition of the work on HSV1 is personally gratifying as, like most people, I am heartened to know that my work has achieved something.

I am pleased that the research that I and others are carrying out is now moving forwards in even more exciting directions, including the use of a 3D bioengineered human which, when infected with HSV1, displays many Alzheimer’s-like characteristics.

We are now investigating the effects of and a possible role for vaccinations. This follows an explanation I with my then-senior post-doctoral associate, Curtis Dobson, to account for that certain vaccines decreased the risk of Alzheimer’s disease. We suggested that infections might reactivate latent HSV1 in the brain and that vaccines might decrease the consequent risk of Alzheimer’s disease by reducing the occurrence of such infectious diseases.

For example, in the case of shingles – which is caused by another type of herpes virus, varicella zoster virus (VZV) – I carried out with 91ֱ University epidemiologists showed that vaccination against the disease may protect against the development of Alzheimer’s. Two subsequent studies showed the same result. However, much further work needs to be done to elucidate the findings that certain types of vaccine appear to reduce the risk of Alzheimer’s.

Scraping of a skin lesion showing characteristic giant cells in a patient with chicken pox (Varicella Zoster Virus), a type of herpes.

I, along with researchers at Tufts University, then if VZV (which also causes chickenpox) plays a role similar to HSV1 in causing brain damage leading to the development of Alzheimer’s.

showed that VZV infection of the cells does not lead to the formation of the main characteristic Alzheimer’s features in the brain. However, VZV infection does result in certain other Alzheimer’s-like features, including increased inflammation. And – importantly – VZV was seen to reactivate the latent HSV1 infection in the brain model, with the consequent occurrence of Alzheimer’s-like characteristics. This is consistent with our suggestion that infections reactivate latent HSV1 in the brain.

The that another herpes virus, Epstein Barr, is a cause of another brain disease (multiple sclerosis) strengthens the likelihood of viral involvement in certain other such diseases.

We now plan to find out if other infections cause HSV1 reactivation from latency. If they do, the obvious corollary would be to try to limit infections by vaccination, and by improving standards of hygiene and living conditions – a particular need in developing countries – to reduce microbial transmission.

In addition, we now have some exciting preliminary findings suggesting that percussive brain injury (for example, concussion) can cause HSV1 reactivation. This is a very different type of injury from infection and the results suggest that the virus might be pivotal in the brain’s response to diverse types of damage.

This is an exciting field of study and I hope bright young scientists will enter it. Nobody said being a scientist was easy, but with the right encouragement from family, friends and open-minded peers, it is amazing what challenges can be overcome.

, Professor Emeritus of Molecular Neurobiology at the University of Manchester and a Visiting Professorial Fellow,

This article is republished from under a Creative Commons license. Read the . For you: more from our :

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Wed, 16 Nov 2022 08:44:59 +0000 https://content.presspage.com/uploads/1369/500_ruthitzhaki.jpg?10000 https://content.presspage.com/uploads/1369/ruthitzhaki.jpg?10000
91ֱ of Alzheimer’s patients launched in bid to find early test /about/news/study-of-alzheimers-patients-launched-in-bid-to-find-early-test/ /about/news/study-of-alzheimers-patients-launched-in-bid-to-find-early-test/535435A new study by scientists at PharmaKure -  a UK based pharmaceutical company spun out from The University of Manchester -is to examine blood biomarkers in Alzheimer’s disease patients.

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A new study by scientists at PharmaKure -  a UK based pharmaceutical company spun out from The University of Manchester -is to examine blood biomarkers in Alzheimer’s disease patients.

The study of the patients tested by either PET brain imaging or amyloid deposits in cerebrospinal fluid (CSF) aims to identify a blood test which could help with earlier diagnosis of the disease.

Certain blood biomarkers of amyloid- (Total, A40 and A42), aggregated α-synuclein, aggregated Tau (Total and pTAU (181), NFL and DJ-1 have been associated with Alzheimer’s Disease pathology.

The study is to evaluate the relationship of all these aggregated forms of biomarkers, including oligomers in the blood, to historical PET scan and CSF findings.

Launched this month (October 2022), participants of the study will be aged 50 to 80, who have had an Amyloid PET scan or CSF Amyloid assessment in the last five years that diagnosed the disease.

Dr Farid Khan, CEO at PharmaKure said: “Every three seconds someone in the world develops dementia. 850,000 in the UK and 44 million worldwide suffer from Alzheimer’s or dementia related illnesses and this takes a terrible toll on patients and their families.

“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.

“Our hope is this study may lead to a blood test which could help with earlier diagnosis of this disease.

“That could lead to better health outcomes, lower health system costs and improved quality of life of patients by offering treatments earlier.”

Professor Andrew Doig of The University of manchester and co-founder of PharmaKure said: “Blood tests give further understanding of Alzheimer’s Disease pathology and an insight into formulating strategies for improving clinical outcomes by selecting future treatments that are tailored to the right patient group.

“In the progression of Alzheimer’s Disease, it is not clear whether blood biomarkers are associated with brain imaging scans or amyloid in the CSF.  This study could enable us to learn how to get early warning signs of cognitive decline in blood.”

Alzheimer's disease is a fatal illness that causes progressive decline in memory and other aspects of cognition. It is the most common form of dementia, accounting for 60 to 80 percent of all cases.

In 2020, the total cost of cost of care for people with dementia in the UK was £34.7 billion. Globally, the cost was $360 billion and by 2050 the costs could be a $1 trillion according to Alzheimer’s Research UK.

In the US alone, there was an increase of 8 million new caregivers from 2015 to 2020.

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Tue, 04 Oct 2022 11:05:00 +0100 https://content.presspage.com/uploads/1369/500_istock-000083379035-full.jpg?10000 https://content.presspage.com/uploads/1369/istock-000083379035-full.jpg?10000
Researchers win international award for study on supporting care home residents /about/news/researchers-win-international-award-for-study-on-supporting-care-home-residents/ /about/news/researchers-win-international-award-for-study-on-supporting-care-home-residents/527503A study led by researchers at the University of Manchester has been selected by the Mather Institute as the Gold Award recipient of their 2022 Innovative Research on Aging Awards.

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A study led by researchers at the University of Manchester has been selected by the Mather Institute as the Gold Award recipient of their 2022 Innovative Research on Aging Awards.

Now in their 7th year, the awards were created by Mather Institute to inspire evidence-based next practices that can improve the lives of older adults.

As an internationally recognized resource for research and information about wellness, aging, and trends in senior living, Mather Institute invited submissions by researchers from universities and organizations around the world for this year’s awards, which cover a variety of categories from Aging in Place to Technological Advancements for Older Adults, and beyond. The University of Manchester research was honoured in the award category of ‘Health and Well-Being of Senior Living Residents’ based on an innovative 2021 study on the importance of purpose in life to people living in long-term care facilities.

The study authors, Dr Rebecca Owen, Dr Laura Brown, and Professor Katherine Berry, from the Division of Psychology and Mental Health at the University of Manchester, interviewed residents from four care homes about their views and experiences about:

  • What purpose in life means to them.
  • What helps give them a sense of purpose.
  • The extent to which they would like to engage in more purposeful activities.
  • How long-term care providers could help or hinder this.

