Latest news with #UKDementiaResearchInstitute
Yahoo
3 days ago
- General
- Yahoo
Sleep disorders increase dementia risk
People who experience sleep disorders are at greater risk of developing neurodegenerative conditions, including dementia, new research has found. The study, conducted by researchers at Cardiff University, found that diagnoses of sleep disorder made people up to twice as likely to develop a neurodegenerative disease in the 15 years that followed. The peer-reviewed study used data from more than a million electronic health records. "This increased risk was occurring independently of genetic risk factors for Alzheimer's and Parkinson's, with sleep disorders almost 'compensating' for low genetic risk," said Prof Valentina Escott-Price, from the UK Dementia Research Institute at Cardiff University. Call for danger warnings to rugby parents over dementia fears I love dad to bits - but being his carer has broken me The researchers examined data from three biobanks – facilities that store biological samples and are used for health research – from which they were "able to obtain accurate, timestamped records of when people experienced sleep disorders". The team analysed those who had been diagnosed with one of more sleep disorder, grouping them into those associated with "circadian rhythm" – or body clock – such as sleepwalking and narcolepsy, and "non-organic" sleep disorders not linked to a known psychological condition, including generalised insomnia and nightmares. The key findings were: Circadian sleep disorders and non-organic sleep disorders were associated with an increased risk of dementia in the 10 to 15 years that followed. The risk was further increased for those with multiple sleep disorders. Circadian sleep disorders increased the risk of Alzheimer's in the 10 to 15 years following sleep disorder diagnosis. Circadian sleep disorders and non-organic sleep disorders increased the risk of vascular dementia in the 5 to 10 years following sleep disorder diagnosis. The risk was further increased for those with multiple sleep disorders. Circadian sleep disorders and non-organic sleep disorders increased risk of Parkinson's in the 10 to 15 years following sleep disorder diagnosis. Dr Emily Simmonds, bioinformatician at the UK Dementia Research Institute at Cardiff University, said the study aimed to "understand the complicated relationship between sleep and dementia". She said: "People living with dementia often experience sleep problems, but there is not yet enough evidence to say for sure whether poor sleep increases risk of dementia. "Our results are compelling, indicating a clear increased risk of neurodegenerative disease following a sleep disorder." Prof Escott-Price, also from Cardiff University, said that while further investigation is needed the research "points towards sleep disorders as a risk factor for these conditions". Future research will examine whether improving sleep through the use of medication leads to a reduction in risk.
Yahoo
3 days ago
- General
- Yahoo
Sleep disorders increase dementia risk
People who experience sleep disorders are at greater risk of developing neurodegenerative conditions, including dementia, new research has found. The study, conducted by researchers at Cardiff University, found that diagnoses of sleep disorder made people up to twice as likely to develop a neurodegenerative disease in the 15 years that followed. The peer-reviewed study used data from more than a million electronic health records. "This increased risk was occurring independently of genetic risk factors for Alzheimer's and Parkinson's, with sleep disorders almost 'compensating' for low genetic risk," said Prof Valentina Escott-Price, from the UK Dementia Research Institute at Cardiff University. Call for danger warnings to rugby parents over dementia fears I love dad to bits - but being his carer has broken me The researchers examined data from three biobanks – facilities that store biological samples and are used for health research – from which they were "able to obtain accurate, timestamped records of when people experienced sleep disorders". The team analysed those who had been diagnosed with one of more sleep disorder, grouping them into those associated with "circadian rhythm" – or body clock – such as sleepwalking and narcolepsy, and "non-organic" sleep disorders not linked to a known psychological condition, including generalised insomnia and nightmares. The key findings were: Circadian sleep disorders and non-organic sleep disorders were associated with an increased risk of dementia in the 10 to 15 years that followed. The risk was further increased for those with multiple sleep disorders. Circadian sleep disorders increased the risk of Alzheimer's in the 10 to 15 years following sleep disorder diagnosis. Circadian sleep disorders and non-organic sleep disorders increased the risk of vascular dementia in the 5 to 10 years following sleep disorder diagnosis. The risk was further increased for those with multiple sleep disorders. Circadian sleep disorders and non-organic sleep disorders increased risk of Parkinson's in the 10 to 15 years following sleep disorder diagnosis. Dr Emily Simmonds, bioinformatician at the UK Dementia Research Institute at Cardiff University, said the study aimed to "understand the complicated relationship between sleep and dementia". She said: "People living with dementia often experience sleep problems, but there is not yet enough evidence to say for sure whether poor sleep increases risk of dementia. "Our results are compelling, indicating a clear increased risk of neurodegenerative disease following a sleep disorder." Prof Escott-Price, also from Cardiff University, said that while further investigation is needed the research "points towards sleep disorders as a risk factor for these conditions". Future research will examine whether improving sleep through the use of medication leads to a reduction in risk.
