Latest news with #Parkinson's
Daily Mirror
20 hours ago
- Health
- Daily Mirror
'I thought I'd burnt toast but it was symptom of very serious condition'
Gareth Evans, 57, from Cardiff, was diagnosed with Parkinson's in 2018 after he started to show symptoms in his mid 40s - including depression and unusual smells When Gareth Evans, a staunch rugby fan and carpenter, reached his mid-40s, peculiar signs began to emerge, indicating something was amiss. Known for his activity levels and joyful nature both at work and at home, Gareth suddenly found himself grappling with inexplicable sadness and unprovoked tearfulness while on the job. Experiencing involuntary arm twitches and sensing the phantom scent of burnt toast further compounded his confusion. Despite the jigsaw of symptoms, it wasn't until medical professionals stepped in that the perplexing picture was completed with a diagnosis of Parkinson's – an illness with no known cure. Gareth grappled with depression, one of the initial indicators of his condition but remained without answers for some time. "Depression... it comes with Parkinson's," he recounted. The reality of the disease dawned on him as he tried to cope with overwhelming emotions. "I didn't understand it. I'd go into work and I'd feel very sad and I would cry." Concealing his struggle became second nature to Gareth, who worked at the Cardiff and Vale University Health Board. "I would come home and I'd cry in the shower, but I was very good at hiding it, didn't talk about it, and didn't get any help and that just got worse and worse." He was acutely aware that something was amiss but couldn't pinpoint the problem. "I just knew there was something wrong. I just didn't know what." It wasn't until unmistakable physical manifestations became evident that Gareth sought assistance. Now 57-years-old, he reflects: "I worked for 34 years for the health service. So I was actually at work and I looked down onto my left arm, and I could see the muscle just on the forearm... it was twitching, twitching a lot. "I couldn't control it, couldn't stop it and I had this for a while, you know, for a couple of days." "So actually, I went to see a friend of mine who worked in the hospital and I asked her advice and she told me I needed to get it sorted." Gareth ultimately sought help from his GP and was referred to a specialist at the University Hospital of Wales, ,reports Wales Online. After receiving his diagnosis on September 21, 2018, he admits he "cried like a baby". The revelation offered clarity for his past ailments, but the subsequent reality of living with the condition has drastically impacted his life. "First of all, the depression just wasn't me, because I've always enjoyed life to the full," Gareth shared. He explained that the emotional toll of depression hit him harder than the Parkinson's itself, saying, "The depression knocked me for a six, more so than the actual Parkinson's, to be honest." Now, years after the diagnosis date, he faces significant challenges: "But it affects me now, like 10 years on if you want to go from the diagnosis date. I can't walk properly. If I don't take my tablets, I get these terrible cramps." Recalling a harrowing episode, Gareth said, "I was walking the dog one day and I forgot to take my tablet and I was stuck in the field for 40 minutes. I just couldn't move." Compounded by bad weather, his situation worsened: "It was tipping down with rain and all my muscles had seized up." Painfully immobilised by cramps, Gareth described the recurring struggle: "I had a terrible cramp and it was very, very painful. This sort of thing happens quite a lot. It affects your internal organs as well. "It affects you bladder. So you're constantly back and forth to the toilet. You think you need a wee, but then you don't, and then you do, and that affects you there. But I must admit, I don't really let it get to me too much now. I'm in control of it." Nearly 8,300 people in Wales are currently living with Parkinson's. The progressive neurological condition caused by a lack of dopamine in the brain. The disease causes both motor symptoms such as tremor, stiffness, and slowness of movement, as well as less commonly recognised non-motor symptoms including sleep disturbances, memory issues, and constipation among others. It can also sometimes lead to phantosmia – where patients perceive smells, such as burnt toast, that aren't actually there. In recent years, Parkinson's has come to renewed public attention as a result of Michael J Fox's campaigning on the issue. The Back to the Future star has been open about his experience with the condition, and has won awards for his advocacy for a cure for the disease. For Gareth, once he had fully taken in the advice from experts and come to terms with the diagnosis, he felt he could move on and get back to work. But while Gareth's return was accommodated well by his employers, in light of his diagnosis he soon had to retire upon his doctor's advice. Recalling how he dealt with his retirement, he said: "The first few months, I just sat in the window, looking out at the rain, beating down onto the patio, and I'm thinking, 'Is this it? Is this what retirement is about?' "Like I said, I'm a very headstrong person, and I've been involved in team sports all my life, mostly rugby. So you know when you're down, and you know you can do something about it. "So, I decided to... enjoy as much as possible and get out and about if I can. Look after my grandchildren and my wife."It was a case of, 'it's not going to