 

They then analysed the interviews for common themes that revealed opportunities for senior living providers to support residents to maintain a sense of purpose in their facilities.

“The Innovative Research on Aging Award honours the study authors for providing insights into the importance that long-term care residents place on purpose in life, how purpose in life can be promoted through resident programs, and the barriers and facilitators to engagement that residents face,” said Cate O’Brien, PhD, VP and Director of Mather Institute. “These awards honour excellent applied research with practical implications for the senior living industry. We hope these award-winning studies will spark ideas in senior living organizations across the country and around the world.”

“We are delighted that our research has been recognised by the Mather Institute in this way”, said study author Dr Laura Brown. “Our findings clearly show how important it is to many care home residents to maintain a sense of purpose, and provide valuable insights into how care home staff can support this. We hope that this award enables long-term care facilities around the world to benefit from these findings in order to help their residents to age well.”  

A full complimentary report on the Innovative Research on Aging Award recipients, Revealing Research 2022, is available for download at . The full version of the original research (Owen et al., 2021), published in the journal ‘Aging and Mental Health’, can be found

Founded in 1941, Mather is a nondenominational not-for-profit organization based in Evanston, Illinois, that creates Ways to Age Well.SM Mather Institute is its research area of service, and serves as an award-winning resource for research and information about wellness, aging, trends in senior living, and successful aging service innovations. To learn more, find your way to .

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Fri, 02 Sep 2022 09:11:07 +0100 https://content.presspage.com/uploads/1369/500_stock-photo-helping-hands-care-for-the-elderly-concept-240339163.jpg?10000 https://content.presspage.com/uploads/1369/stock-photo-helping-hands-care-for-the-elderly-concept-240339163.jpg?10000
Researcher wins award for film raising awareness of Deaf people affected by dementia. /about/news/researcher--wins--award-for-film-raising-awareness-of-deaf-people-affected-by-dementia/ /about/news/researcher--wins--award-for-film-raising-awareness-of-deaf-people-affected-by-dementia/523355A gallery of “breath-taking” images and videos which shine a light on crucial dementia research have been released today by Alzheimer’s Society’s first ever research image competition which was won by a University of Manchester researcher.

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A gallery of “breath-taking” images and videos which shine a light on crucial dementia research have been released today by Alzheimer’s Society’s first ever research image competition which was won by a University of Manchester researcher.

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 *

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Tue, 09 Aug 2022 08:15:51 +0100 https://content.presspage.com/uploads/1369/500_aslogo.png?10000 https://content.presspage.com/uploads/1369/aslogo.png?10000
Viral role in Alzheimer's Disease discovered /about/news/viral-role-in-alzheimers-disease-discovered/ /about/news/viral-role-in-alzheimers-disease-discovered/522682Researchers from Oxford’s Institute of Population Ageing, Tufts University and the University of Manchester have discovered that common viruses appear to play a role in some cases of Alzheimer’s disease (AD).

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Researchers from Oxford’s Institute of Population Ageing, Tufts University and the University of Manchester have discovered that common viruses appear to play a role in some cases of Alzheimer’s disease (AD).

The causes of most cases of Alzheimer’s are currently unknown, but there is growing evidence to suggest microbial organisms are involved, in particular, herpes simplex virus type 1 (HSV-1), the so-called cold sore virus.  This virus has long been known to reside lifelong, after infection in the peripheral nervous system, usually in a dormant form, from which it can be reactivated by events such as stress and immune-mediated mechanisms.

Professor Ruth Itzhaki has been researching the potential role of HSV-1 in AD for more than 30 years, beginning at the University of Manchester, where her team discovered HSV-1 DNA is present in the human brain in a high proportion of older people - the first microbe to be detected definitively in normal human brains. The researchers later indicated that the virus, when in the brain, in combination with a specific genetic factor, confers a high risk of developing AD. 

Subsequent studies revealed major links between the effects of the virus and the characteristic features of AD, and showed also that treating laboratory-grown HSV1-infected cells with antivirals protected against AD.

Further strong support for a major causal role for HSV-1 in AD was demonstrated by Dana Cairns in David Kaplan’s laboratory at the Tufts School of Engineering, using a 3D bioengineered human brain tissue model. This study showed HSV-1 infection of human-induced neural stem cells (hiNSCs) caused changes that resembled changes observed in AD patients’ brains - amyloid plaque-like formations (PLFs), gliosis, neuroinflammation, and decreased functionality.

In the latest study, published today in the Journal of Alzheimer's Disease, Professor Itzhaki, now working at Oxford’s Institute of Population Ageing, jointly with researchers at Tufts, expanded the study of viral roles in AD to include another type of herpes virus, varicella zoster virus (VZV), which causes chickenpox and shingles.

They investigated whether VZV can play a similar role to HSV-1 - that might implicate VZV directly in AD development. Using both laboratory-grown brain cells and a 3D brain model, the researchers looked at whether VZV infection caused the accumulation of beta amyloid (Aβ) and abnormally phosphorylated tau (P-tau) and other AD-like features, as is the case with HSV-1.

They found VZV infection of lab-grown brain cells does not lead to the formation of Aβ and P-tau, the main components respectively of the characteristic AD plaques and neurofibrillary tangles in the brain. However, they did find VZV infection resulted in both gliosis and up-regulation of inflammatory cytokines. This makes it unlikely that VZV could be a direct cause of AD, but suggests instead it has an indirect effect by reactivating dormant HSV-1.

They also found upon VZV infection of cells containing latent HSV-1, reactivation of HSV1 occurred and a dramatic increase in levels of Aβ and P-tau, suggesting severe VZV infection in humans, as in shingles, could reactivate latent HSV-1 in brain, which, in turn, could lead to formation of AD-like damage.

Professor Itzhaki, Visiting Professorial Fellow at the Oxford Institute of Population Ageing and Emeritus Professor at the University of Manchester, said: “This striking result appears to confirm that, in humans, infections such as VZV can cause an increase in inflammation in the brain, which can reactivate dormant HSV-1

“The damage in the brain by repeated infections over a lifetime would lead eventually to the development of AD/dementia.

“This would mean vaccines could play a greater role than just protecting against a single disease, because they could also indirectly, by reducing infections, provide some protection against Alzheimer’s.”

In fact, researchers at 91ֱ University in an epidemiological study, together with Professor Itzhaki, discovered that vaccination against shingles reduced the risk of AD/dementia (Lophatananon et al., BMJ Open, 2021).

The results should help to elucidate the pathways whereby infections increase the risk of AD/dementia and the ways this disease could be combatted by using appropriate antivirals for treatment, or just possibly, for prevention.

Current studies by the three authors, not on infections but using the same cell model system, support the probability that reactivation of HSV1 in brain is pivotal to the brain’s response to damage and to the development of AD.

The full paper, ‘Potential involvement of Varicella Zoster Virus in Alzheimer’s Disease via reactivation of quiescent Herpes Simplex Virus Type 1’, is published in the Journal of Alzheimer's Disease.