Yahoo
3 days ago
- General
- Yahoo
Nightmares linked to higher dementia risk, study finds
People who have nightmares or sleepwalk are twice as likely to develop vascular dementia than those who sleep soundly, a study has found. Scientists have long known that serious sleep disorders increase the risk of neurodegenerative conditions, but the latest research has shed more light on the connection. Analysis of more than a million people's medical records has found individuals with sleep problems who have not been diagnosed with anything physically wrong are also at increased risk. So-called 'non-organic' sleep disorders which are not linked to a known physiological condition include night terrors, sleepwalking, nightmares, and forms of insomnia and hypersomnia. Sufferers from these disorders were found to be more than twice as likely to be diagnosed with vascular dementia in later life, and to be at 67 per cent higher risk of dementia and 68 per cent higher risk of Parkinson's disease. The study, led by Cardiff University, involved data from three biobanks containing the records of people in Britain and Finland. The research compared the subjects' sleeping patterns with their genes and their long-term health outcomes. 'By using biobank data, we had timestamped records of when people had sleep disorders, and exactly when they were subsequently diagnosed with a neurodegenerative disease – rather than relying on self-reporting,' said Dr Emily Simmonds, one of the study authors and a bioinformatician at the UK Dementia Research Institute at Cardiff University. 'Our results are compelling, indicating a clear increased risk of neurodegenerative disease following a sleep disorder, across three large biobank datasets.' The scientists found people often experienced sleep disorder symptoms up to 15 years before they started seeing symptoms of the neurodegenerative conditions. Kristin Levine, a study co-author from the US National Institutes of Health's (NIH) Centre for Alzheimer's and Related Dementias, said: 'One of the exciting things about identifying people at higher risk of developing a neurodegenerative disease 10-15 years before diagnosis, is that it gives us time to implement treatments that may delay or prevent development of disease.' A link was seen between sleep problems and the neurodegenerative diseases even in people whose genes put them at low risk, the study authors found. 'Perhaps most interestingly, this increased risk was occurring independently of genetic risk factors for Alzheimer's and Parkinson's, with sleep disorders almost 'compensating' for low genetic risk,' said Hampton Leonard from the NIH Centre, the study's co-leader. 'One would expect that if sleep disorders were caused by neurodegeneration, genetic risk of sleep disorder and neurodegenerative disease would line up. Further investigation is needed, but this points towards sleep disorders as a risk factor for these conditions.' The scientists hope future research will build on their findings, and investigate if any interventions that target sleep problems can improve the outlook for neurodegenerative conditions. The study is published in npj Dementia. Broaden your horizons with award-winning British journalism. Try The Telegraph free for 1 month with unlimited access to our award-winning website, exclusive app, money-saving offers and more.