get better. So I've got to live with it and work with it'." It wasn't long before he found solace in his retirement, and found surprising new ways of coping. "I started painting, believe it or not," he said. "Another symptom I've got with Parkinson's is insomnia. I don't sleep very well. So I get up at night and I paint, painting by numbers. "I find that quite relaxing. Now that you might think is strange because I've got a tremor. I tremor most of the time. "So when I actually paint, because your brain tells you to concentrate and you literally go in and you paint, the painting by number is a very fine painting. You don't tremor because you use your brain." One of his favourite creations is a painting of his wife's grandfather, a World War two veteran. He explained: "I've got a painting on my wall in my kitchen and it's my wife's grandfather. He was just a couple of days short of 102 before he passed and I painted him and he's sitting in an armchair with his World War two medals across his chest." Gareth also now helps other people diagnosed with Parkinson's to come to terms with their diagnosis. He explained: "Funny enough, I actually do talk to people who are recently diagnosed and need help. "They'll come over to my house or they'll phone me. We tend to stick together, belong to a Facebook page for Parkinson's. "We all stick together and we help each other out... talking's the best thing." Newly diagnosed patients often went through similar emotions, he added. "The biggest thing is fear, knowing it's not going to get better, it's going to get worse, and there is no cure. The tablets I take actually work for me but, believe it or not, they've been out since the '60s annd '70s with all these tablets, they'd been around for years and years, and [doctors working in the field of] Parkinson's are trying to find a cure. "I'm hoping come September to actually go on a trial with my consultant. I've asked to put my name forward and become a guinea pig, so to speak. Because you've just got to try something, you've just got to give it a go." Gareth has thrown his weight behind fundraising, raising significant funds for Parkinson's charities through quizzes, marathons, and rugby matches. Earlier this month – on May 4 – Gareth raised £8,000 when he underwent a sponsored head shave and wax at the Maltsters Arms pub in Whitchurch, Cardiff. He said: "I'll always help, no matter what charity, and if I am able to do anything, I'll do it. "This last one, this one we've done, all I had to do was sit down and have my hair cut. It was the easiest £8,000 I've ever been involved in making! "I've done charity rugby games as well because, when I was first diagnosed, I wanted to raise some money for Parkinson's, so I organised a rugby game. All the people I've been involved with over the years, coaching, playing with, playing against, they all turned up for me. We raised £1,680 that day. That was just one day. "Another time in work, when I used to work, I used to have a 'fat club', we used to call it the 'Big Boy's Belly Fat Club' and the boys used to pay a pound a week and I would have my scales in work and I'd weigh them and I'd write their weight down on the board to encourage them for next week to come in lighter. "This went on for a couple of years and a lot of people got to know about it. Again, we raised money and it was all sent over to Parkinson's." This Friday, Gareth is organising an auction in aid of Parkinson's charity, where shirts donated by Wales rugby stars Rhys Patchell and Ben Thomas will go under the hammer. Meanwhile, Gareth wishes people were more aware of Parkinson's and how to approach people with the disease. He recalled: "(At) Christmas time, I went to watch Cardiff rugby play. I wasn't feeling well. I couldn't explain why I was feeling like it, but I wasn't very well and I decided to leave the rugby halftime. "My wife was picking me up in town because of my condition. I became so bad quickly and I didn't know what it was. I had a chest infection as well. "I approached a man in Queen Street and I asked him for help because I was walking with cramps and I was stiff. I wasn't drunk by any means but this guy thought I was drunk, and I asked him for his help. He gave me the F-word, told me to go away. "It made me cross, because that was the first time that had ever happened. So I just want people, you know, who haven't got Parkinson's, to just realise when you look at somebody and they're a little bit different to normal, just think to yourself it could be something medical. "It could be something causing that problem. Give them a chance, there's always a story behind everybody." In the meantime, Gareth says he's had amazing support from his family. He said: "My wife, she keeps me motivated. My family, my children, my grandchildren. I'm a very lucky man. I've got a fantastic family and I've got a fantastic circle of friends and colleagues. I've been fortunate enough to be recognised in work and I actually went to meet the royal family at a garden party a couple of years ago. " Gareth added: "I've got three granddaughters and they're brilliant, six, four, three, and 18 months - nearly two. And my wife looks after them on a Tuesday, they come here to our house every Tuesday and I sit there and I just watch them and it makes me happy because I live through them. "You look at your children and you... You see them doing well, and you just think to yourself, 'I've done something right in life, having a good family'. That's my unit, what I call my unit. My children."