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Tue, 02 Aug 2022 03:25:00 +0100 https://content.presspage.com/uploads/1369/500_hsv-1-em.png?10000 https://content.presspage.com/uploads/1369/hsv-1-em.png?10000
Blood vessel breakthrough major step towards Alzheimer’s treatment /about/news/blood-vessel-breakthrough-major-step-towards-alzheimers-treatment/ /about/news/blood-vessel-breakthrough-major-step-towards-alzheimers-treatment/514855Discovery could lead to development of drugs that halt disease progression and stop memory lossA breakthrough in our understanding of Alzheimer’s disease has revealed changes to blood vessels in the brain, potentially presenting a path for developing new drugs to help fight the disease, according to University of Manchester research funded by the British Heart Foundation (BHF) and published today in Proceedings of the National Academy of Sciences (PNAS)1

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A breakthrough in our understanding of Alzheimer’s disease has revealed changes to blood vessels in the brain, potentially presenting a path for developing new drugs to help fight the disease, according to University of Manchester research funded by the British Heart Foundation (BHF) and published today in Proceedings of the National Academy of Sciences (PNAS)1.

Alzheimer’s Disease is traditionally thought of as a disease of the brain cells, where a protein called Amyloid-beta (Aβ) accumulates and forms plaques. There is growing evidence that the blood supply to the brain is also affected, however, how this happens is unknown.

Now, researchers at the University of Manchester have found that a smaller version of the protein - called Amyloid-β 1-40 (Aβ 1-40) - builds up in the walls of the small arteries and reduces blood flow to the brain.

The surface of the brain is covered with small arteries, called pial arteries, that control the brain’s supply of blood and oxygen. If these arteries become narrowed for too long, the brain can’t get enough nutrients. This is one of the causes of memory loss seen in people with the disease.

When the team looked at pial arteries of older mice with Alzheimer’s that produced too much Aβ1-40, they found that the arteries were narrower compared to those of healthy mice.

This narrowing was found to be caused by Aβ 1-40 switching off a protein called BK in cells lining blood vessels. When it is working normally, BK sends a signal which causes arteries to widen.

To confirm that Aβ 1-40 stopped BK from working properly, they soaked healthy pial arteries in Aβ 1-40 and measured the signals sent by the BK protein after one hour. Aβ 1-40 weakened these signals, which caused the arteries to narrow.

The researchers now plan to investigate which part of Aβ 1-40 blocks the BK protein, so drugs to stop this from happening can be developed and tested as a much-needed treatment to prevent Alzheimer’s disease from progressing and save people the heartache of losing their memory.

Dr Adam Greenstein, lead BHF-funded researcher and Clinical Senior Lecturer in Cardiovascular Sciences at the University of Manchester said:  “To date, over 500 drugs have been trialled as a cure for Alzheimer’s disease. All of them have targeted the nerves in the brain and none of them have been successful. By showing exactly how Alzheimer’s disease affects the small blood vessels, we have opened the door to new avenues of research to find an effective treatment.”

Professor Metin Avkiran, Associate Medical Director at the British Heart Foundation said: “This research is an important step forward in our understanding of Alzheimer’s disease. More than half a million people in the UK are living with the condition, and that number is set to rise as our population gets older. These findings could lead to a desperately needed treatment for this devastating condition.”

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Mon, 20 Jun 2022 20:00:00 +0100 https://content.presspage.com/uploads/1369/500_istock-000083379035-full.jpg?10000 https://content.presspage.com/uploads/1369/istock-000083379035-full.jpg?10000
Trial of comms scheme for carers of people with dementia launches /about/news/trial-of-comms-scheme-for-carers-of-people-with-dementia-launches/ /about/news/trial-of-comms-scheme-for-carers-of-people-with-dementia-launches/506729A unique psychological and social intervention which trains family and informal carers to communicate more effectively with the person they support is being trialed in 91ֱ.

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A unique psychological and social intervention which trains family and informal carers to communicate more effectively with the person they support is being trialed in 91ֱ.

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.”

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Wed, 18 May 2022 14:08:00 +0100 https://content.presspage.com/uploads/1369/500_shutterstock-1754653154.jpg?10000 https://content.presspage.com/uploads/1369/shutterstock-1754653154.jpg?10000
Scientists launch study of how ageing is influenced by skin bacteria. /about/news/scientists-launch-study-of-how-ageing-is-influenced-by-skin-bacteria/ /about/news/scientists-launch-study-of-how-ageing-is-influenced-by-skin-bacteria/497474A new network of scientists from across the UK, including The University of Manchester, has been launched to study how ageing is influenced by skin bacteria.

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A new network of scientists from across the UK, including The University of Manchester, has been launched to study how ageing is influenced by skin bacteria.

The move follows recent studies which have shown communities of bacteria that live in the skin - known as the microbiome - are a more accurate predictor of age than the gut microbiome.

However, there is little knowledge on the processes involved in which the skin microbiome affects ageing.

Called Skin Microbiome in Healthy Ageing (SMiHA), the network is a multi-disciplinary UK research community comprising of universities, industry, and healthcare practitioners.

It is a jointly funded by the Biotechnology and Biological Sciences Research Council and the Medical Research Council.

It will study how changes in the composition of the skin microbiome reflect acceleration or deceleration of the ageing process and age specific disorders.

The network is led by Julie Thornton Professor of Cutaneous Biology and Director of the Centre for Skin Sciences, University of Bradford, and Scientific Director, Plastic Surgery and Burns Unit.

Other members of the network are from the University of Liverpool, Queen Mary University London and the University of East Anglia.

Around 50% of the UK population have a microbiome associated skin complaint, such as infant eczema or teenage acne each year. Management of infected wounds alone utilise 5.5% of total NHS expenditure.

Skin complaints are the most frequent problems seen by GPs, and poor skin health and chronic skin conditions, such as infected wounds, often impacts on the elderly.

Professor Andrew McBain a microbiologist from The University of Manchester said: “We formed this network to help skin microbiome research come up with solutions to age-related conditions.

“We hope to achieve that through creating more knowledge about the aging skin microbiome.

”We believe that this will create better outcomes and quality of life for many people.”

The network itself is a member of a the UK Ageing Network which encompasses 11 interdisciplinary research networks bringing researchers and stakeholders from different disciplines together to create new knowledge and better outcomes for older people.

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Thu, 10 Mar 2022 11:23:25 +0000 https://content.presspage.com/uploads/1369/500_skin.jpg?10000 https://content.presspage.com/uploads/1369/skin.jpg?10000
Trial of groundbreaking ‘buddy’ scheme for older adults launches /about/news/trial-of-groundbreaking-buddy-scheme-for-older-adults-launches/ /about/news/trial-of-groundbreaking-buddy-scheme-for-older-adults-launches/492111The trial of a groundbreaking volunteer buddy scheme aimed at improving mobility in older adults is being launched today in Stoke, 91ֱ and Cardiff.

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The trial of a groundbreaking volunteer buddy scheme aimed at improving mobility in older adults is being launched today in Stoke, 91ֱ and Cardiff.