Time of India
01-05-2025
- Health
- Time of India
In breakthrough study, scientists watch dementia unfold using live brain cells
For the first time, a team of researchers have used living human brain tissue to see how dementia unfolds in the brain cells. "Experts said the new way of studying the disease could make it easier to test new drugs and boost the chances of finding ones that work," The Guardian reported citing a study by researchers from the University of Edinburgh. "In the study, scientists and neurosurgeons in Edinburgh teamed up to show for the first time how a toxic form of a protein linked to Alzheimer's, amyloid beta , can stick to and destroy vital connections between brain cells." Amyloid beta is a sticky protein that plays a big role in dementia, especially Alzheimer's. In a healthy brain, it's cleared out regularly. But sometimes, it starts to pile up and form clumps or plaques between brain cells kind of like unwanted gunk. These clumps mess with how brain cells talk to each other and can trigger inflammation, making things worse over time. This buildup is one of the early signs doctors look for when diagnosing Alzheimer's. For the study, the researchers collected tiny fragments of health brain tissue from cancer patients who were admitted at the Royal Infirmary of Edinburgh. The collected tissues were put in glass bottles filled with oxygenated artificial spinal fluid and taken to the lab for study. "There, samples were sliced into thin pieces, less than a third of a millimetre thick, and laid out in small dishes. Each piece of living brain tissue was kept in a nutrient-rich liquid, inside an incubator at 37C to mimic body temperature," the report says. The team found that when exposed to the toxic protein, the brain did not attempt to repair damage. "Even small changes in natural levels of amyloid beta – increasing or decreasing – were enough to disrupt brain cells. This suggests that the brain requires a finely tuned sweet spot of the protein to function properly," Dr Claire Durrant, a Race Against Dementia fellow and UK Dementia Research Institute emerging leader at the Centre for Discovery Brain Sciences at the University of Edinburgh told the media outlet. Hope for a cure for dementia? 'The use of living human tissue samples generously donated by people undergoing surgery to remove brain tumours allows scientists to probe how living human brain reacts to toxic proteins produced in Alzheimer's, and in future will allow testing of whether new treatments are effective in human brain," Prof Tara Spires-Jones, group leader at the UK Dementia Research Institute told the media. This breakthrough will help scientists focus on identifying drugs most likely to prevent the loss of synapses—critical connections that enable communication between brain cells and are essential for healthy brain function. Alzheimer's targets these synapses, and their deterioration is a strong predictor of memory loss and impaired cognitive abilities. Dementia in the US Dementia is becoming a major health challenge in the U.S., especially as the population ages. Right now, over 6 million Americans are living with Alzheimer's disease, the most common form of dementia, and that number is expected to double in the next couple of decades. It's not just about forgetting names or where you put your keys; dementia slowly affects thinking, reasoning, memory, and even basic day-to-day functions. It can hit families hard, both emotionally and financially, as care needs increase over time. What's worrying is that many people still confuse dementia with normal aging, which delays diagnosis and treatment. Scientists are exploring everything from lifestyle changes to experimental drugs that target harmful proteins like amyloid beta and tau. The goal? Help people with dementia live with dignity and independence for as long as possible. It's a tough journey, but with awareness, compassion, and science, there's hope on the horizon. Masterclass for Students. Upskill Young Ones Today!– Join Now
Business Mayor
30-04-2025
- Health
- Business Mayor
Living human brain tissue used to mimic Alzheimer's in breakthrough study
Scientists have used living human brain tissue to mimic the early stages of Alzheimer's disease, the most common form of dementia, in a breakthrough that will accelerate the hunt for a cure. In a world first, a British team successfully exposed healthy brain tissue from living NHS patients to a toxic form of a protein linked to Alzheimer's – taken from patients who died from the disease – to show how it damages connections between brain cells in real time. The groundbreaking move offered a rare and powerful opportunity to see dementia developing in human brain cells. Experts said the new way of studying the disease could make it easier to test new drugs and boost the chances of finding ones that work. Dementia presents a big threat to health and social care systems across the world. The number of people affected is forecast to triple to nearly 153 million by 2050, which underlines why finding new ways to study