Yahoo
a day ago
- Health
- Yahoo
Why fava beans taste gross (and how scientists want to fix them)
Beef production is a significant source of planet-warming greenhouse gasses, and its land use often leads to deforestation. Plant-based food products are thus widely considered to be a more sustainable alternative. But there's one problem: to most people, they don't taste nearly as good as a juicy ribeye steak. In particular, people don't like fava beans (also called faba beans) because of their bitterness and the dry sensation they cause in the mouth, according to a Finnish consumer study reported by the University of legume, however, has incredible potential. It's highly nutritious and provides a great source of amino acids. What's more, dried faba beans have more protein than red meat, and some studies have even suggested that eating them improves the motor skills of patients with Parkinson's disease. 'People avoid faba beans in cooking and in the food industry especially because of their bitterness. In their current form, faba bean products have not sold very well either,' Fabio Tuccillo, a sensory and consumer scientist conducting his doctoral research at the University of Helsinki, explained in a statement. 'They are often also heavily seasoned to cover the bitter taste. Therefore, it is important to identify the compounds that cause unpleasant flavours.' [ Related: A new ingredient could revolutionize white bread. ] The idea is that if scientists discover the compounds behind these flavors, they can modify them through new technologies, processing methods, and even plant-breeding approaches to make fava beans a better-tasting ingredient for plant-based foods. In this spirit, Tuccillo reveals in his doctoral thesis that the bitterness and mouth-drying feeling is associated with compounds called vicine and convicine, in addition to several amino acids including phenylalanine, according to the university. He also identified compounds responsible for the beans' cereal-like smell. Fava beans 'can be used in a diverse range of food products, such as bread, pastry and other products. Once we know how to reduce the unpleasant flavour and sensation, we can produce increasingly pleasant faba bean raw materials,' explained Tuccillo, who is defending his doctoral thesis today. 'Improving the sensory quality of raw materials made from faba beans is necessary, if the aim is to succeed in the food market with products supporting sustainable development and plant-based diets.' Perhaps we'll all be enjoying delicious fava bread sooner than you think.