The study led by The University Birmingham in collaboration with The Universities of Manchester, , Cardiff Metropolitan, Cardiff, Exeter, the Royal Voluntary Service and Sport Cardiff, follows a successful small-scale trial carried out previously in Bristol.

The 91ֱ study team are looking for around 200 over-65s in the 91ֱ area who are starting to find everyday activities such as getting up from a chair, climbing the stairs and walking to the shops harder than it used to be.

The aim is to test if the volunteers - who are themselves over 55- can support people getting out and about, be more active, increase and maintain their mobility.

Chief Investigator, Professor Afroditi Stathi, from The University of Birmingham said: “As people get older, everyday activities, like walking and climbing the stairs, can become more difficult.

“The Covid-19 pandemic has made this issue even worse as many people haven’t been able to get out and about as much as normal and so have become less mobile and active.

“This deconditioning can affect people’s ability to live independently and makes life a lot less enjoyable.

“Contrary to the common belief that physical decline is inevitable in later life, we have strong evidence from our studies that it is possible to delay this physical decline, or even reverse it, by keeping active.

“But we know becoming more active is a lot easier said than done for many people.”

Called the new volunteer buddy scheme will pair people 65 and above with a volunteer for six months.

The pair will choose local activities to try out together over the first three months such as exercise classes, dancing, a choir or just a local walk.

Over three months, the volunteer will support the participant to continue the activities independently, through phone calls and further face to face support.

The ACE study will assess if the volunteer buddy scheme can support people in getting out and about and so being more active and help them increase their mobility and maintain it for longer.

The team will follow up people who are taking part after 6, 12 and 18 months, to find out how successfully they have been in maintaining their new levels of activity allowing them to live independently and to get the most out of life.

Dr Helen Hawley-Hague from The University of Manchester added: ‘An older person who remains mobile and active is more likely to stay healthy – both mentally and physically – and to enjoy their independence and a higher quality of life for longer.

“We have already had positive results from testing this buddy scheme on a small scale. Now, it is the time to get some definitive answers about how well the ACE programme supports older people, with mobility limitations, to increase and maintain they physical function and independence.’

Pictures are from the initial small scale trial.  Credit:  Alex Rotas (alexrotasphotography.co.uk).

Anyone interested in taking part in or volunteering for ACE, contact Amy Davies on Tel  07442943716 or email amy.davies@manchester.ac.uk or visit our website  for more information.

ACE volunteers will be managed through the Royal Voluntary Service (RVS), a UK-wide volunteering organisation. The study will take place in three areas: Stoke-on-Trent, 91ֱ and Cardiff. If the programme is shown to be effective, it will be rolled out nationally.

ACE is funded by the National Institute for Health Research (NIHR) – Public Health Research Programme

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Wed, 02 Feb 2022 10:44:00 +0000 https://content.presspage.com/uploads/1369/500_reacteaston1-31.jpg?10000 https://content.presspage.com/uploads/1369/reacteaston1-31.jpg?10000
Jeff Bezos is looking to defy death – this is what we know about the science of ageing /about/news/jeff-bezos-is-looking-to-defy-death--this-is-what-we-know-about-the-science-of-ageing/ /about/news/jeff-bezos-is-looking-to-defy-death--this-is-what-we-know-about-the-science-of-ageing/490653Jeff Bezos is on a mission to conquer ageing. He has just from GlaxoSmithKline to help lead Altos Labs, the ambitious new anti-ageing company with billions of investment. So what does science really say about this? Could we beat ageing?

Ageing isn’t just a change in how we feel or look, ageing happens at a cellular level. In a lab culture dish, adult skin cells divide roughly 50 times before stopping. But skin cells from a newborn baby can divide 80 or 90 times. And on the flip side, cells from someone elderly divide only around .

Ageing is also evident in our genes. Our genetic material is modified over time – chemicals can be attached that change which genes are switched on or off. These are called , and they build up as we age. Another kind of change takes place at the ends of our cell’s DNA. Repeating segments of DNA called telomeres act like the plastic tip of a shoelace, preventing the twisted coils of genetic material from fraying at the ends or knotting together. But these telomeres shorten each time a cell divides. We don’t know if short telomeres are merely a mark of ageing, like grey hair, or are part of the process by which cells age.

Cells, chromosomes and telomeres

 

To keep alive and keep dividing, immune cells stop their telomeres shortening when they multiply, . This is probably a contributing factor in their apparent immortality. Drugs that stop telomerase from working also show (although cancer cells can evolve resistance).

Bigger question

Given that ageing has such a profound effect on our cells and genes – the effects mentioned here being just some examples – a much bigger question emerges: why does this happen? Why do we age?

It was once thought that ageing happened for the continuing evolution of species. In other words, the evolution of a species requires a turnover of individuals. However, one problem with this idea is that most life on Earth doesn’t ever reach old age. Most animals are killed by predators, disease, the climate or starvation. So an inbuilt limit on an animal’s lifespan may not be important to evolution.

Another view is that ageing is simply a side-effect of the damage that builds up over time caused by metabolism or exposure to ultraviolet light from the Sun. We do know that genes are damaged as we age, but it is not proven that this drives ageing directly. Another possibility is that ageing might have evolved as a defence against cancer. Since cells accumulate genetic damage over time, they may have evolved a process to not persist in the body for too long, in case this damage eventually causes a cell to turn cancerous.

As we age, some of the body’s cells enter a state called senescence, in which a cell stays alive but stops dividing. Senescent cells accumulate in the body over a lifetime – especially in the skin, liver, lung and spleen – and have both beneficial and detrimental effects.

They are beneficial because they secrete chemicals that help repair damaged tissue, but over a long period of time, as senescent cells increase in number, they can disrupt the normal structure of organs and tissues. These cells could be an underlying cause of many of the problems we associate with ageing. Mice in which senescent cells were cleared were profoundly delayed in showing .

We can describe a lot of what happens during ageing at the level of what physically happens to our genes, cells and organs. But the fundamental question of why we age is still open. In all likelihood, there is more than one correct answer.

Of course, nobody knows whether Bezos’s company can succeed in helping extend the human lifespan. But what is clear is that by studying ageing, exciting new discoveries are bound to emerge. Never listen to anyone who says the big questions have already been answered. As I’ve recently detailed in a book about new technology and the human body, , I’m confident that dramatic breakthroughs will profoundly change the experience of being human in the coming century.The Conversation

, Professor of Immunology,

This article is republished from under a Creative Commons license. Read the .

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Fri, 21 Jan 2022 13:20:34 +0000 https://content.presspage.com/uploads/1369/500_stock-photo-active-old-age-people-and-lifestyle-concept-happy-senior-couple-riding-bicycles-at-summer-park-707244118.jpg?10000 https://content.presspage.com/uploads/1369/stock-photo-active-old-age-people-and-lifestyle-concept-happy-senior-couple-riding-bicycles-at-summer-park-707244118.jpg?10000
Housing for people living with dementia must reflect their specific needs – finds new Greater 91ֱ report /about/news/housing-for-people-living-with-dementia-must-reflect-their-specific-needs--finds-new-greater-manchester-report/ /about/news/housing-for-people-living-with-dementia-must-reflect-their-specific-needs--finds-new-greater-manchester-report/485749The lives of people living with dementia in Greater 91ֱ, alongside carers and loved ones, can be improved through better access to housing that reflects the changing needs and diversity of the population, according to the finding of a new report published today (Friday 10 December).