the disease and speed up the search for treatments is a health priority. In the study, scientists and neurosurgeons in Edinburgh teamed up to show for the first time how a toxic form of a protein linked to Alzheimer's, amyloid beta, can stick to and destroy vital connections between brain cells. Tiny fragments of healthy brain tissue were collected from cancer patients while they were undergoing routine surgery to remove tumours at the Royal Infirmary of Edinburgh. Living brain tissue cultures are placed inside an incubator set at 37C to mimic body temperature. Scientists dressed in scrubs were stationed in operating theatres alongside surgical teams, ready to receive the healthy brain tissue, which would otherwise have been discarded. Once the pieces of brain were retrieved, scientists put them in glass bottles filled with oxygenated artificial spinal fluid before jumping into taxis to transport the samples to their lab a few minutes away. 'We pretty much ran back to the lab,' said Dr Claire Durrant, a Race Against Dementia fellow and UK Dementia Research Institute emerging leader at the Centre for Discovery Brain Sciences at the University of Edinburgh. There, samples were sliced into thin pieces, less than a third of a millimetre thick, and laid out in small dishes. Each piece of living brain tissue was kept in a nutrient-rich liquid, inside an incubator at 37C to mimic body temperature. 'And then we start experiments almost straight away,' Durrant said. Fragments of human brain were kept alive in dishes for up to a fortnight, with the patient's permission. Researchers extracted the toxic form of amyloid beta from people who died from Alzheimer's disease and then applied it to the healthy living brain tissue in their dishes. 'We're trying to mimic Alzheimer's disease,' said Durrant. From left: Dr Claire Durrant, Sir James Dyson and Sir Jackie Stewart. Photograph: Douglas Robertson Unlike when exposed to a normal form of the protein, the brain did not attempt to repair damage caused by the toxic form of amyloid beta, her team found. Even small changes in natural levels of amyloid beta – increasing or decreasing – were enough to disrupt brain cells. This suggests that the brain requires a finely tuned sweet spot of the protein to function properly, Durrant said. 'Working alongside the neurosurgical team at the University of Edinburgh, we have shown that living human brain slices can be used to explore fundamental questions relating to Alzheimer's disease,' she said. Read More Scottish government wants drug possession to be legal skip past newsletter promotion Our morning email breaks down the key stories of the day, telling you what's happening and why it matters Privacy Notice: Newsletters may contain info about charities, online ads, and content funded by outside parties. For more information see our Privacy Policy. We use Google reCaptcha to protect our website and the Google Privacy Policy and Terms of Service apply. after newsletter promotion 'We believe this tool could help accelerate findings from the lab into patients, bringing us one step closer to a world free from the heartbreak of dementia.' The breakthrough will enable scientists to home in on drugs with the best chance of preventing the loss of synapses – connections that allow the flow of messages between brain cells and are vital to healthy brain function. Alzheimer's attacks synapses and their loss strongly predicts reduced memory and thinking abilities. Durrant's team also found that brain slices taken from the temporal lobe, a region known to be affected early in Alzheimer's, released higher levels of tau, another key disease protein. This may explain why this part of the brain is particularly vulnerable in early Alzheimer's, as increased tau release may enable toxic forms of this protein to spread faster between cells. The research was backed by Race Against Dementia, a charity formed by Sir Jackie Stewart after his wife's dementia diagnosis, and a £1m donation from the James Dyson Foundation, a charity supporting medical research and engineering education. Dyson said the breakthrough represented progress 'towards solving one of the most devastating problems of our time'. 'Working with brain surgeons and their consenting patients to collect samples of living human brain and keep them alive in the lab is a groundbreaking method,' he said. 'It allows researchers to better examine Alzheimer's disease on real human brain cells rather than relying on animal substitutes, such as mice.' Prof Tara Spires-Jones, group leader at the UK Dementia Research Institute, hailed the important development. Seeing early Alzheimer's in real-time provided a new tool for scientists to better understand the disease and how to treat it, she said. She said: 'The use of living human tissue samples generously donated by people undergoing surgery to remove brain tumours allows scientists to probe how living human brain reacts to toxic proteins produced in Alzheimer's, and in future will allow testing of whether new treatments are effective in human brain.'