USA Today
a day ago
- Health
- USA Today
A potential new treatment for Parkinson's shows early promise
A potential new treatment for Parkinson's shows early promise | The Excerpt On a special episode (first released on May 29, 2025) of The Excerpt podcast: Parkinson's is a disease that afflicts an estimated 90,000 Americans every year. Dr. Lorenz Studer and Dr. Viviane Tabar of Memorial Sloan Kettering Cancer Center, joined USA TODAY The Excerpt to share more about a new stem cell-based therapy that creates nerve cells. The treatment is showing early promise. Hit play on the player below to hear the podcast and follow along with the transcript beneath it. This transcript was automatically generated, and then edited for clarity in its current form. There may be some differences between the audio and the text. Podcasts: True crime, in-depth interviews and more USA TODAY podcasts right here Karen Weintraub: Hello, and welcome to The Excerpt. I'm USA TODAY Health Reporter Karen Weintraub. Today is Thursday, May 29th, and this is a special episode of The Excerpt. You've no doubt heard of the chemical dopamine. It's often referenced as part of the brain's reward system when we do something pleasurable. Dopamine, or a lack thereof, also plays a critical role in the onset of Parkinson's, a disease that afflicts an estimated 90,000 Americans every year. Treatment for Parkinson's focuses on managing its many symptoms, as there is no cure. But a new stem cell therapy developed at Memorial Sloan Kettering Cancer Center for advanced Parkinson's is showing early promise. What's behind this incredible discovery and just how hopeful should patients be? Here to talk about this exciting new treatment and its impact on patients are the two physicians who helped make it a reality. Dr. Viviane Tabar and Dr. Lorenz Studer. Drs. Tabar and Studer, thanks so much for joining The Excerpt. Dr. Tabar, when someone is diagnosed with Parkinson's disease, what exactly is happening to their brain and their body? Dr. Viviane Tabar: Well, we think that at the time an individual is diagnosed with Parkinson's disease, they have already experienced degeneration or loss of a large number of their dopamine neurons. We are all born with a limited number of large, beautiful dopamine neurons that live in our brainstem and that project to multiple areas in the brain. They're involved in a lot of intricate activities, but an important element of their function is to modulate movement. So the individual very commonly will come to clinical attention because of movement difficulties, albeit there are other symptoms, loss of smell, gastrointestinal symptoms, difficulties with sleep, and it's a complex picture. But it's important to remember that at the time they receive this diagnosis, which today is still vastly made on a clinical basis, on an examination of the individual and listening to their symptoms, they have already lost probably 50% or more of their dopamine neurons and their projections. A potential new treatment for Parkinson's shows early promise A new stem cell-based therapy creates cells that make dopamine, a chemical that's critical to the disease. Karen Weintraub: And what are some of the everyday challenges your patients face? You mentioned motor control, cognitive issues also I think? Dr. Viviane Tabar: For the majority of patients, and keep in mind that Parkinson's is a disease that spans a variety of symptoms and spectrum of progression and intensity, for most patients it starts with manageable symptoms that they control well, could be a tremor, could be some stiffness in their gait. And for the majority, I would say cognitive change comes late, assuming a proper diagnosis of Parkinson's. So it becomes paradoxically even more problematic because it starts interfering with activities of daily living, your ability to get to and from your job. You're still high-performing, but you are impaired gradually. And you're fully cognitively there often, and so you're very aware of the slow degeneration that's essentially relentless. Karen Weintraub: And you mentioned jobs. Are people affected by Parkinson's primarily older, retiree age, or are there other groups at risk as well? Dr. Viviane Tabar: We didn't say necessarily retirees. Parkinson's, the sporadic form of it, which is the most common form, I mean by that the form that's not inherited, that happens commonly in the sixties or later. But nowadays, people in their fifties and sixties are considered at their prime still at work. Karen Weintraub: And others who are affected, we think of Michael J. Fox who is certainly younger when he started developing symptoms. Dr. Viviane Tabar: There are forms of Parkinson's that occur in a younger individual at a younger average age, and that is commonly related to specific mutations. And so the majority of Parkinson's disease occurs what we call sporadically, so without a hereditary or identified specific mutation that we are aware of. But some is related to a mutation, and those tend to occur at a younger age, but that's not the majority. Karen Weintraub: And is it clear what causes Parkinson's? You mentioned the neurons, but is there still some mystery there, and can the causes vary from person to person? Dr. Viviane Tabar: There is a lot of mystery. So in simple terms, we do not know the etiology of Parkinson's disease very specifically. Many things have been invoked, the environment, environmental toxins, a genetic predisposition outside of the genetic forms of the disease. And we can talk a lot about some exciting science trying to