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The lives of people living with dementia in Greater 91ֱ, alongside carers and loved ones, can be improved through better access to housing that reflects the changing needs and diversity of the population, according to the finding of .

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.

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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.]]> Fri, 10 Dec 2021 07:25:00 +0000 https://content.presspage.com/uploads/1369/500_manchesterhousingestate.png?10000 https://content.presspage.com/uploads/1369/manchesterhousingestate.png?10000
Hard of hearing over-70s report memory loss and mental health problems in lockdown /about/news/hard-of-hearing-over-70s-report-memory-loss-and-mental-health-problems-in-lockdown/ /about/news/hard-of-hearing-over-70s-report-memory-loss-and-mental-health-problems-in-lockdown/443345People with hearing difficulties experience heightened self-reported depression, loneliness, and memory problems during the COVID-19 lockdown, according to an online survey of the over 70s.

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People with hearing difficulties experience heightened self-reported depression, loneliness, and memory problems during the COVID-19 lockdown, according to an online survey of the over 70s.

The study, published in the International Journal of Audiology, was carried out by experts at The University of Manchester, The University of Sheffield and Lancaster University.

Eighty people over seventy with mixed hearing abilities completed two detailed questionnaires, 12 weeks apart, during May and June 2020 when lockdown restrictions were in place.

The study was funded by Deafness Support Network (DSN), a Cheshire based charity, and supported by the (BRC) and NIHR Sheffield Biomedical Research Centre.

NIHR 91ֱ BRC bridges the gap between new discoveries and individualised care through pioneering research. The BRC’s Hearing Health theme is improving the lives of adults and children by preventing potentially devastating congenital deafness, diagnosing acquired age-related hearing deficits, and developing new treatments.

Lead author Dr Jenna Littlejohn from The University of Manchester, DSN and NIHR 91ֱ BRC said: “Hearing loss, one of the leading causes of disability in older adults, is already commonly associated with increased rates of depression, social isolation, and risk of dementia and cognitive decline.

“However this study shows that these problems are even more acute during the lockdown for people over 70, who were among the ‘clinically vulnerable’ people asked to shield.”

She added: “Because we were not able to conduct face to face interviews during the lockdown, this study was clearly not able to estimate the effects of the pandemic on the over seventies without internet access.

“However, it would be logical to suspect that these negative associations could be even stronger in people who do not have access to the internet as they may be even more socially isolated: video calls have been lifelines for many.”

Cancellation of medical appointments, the use of face masks and the limitation in the use of technology due to hearing loss are thought to all be important factors.

Many routine face-to-face audiology appointments have been postponed, suspended, or offered remotely.

Face masks act as a direct barrier to communication and are particularly problematic for people with hearing loss who also rely on lip reading and facial expression.

And the enforced social distancing means people with hearing loss might struggle to use telephone and video calls to stay in touch with family and friends.

Around 70 per cent of people over the age of 70 have hearing loss according to the World Health Organisation. The 8.3 million people in the UK with the condition are likely, argue the team, to be selectively disadvantaged by the coronavirus pandemic.

Dr Littlejohn said: “We suspect the use of face coverings and limited group meetings may remain for a while yet, and so our work into the longer-term collateral effects of the pandemic is ongoing.

We need to ensure people with hearing loss get the correct support from health and social care professionals in terms of supporting mental health and investigating the risk of cognitive impairment due to the enforced social isolation on these people.

“The more data we have, the better we can inform the health and social care professionals who are responsible for them.”

The paper ‘Self-reported hearing difficulties are associated with loneliness, depression and cognitive dysfunction during the COVID-19 pandemic’ is published in the

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Wed, 17 Mar 2021 13:04:00 +0000 https://content.presspage.com/uploads/1369/500_hearing-aid.jpg?10000 https://content.presspage.com/uploads/1369/hearing-aid.jpg?10000
Face masks are a challenge for people with hearing difficulties /about/news/face-masks-are-a-challenge-for-people-with-hearing-difficulties/ /about/news/face-masks-are-a-challenge-for-people-with-hearing-difficulties/388867Face masks are a challenge for people with hearing difficulties ,

The use of face masks by the public is a controversial topic and . Evidence suggests that while face coverings and surgical masks can prevent large particles spreading from an infected person wearing a mask to someone else, they don’t trap .

A mask may also increase a person’s risk of contracting COVID-19 by encouraging them to touch their face as they fit and adjust it. Exhaled air can irritate the eyes, which might also tempt the wearer to wipe them.

On the other hand, wearing a mask may stop people with coronavirus spreading it to others (although the evidence for this is currently weak). As governments search for a surefooted transition to whatever the new norm will be, there is a danger that a policy of encouraging the public to wear face masks may precede the evidence.

Unintended consequences

It’s important to consider some of the unintended consequences. Wearing a face mask may impair the ability for some people to communicate with ease because it prevents lip reading and it can reduce the level of speech transmitted from the mouth.

At the very least, removing visual cues can make communication more taxing because of the mental exertion required to listen, especially when there is background noise. As a result, even if a person can follow what is said, they have fewer mental resources left to think about and recall what they heard.

Research has shown there are beneficial effects of wearing surgical masks made from a transparent material that , but these aren’t widely available. And there have , rather than masks, which may offer a solution. But the public has yet to adopt this solution.

The increased effort needed to listen and communicate is exacerbated in people who have a hearing loss. According to the WHO, there are .

Hearing loss leads to communication difficulties between family members, colleagues and friends. It is associated with such as poor social interactions, isolation, depression and anxiety, increased risk of dementia and reduced quality of life. In fact, there are probably many people with hearing loss who were able to manage but would struggle with the widespread use of masks.

Mask misery

An unintended consequence of wearing a face mask might be that social distancing is replaced with social isolation and poor mental wellbeing in older adults with hearing loss. A huge section of society could be subjected to mask misery.

It is also not clear whether wearing a face mask provides a false reassurance about risk reduction (encouraging people to relax behaviours that are known to interrupt transmission, such as keeping at least two metres apart), or if it acts as a reminder to steer clear of people.

Coronavirus tends to take a , many of whom are likely to suffer from hearing loss. This means that those admitted to a hospital are especially vulnerable.

The N95 and FFP3 respirator masks for frontline health and care workers , but they are much more likely to distort and reduce the level of speech. This makes communication particularly difficult at a time of heightened anxiety and when the content of conversations is novel and unpredictable. Imagine the apprehension of being greeted by someone in full PPE wearing a fitted mask and muffled speech competing with the hiss of oxygen from a breathing mask or nasal cannula.

Practical advice for the hard of hearing

So what can you do to improve communication if you have a hearing loss and are confronted by someone wearing a face mask?

  1. Ask them to reduce the background noise as much as possible or move to a quieter location.

  2. Ask them to talk slowly and not shout.

  3. If you have a hearing aid, make sure to wear it.

  4. Some hospitals provide portable hearing amplifiers to help with communication if you have lost your hearing aid or it has stopped working.

  5. If you don’t have a hearing aid but need one, you can always download a hearing aid app to your mobile phone that can provide amplification to improve speech understanding. Or you can find an app that translates speech into text in real-time.The Conversation

, Ewing Professor of Audiology,

This article is republished from under a Creative Commons license. Read the .

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Thu, 30 Apr 2020 13:25:25 +0100 https://content.presspage.com/uploads/1369/500_healthworker.jpg?10000 https://content.presspage.com/uploads/1369/healthworker.jpg?10000
Advice for people with dementia and carers in lockdown issued /about/news/advice-for-people-with-dementia-and-carers-in-lockdown-issued/ /about/news/advice-for-people-with-dementia-and-carers-in-lockdown-issued/388200New guidance has been published to support people with dementia and their carers facing isolation and reduced services as a result of COVID-19.

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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.

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Mon, 27 Apr 2020 11:12:00 +0100 https://content.presspage.com/uploads/1369/500_elderlyman.jpg?10000 https://content.presspage.com/uploads/1369/elderlyman.jpg?10000
New assessment could identify risks of frailty /about/news/new-assessment-could-identify-risks-of-frailty/ /about/news/new-assessment-could-identify-risks-of-frailty/365330Signs of frailty, and the risks it brings, could be identified in young and old people alike through a new assessment developed in a study by researchers at the Universities  of Strathclyde, 91ֱ, Liverpool, Edinburgh and Yale.

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Signs of frailty, and the risks it brings, could be identified in young and old people alike through a new assessment developed in a study by researchers at the Universities of Strathclyde, 91ֱ, Liverpool, Edinburgh and Yale.

Increasing risk of frailty is a defining characteristic of the ageing process but it has no precise clinical definition and there are currently no analytical techniques that can accurately quantify its status.

Furthermore, little is known about the underlying biological mechanisms of frailty but the new research has revealed a set of blood biomarkers that can predict its extent. Further down the line it could potentially achieve this with people as young as in their 20s or 30s.

The assessment could also determine whether a patient would be able to withstand intensive courses of treatment, such as chemotherapy, as well as helping to understand, prevent, cure or minimise age-related impairments.

The research has been published in the journal Nature Communications.

Dr Nicholas Rattray, a Chancellor’s Fellow with Strathclyde Institute of Pharmacy and Biomedical Sciences, led the study. He said: “Being able to measure the frailty status of a person is currently a very subjective clinical assessment and is ultimately causing a delay in the personalisation of therapeutic options for frail patients.

“By using cutting-edge analytical techniques such as mass spectrometry based metabolomics, this research has opened the door to developing ways to rapidly and accurately quantify frailty and apply this knowledge directly within the clinical environment.

“We believe this assessment is the first of its kind. It could lead to a far deeper understanding of the ageing process and how to potentially develop intervention strategies for ageing poorly.”

Professor Roy Goodacre from the University of Liverpool said: “I am excited by this work as this shows that large-scale metabolomics has for the first time shown clear biochemical changes in people with frailty which may with future work lead to therapy to help revert these individuals back to a resilient phenotype which will improve quality of life.”

Professor James Nazroo, from The University of Manchester said “These crucially important findings pave the way for providing accurate diagnostic procedures for identifying risk of frailty, but also for understanding the mechanisms that lie behind that risk and the possibility of intervening to reduce risk and the negative consequences that follow from frailty.”

Professor Neil Pendleton from the University of Manchester said “identification of frailty is complex requiring expertise not widely available. Using these findings could offer potential to expand opportunities for diagnosis when interventions are possible.”

Although there is currently no widely accepted clinical or biomedical definition of frailty, there exists a series of clinical scoring metrics, or frailty indices, which can help in the assessment of a patient’s resilience. They include measures of physical fitness, falls and fractures, vision, hearing, chronic diseases and depression.

The researchers analysed blood serum samples from 1191 people aged between 56 and 84 and followed up on 786 of the participants four years later. They weighed and identified molecules in the samples from the blood of 1200 elderly people, using machine learning to categorise bio-signatures of frailty.

A set of 12 metabolites – substances produced in metabolism – were identified and were found to differentiate between frail and non-frail people.

The research has been funded by the UK Medical Research Council.

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Tue, 05 Nov 2019 10:00:00 +0000 https://content.presspage.com/uploads/1369/500_elderlyman.jpg?10000 https://content.presspage.com/uploads/1369/elderlyman.jpg?10000
Ageing equally: what makes a good place in which to grow older? /about/news/ageing-equally-what-makes-a-good-place-in-which-to-grow-older/ /about/news/ageing-equally-what-makes-a-good-place-in-which-to-grow-older/361121Researchers at The University of Manchester have collaborated with Oldham Coliseum to explore how the experiences of women aged over 50 can help to map out what makes a good place in which to grow old.

The project involved a group of women aged 50 and over who attend the Glodwick Luncheon Club at the Oldham Pakistani Community Centre who attended trips to venues such as the Whitworth Art Gallery and workshops held by artists including Najma Khalid and Robina Ullah to explore the themes of ageing, home and place through textiles.

This collaboration has culminated in a performance and exhibition called , which will take place on 10 October from 2pm-3pm. The event is free to attend and addresses how women in this demographic want to engage more in their community, but find it difficult due to barriers such as language or shared accommodation infrastructure.

By using material culture and practices such as embroidery, many of these women (most of whom are first-generation migrants) have created a sense of home for themselves, with the textile industry bringing many of those of Pakistani origin to Oldham decades ago. The signifiers of textiles and their sense of home to this community is examined at this event, as is how Oldham is a good place to grow old, and how it could be better.

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Tue, 08 Oct 2019 16:37:36 +0100 https://content.presspage.com/uploads/1369/500_ageing2-412293.jpg?10000 https://content.presspage.com/uploads/1369/ageing2-412293.jpg?10000
Northern millennials less likely to live into their 50s than their southern English counterparts /about/news/northern-millennials-less-likely-to-live-into-their-50s-than-their-southern-english-counterparts/ /about/news/northern-millennials-less-likely-to-live-into-their-50s-than-their-southern-english-counterparts/324721By Professor 

 

File 20190130 108355 1r6ttok.jpg?ixlib=rb 1.1

 

 

There is a stark disparity in wealth and health between people in the north and south of England, commonly referred to as England’s “north-south divide”. The causes of this inequality are complex; it’s influenced by the environment, jobs, migration and lifestyle factors – as well as the long-term political power imbalances, which have in the south, especially in and around London.

 

Life expectancy is also lower in the north, mainly because the region is more deprived. But of national mortality data highlights a shockingly large mortality gap between young adults, aged 25 to 44, living in the north and south of England. This gap first emerged in the late 1990s, and seems to have been growing ever since.