dissect what's going on, the role of inflammation, et cetera. But the short answer to your question is we're not able today to tell a patient what caused their Parkinson's, again, outside the relatively uncommon hereditary forms. Karen Weintraub: And can you walk us a little bit through how Parkinson's progresses over time? Is there a sort of a path, many paths, what does that look like? Dr. Viviane Tabar: So yes, there are many paths, but let's take an average situation. The patient would reach out to a physician, eventually come to the attention of a neurologist, they're examined, their brain scan is obtained. In the case of Parkinson's, often that scan is fine and normal to age and the symptoms are identified often, as we said earlier, motor symptoms. The common situation is that they get started on a form of dopamine that can reach the brain, and that makes them feel better and that is often referred to as the honeymoon period. And that goes on for a few years where the patient is almost back to normal but dependent on the medicine. And as time goes by, the disease process is such that they are losing more and more of their dopamine neurons. And at some point we start or the treating neurologist starts escalating the dose of the medication. And there are other medications that can support that. But essentially within a few years or several years depending, they reach a point where they're starting to experience side effects from the medication and a shortening of the periods where they are feeling okay and functioning. And that is where we start getting stuck in that there are no new medications that, I shouldn't say no new medications, there's always new medications, no formulations that try to extend the ability to help the individual. But you clearly plateau in terms of the effectiveness of pharmacological therapy for a lot of patients, not all. There are options that are surgical like inserting electrodes that is called deep brain stimulation, which will work for some patients. But we reach a point where the patient has lost most of their dopaminergic neurons and there is not much more that can be offered today to help the individual. Hence, the idea of what if we could replace those degenerated dopamine neurons? Karen Weintraub: Which brings us to Dr. Studer. Dr. Studer, when did you first think about using stem cells as a possible way to treat Parkinson's? Dr. Lorenz Studer: Well, it's really a very long story. In fact, it's I think nearly three decades when we first had the idea of doing so, which was the question, "Now, can we really replace cells in the brain and what will be the right source?" In fact, that was the goal of my laboratory starting 25 years ago, finding exactly what's the source of dopamine neurons. The challenge is how do you make this very, very specific nerve cell in the brain? And so that was a long journey, took us at least 10 years of basic research to understand, now what is the code of development? It's a little bit like trying to go through the steps that the cells go in normal development, but give them those signals one by one in a culture dish. And so it's a little bit like a code that we need to decipher and then to apply to the cells. And by 2011, we could do that finally in a study that showed that we did a good job because when we implant those cells back into a mouse, in a rat or in a monkey model of Parkinson's disease, we see benefit in that model. And that really then opened up the whole next new step, now can we do that not just in a animal model, but maybe eventually in humans? That was what they call the proof of concept. But then obviously it was not a long journey to get to the ultimate clinical patient. Karen Weintraub: And how might the stem cell therapies transform the treatment landscape? What opportunities does this offer? And are there specific symptoms that you expect to get better or everything or certain symptoms? Dr. Lorenz Studer: The dopamine acts primarily on the movement-related symptoms. That's the area where we think we can make the biggest impact. Whether it's also going to affect all the symptoms, it's more questionable. Now, for example, again, we said the patients can have loss of smell, they can have problems with severe constipation, and at later stage of the disease, cognitive issues. And at this point we don't have a good reason to believe that this therapy will also help with those symptoms. This has to be tested. It could be indirect effects, but the main effect we expect is that the movement disorder should improve. Again, we don't want to overstate it, but in a dream scenario, it would be you have still Parkinson's disease, so you cannot cure Parkinson's disease, but maybe if it worked, ideally you could cure the movement disorder component of Parkinson's disease. And so I think that's really what we are trying to develop with this type of cell therapy. And maybe in the future this will open up the same approach for all the cell types that might affect all the symptoms as well. So it's also kind of opening up the door to many other cell therapies in Parkinson's itself and maybe in other diseases as well, because it's one of the first cases now where really you actually replacing nerve cells in the brain, which sounds like a little bit of a science fiction approach. But I think this is one of the first examples where we really tried to attempt that and hopefully opening the door now for applications in the future. Karen Weintraub: And you said we can't call this a cure, obviously it's early days, but what would it take