 

In 1995, there were 2% more deaths among northerners aged 25 to 34 than southerners (in other words, 2% “excess mortality”). But by 2015, northerners in this age group were 29% more likely to die than their southern counterparts. Likewise, in the 35 to 44 age group, there was 3% difference in mortality between northerners and southerners in 1995. But by 2015, there were 49% more deaths among northerners than southerners in this age group.

 

Excess mortality in the north compared with south of England by age groups, from 1965 to 2015. Follow the lines to see that people born around 1980 are the ones most affected around 2015.

While mortality increased among northerners aged 25 to 34, and plateaued among 35 to 44-year-olds, southern mortality mainly declined across both age groups. Overall, between 2014 and 2016, northerners aged 25 to 44 were 41% more likely to die than southerners in the same age group. In real terms, this means that between 2014 and 2016, 1,881 more women and 3,530 more men aged between 25 and 44 years died in the north, than in the south.

What’s killing northerners?
To understand what’s driving this mortality gap among young adults, our team of researchers looked at the causes of death from 2014 to 2016, and sorted them into eight groups: accidents, alcohol related, cardiovascular related (heart conditions, diabetes, obesity and so on), suicide, drug related, breast cancer, other cancers and other causes.

Controlling for the age and sex of the population in the north and the south, we found that it was mostly the deaths of northern men contributing to the difference in mortality – and these deaths were by cardiovascular conditions, alcohol and drug misuse. Accidents (for men) and cancer (for women) also played important roles.

From 2014 to 2016, northerners were 47% more likely to die for cardiovascular reasons, 109% for alcohol misuse and 60% for drug misuse, across both men and women aged 25 to 44 years old. Although the national rate of death from cardiovascular reasons , the longstanding gap between north and south remains.

 

Death and deprivation

The gap in life expectancy between north and south is usually put down to socioeconomic deprivation. We considered further data for 2016, to find out if this held true for deaths among young people. We found that, while two thirds of the gap were explained by the fact that people lived in deprived areas, the remaining one third could be caused by some unmeasured form of deprivation, or by differences in culture, infrastructure, migration or extreme weather.

 

    

Mortality for people aged 25 to 44 years in 2016, at small area geographical level for the whole of England.

Northern men faced a higher risk of dying young than northern women – partly because overall mortality rates are higher for men than for women, pretty much at every age, but also because men tend to be . Although anachronistic, the expectation to have a job and be able to sustain a family weighs more on men. Accidents, alcohol misuse, drug misuse and suicide are all strongly associated with low socioeconomic status.

Suicide risk is twice as high among the most deprived men, compared to the most affluent. Suicide risk with unemployment, and substantial increases in suicide have been observed during periods of recession – especially among men. tells us that unskilled men between ages 25 and 39 are between ten and 20 times more likely to die from alcohol-related causes, compared to professionals.

Alcohol underpins the steep increase in liver cirrhosis deaths in Britain from the 1990s – which is when the north-south divide in mortality between people aged 25 to 44 also started to emerge. has shown that men in this age group, who live in the most deprived areas, are five times more likely to die from alcohol-related diseases than those in the most affluent areas. For women in deprived areas, the risk is four times greater.

It’s also widely known that mortality rates for cancer , and people have worse survival rates in places where smoking and alcohol abuse is more prevalent. Heroin and crack cocaine addiction and deaths from drug overdoses are also with deprivation.

The greater number of deaths from accidents in the north should be considered in the context of transport infrastructure investment, which is heavily skewed towards the south – especially London, which enjoys the lowest mortality in the country. What’s more, if reliable and affordable public transport is not available, people will drive more and expose themselves to higher risk of an accident.

Deaths for young adults in the north of England have been increasing compared to those in the south since the late 1990s, creating new health divides between England’s regions. It seems that persistent social, economic and health inequalities are responsible for a growing trend of psychological distress, despair and risk taking among young northerners. Without major changes, the extreme concentration of power, wealth and opportunity in the south will continue to damage people’s health, and worsen thenorth-south divide.The Conversation

, Professor in Data Science and Health Services Research,

 

 

This article is republished from under a Creative Commons license. Read the .

 

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Report highlights postcode lottery in strength and balance programmes which help people at risk of falls /about/news/report-highlights-postcode-lottery-in-strength-and-balance-programmes-which-help-people-at-risk-of-falls/ /about/news/report-highlights-postcode-lottery-in-strength-and-balance-programmes-which-help-people-at-risk-of-falls/320691Exercise programmes designed to boost the muscle strength and balance of people at risk of falls and injury – such as resistance training, aerobics classes and yoga groups – are not being prioritised by the NHS and local authority commissioners.

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  • Boosting people’s strength and balance through exercise improves their health and wellbeing, reduces the risk of early death and prevents the avoidable hospital admissions caused by falls.
  • By not prioritising these programmes, local authorities and the NHS are missing the opportunity to ease pressure on A&E departments and reduce demand for social care. Falls are a main cause of hip fractures, which cost the NHS around £1bn per year.
  • The Centre for Ageing Better’s project with the University of Manchester’s Healthy Ageing Research Group shows a need for sustained, targeted funding for such programmes, with affordable, accessible and proven options available for everyone.
  • Exercise programmes designed to boost the muscle strength and balance of people at risk of falls and injury – such as resistance training, aerobics classes and yoga groups – are not being prioritised by the NHS and local authority commissioners.

    A new report argues NHS falls rehabilitation services often don’t have the funding or ability to themselves provide strength and balance programmes for more than a few hours over just 6-8 weeks, much less than the 50+ hours over six months needed to make a difference to a person’s ability to do everyday activities.

    The issue can be exacerbated by referral pathways from the NHS to community-led programmes being unclear, with Clinical Commissioning Groups, local authorities and charities failing to join up with one another. A lack of consistent provision can limit the opportunities for people to take up strength and balance training and exercise programmes which will have a real impact on their wellbeing.

    Muscle weakness and poor balance are the two most common modifiable risk factors for falls, which can lead to injuries such as hip fractures and make people more likely to end up in hospital or need social care. Hip fractures alone cost the NHS around £1bn per year.

    Strength and balance activity can mitigate these risks and can lower the chance of suffering a fall, improve energy levels, mood and sleeping patterns and reduce the risk of early death.

    The report shows that, for adults with declining mobility and those experiencing a loss of muscle and bone strength or balance, there can be a corresponding decline in their ability to manage everyday activities like eating, bathing and getting dressed on their own.

    The report recommends that NHS and local authorities support evidence-based programmes, making sure that the most effective approaches to improving strength and balance are accessible and affordable for everyone. Making people aware of the benefit of strength and balance exercises should be a priority, and commissioners must work together to reinforce the information given to patients. There also needs to be improved collaboration between those referring people to programmes and those delivering them.

    Louise Ansari, Director of Communications and Influencing, , said:

    “Improving and retaining strength and balance is vital for our wider health. Despite common misconceptions, falls are not an inevitable part of ageing and can be prevented. Evidence tells us that strength and balance programmes reduce the risk of falls, but lack of communication and effective referral pathways can mean poor or non-existent provision.

    “If we can enable and encourage more people to take up activities to boost their strength and balance, there is significant potential to make savings to health and social care services and help people stay healthy and keep on doing everyday activities for longer.”

    Professor Chris Todd, Professor of Primary Care and Community Health, School of Health Sciences, University of Manchester said:

    “Making people aware of the benefit of strength and balance exercises should be a priority. Prevention is absolutely central to the NHS Long Term Plan, which emphasises a move away from simply treating disease to a system that helps to keep people healthy for longer.

    “Our project shows that if the Long Term Plan’s ambition is to be realised, there needs to be a step change in the way strength and balance training is organised so that it is implemented effectively across the NHS in partnership with local government and the third sector.”

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    Sun damages people with black skin, finds research /about/news/sun-damages-skin-of-older-black-people-finds-research/ /about/news/sun-damages-skin-of-older-black-people-finds-research/320495Premature ageing in the skin of white people caused by repeated exposure to the sun also occurs in black skin - though about 50 years later, according to new research.

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    Premature ageing in the skin of white people caused by repeated exposure to the sun also occurs in black skin - though about 50 years later, according to new research.

    The team - led by University of Manchester scientists – dispel the myth that people with black skin are largely protected from sun damage because of its high content of pigment.

    It has long been known that prolonged exposure to the sun causes premature ageing in white skin.

    The study of 21 people in their early 20s and 18 people in their 60s and 70s is the first to analyse how skin structure and elasticity changes in people with black skin.

    Lead researcher Dr Abigail Langton from The University of Manchester, said: “We know repeated exposure to the sun can age white skin, but very little research has been carried out on black skin.

    “This research shows that black skin is indeed affected by the sun, though it takes far longer for that effect to be felt.”

    The research was carried out in partnership with Johns Hopkins University School of Medicine in Baltimore, the United States.

    The team analysed two skin sites: the buttock, which is protected from sun damage so giving researchers information on how skin may change due to advancing age; and the forearm, which receives regular exposure to the sun.

    They used special equipment to test the elasticity of skin and measured key proteins that help us understand skin health: fibrillin and collagen.

    Protected black buttock skin performed similarly in both young and old people: the older cohort showed only small differences in elasticity. However, the sun exposed black forearm skin showed significant changes: it was much less elastic and fibrillin and collagen were reduced.

    Professor Rachel Watson, from The University of Manchester, said: “Our previous work has shown that there are differences in how skin is organised in black and white skin; clinicians are often unaware of this difference. There is certainly a need to take this into account when considering treatment options for all patients.

    “Most research is carried out in places where there are fewer people from black and ethnic minority backgrounds which might explain the lack of data on black skin.

    “But in Baltimore, around 65% of the population are African Americans – which made it easier for us to recruit volunteers.”

    The study highlights the need for improved public health advice regarding the consequences of prolonged sun-exposure and the importance of using sun protection for all skin types.

    The study is published in the Journal of Investigative Dermatology and is funded by Boots UK, a subsidiary of Walgreens Boots Alliance.

    “Aging in skin of color: Disruption to elastic fiber organization is detrimental to skin’s biomechanical function” is published in the

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    Biggest ever map of human Alzheimer’s brain published /about/news/biggest-ever-map-of-human-alzheimers-brain-published/ /about/news/biggest-ever-map-of-human-alzheimers-brain-published/320101A study of the differences between healthy brains and those with Alzheimer’s Disease has produced largest dataset of its type ever.

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    A study of the differences between healthy brains and those with Alzheimer’s Disease has produced largest dataset of its type ever.

    And the data, developed by a team of researchers led by Dr Richard Unwin at The University of Manchester, is now freely available for any scientist to use.

    The team included researchers from the Universities 91ֱ, Bristol, Liverpool and Auckland.

    The development is an important advance for scientists researching Alzheimer’s.

    The team also show that one region of the brain previously thought to be unaffected by the disease, the cerebellum, displayed a series of changes which they think might protect it from damage caused by Alzheimer’s.

    The Alzheimer’s Research UK funded study is published in the journal Communications Biology today.

    The analysis, mapping the relative levels of over 5,825 distinct proteins across six regions of the brain, generated a massive 24,024 data points.

    The brain regions in the study included the more heavily affected Hippocampus, Entorhinal cortex, Cingulate gyrus and the less affected Motor Cortex, Sensory Cortex, and Cerebellum

    The samples were donated for research by patients at the New Zealand Brain Bank in Auckland.

    Dr Unwin said: “This database provides a huge opportunity for dementia researchers around the world to progress and to follow-up new areas of biology and develop new treatments.

    “It could also help validate observations seen in in animal or cell disease models in humans.

    ”It’s very exciting to be able to make these data public so scientists can access and use this vital information.”

    Alzheimer’s Disease arises in the hippocampus and spreads through pathways in the brain.

    But by looking at different parts of that pathway, the team were able to observe, for the first time, how Alzheimer’s progresses in more detail.

    “We think that the changes we see in the regions affected later on-represent early disease changes, present before cells die,” he said

    “These represent good new targets for drug developers, as we know it’s important to try to intervene early.”

    In the course of the study, the team hit upon new molecules not previously associated with the disease, representing more targets to develop new drugs.

    They also confirm that researchers looking at a range of pathways - including inflammation, Wnt signalling, and metabolic changes in human tissue - are on the right track.

    The team identified 129 protein changes which were present in all areas of the brain studied, with at least 44 not previously associated with the disease.

    But there were hundreds others which change only in the late-affected regions.

    He added: “These new protein changes represent further targets for scientists developing new drugs

    “The cerebellum, previously thought be unaffected, displays a significant response at the molecular level.

    “Many of the changes here are not seen in other regions and this could imply that this region actively protects itself from disease. We won’t know for sure until we carry out more research.”

    Dr Rosa Sancho, Head of Research at Alzheimer’s Research UK, said: “By studying thousands of individual proteins, this exciting research has generated a detailed molecular map of changes that get underway in the brain in Alzheimer’s disease. Making this information freely available online will help researchers to navigate the complex and changing environment of the brain in Alzheimer’s and identify processes that could be targeted by future drugs.

    “There are over half a million people in the UK living with Alzheimer’s and there are currently no treatments that can slow or stop the disease from progressing in the brain. Pioneering research like this is driving progress towards new breakthroughs that will change people’s lives.”

    The paper ‘Regional protein expression in human Alzheimer’s brain correlates with disease severity’ is publihsed in 

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    Hypothesis underpinning dementia research ‘flawed’ /about/news/hypothesis-underpinning-dementia-research-flawed/ /about/news/hypothesis-underpinning-dementia-research-flawed/302759A 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.

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    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 

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    Tue, 16 Oct 2018 15:45:00 +0100 https://content.presspage.com/uploads/1369/500_istock-000083379035-full.jpg?10000 https://content.presspage.com/uploads/1369/istock-000083379035-full.jpg?10000
    New study highlights Alzheimer’s herpes link, experts say /about/news/new-study-highlights-alzheimers-herpes-link-experts-say/ /about/news/new-study-highlights-alzheimers-herpes-link-experts-say/291154A 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.

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    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

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