to get to a cure? More cell types? Dr. Lorenz Studer: Yeah. I think, because again, Parkinson's has more than just a movement disorder. So all that's not just movement-related, there is late stages cognitive problems, gastrointestinal problems, sleep problems, and those are unlikely to be treated with this cell type. So what you can envisage is yes, well, maybe you would have additional cell types that can attack that, or ideally, you brought that up now, what causes Parkinson's disease, it'll be a complementary approach where you would give the cells back, because many dopamine cells are already lost by the time you're diagnosed. So you get that movement-related symptoms hopefully restored, but at the same time, you'll find, like the whole field, many thousands researchers try to do that, find a therapy that can slow down or stop the progression. So you would gain back the function that you've already lost, but you would maybe not get some of those later symptoms. That would be even bigger dream in the future. Karen Weintraub: I was going to ask, Dr. Studer, where the research goes from here? Dr. Lorenz Studer: We always talk about bench to bedside, but there's also a bedside to bench. So where you kind of try to figure out, so what could you do even better now with regard to the cells that they function maybe more quickly or they are more potent or they have some additional features like we discussed? How could it treat some of the other symptoms in the future? So I think that's a big area for Parkinson's disease itself. How can we get the most benefit out of this kind of an approach? But then the other part is really there's so many other very severe diseases now. We talk about Alzheimer's disease, we talk about ELS and other disorders. Each of them might need a different approach, quite different. So in some case we don't think we can just replace nerve cells, but we still learn that maybe other approaches could be used in those specific disorders. And it then gives us a lot of encouragement when we see some progress in one area that this might be not just kind of a one-time go, but we might have opportunities to now give some help to those very difficult to treat neurodegenerative disorders where even today, this has been kind of some of the value of this for many of the drugs. Now, very, very few new drugs came up in the context of neurodegenerative disorders, and I don't think cell therapy is alone going to solve all of that, but it's yet the new tool that is becoming actually clinically a realistic option to replace cells, and I think that's quite exciting. There's some examples, for example, for treating eye disorders, so-called people who get blindness, macular degeneration, where data look quite promising. There's some examples maybe in very severe seizures where [inaudible 00:12:35] could be useful. So I think this is one of the very, very first example now where we now go all the way to this phase three study, but in the lab now we are thinking, "What did we learn? Why did it take us 25 years, for example? How can you make it quicker and what would be some of the next targets?" Because from the stem cell side, we learned a lot. So by now we can pretty much make any cell type of the brain. So that's a language to make this as no longer limiting. What's limiting is now to know what's really needed in each individual patient, which is going to be quite distinct and will take, again, a couple of years, but pretty confident not another 25-year step. Karen Weintraub: Well, we will stay tuned for that very exciting work. Thank you both so much for being on The Excerpt. Dr. Lorenz Studer: Thanks so much. Dr. Viviane Tabar: Thank you for having us. Karen Weintraub: Thanks to our senior producers, Shannon Rae Green and Kaely Monahan, for their production assistance. Our executive producer is Laura Beatty. Let us know what you think of this episode by sending a note to podcasts@ Thanks for listening. I'm USA TODAY Health Reporter Karen Weintraub. Taylor Wilson will be back tomorrow morning with another episode of The Excerpt.
Forbes
a day ago
- Entertainment
- Forbes
Ozzy Osbourne Gives Health Update Amid Upcoming Final Performance
LOS ANGELES, CALIFORNIA - JULY 29: Ozzy Osbourne attends the Ozzy Osbourne Album Special on ... More SiriusXM's Ozzy's Boneyard Channel at at SiriusXM Studios on July 29, 2022 in Los Angeles, California. (Photo byfor SiriusXM) With Black Sabbath and Ozzy Osbourne's final farewell show a month away, Ozzy Osbourne has given an update on his health and how he's preparing for his swan song performance at Back To The Beginning. Since 2018, Osbourne has been battling Parkinson's disease among a number of other physical injuries. Recently Osbounre opened up about the extensive physical therapy and training he's been undergoing on the SiriusXM's Ozzy Speaks show. 'I've got this trainer guy who helps people get back to normal, Osbourne stated. 'It's hard going, but he's convinced that he can pull it off for me. I'm giving it everything I've got." When asked by co-host Billy Morrison on whether or not he's stressed about performing at Back To The Beginning, Osbourne replied, "Sometimes, but what I do, if I start obsessing all the time, I'll be insane by Friday, you know? So, I'm just taking it one day at a time and when I do it one day at a time. You know, when we were talking about this [obsessive-compulsive disorder], whatever. I have that badly. All I can say is I'm giving 120%. If my God wants me to do the show, I'll do it." It's clear that Ozzy Osbourne's health has been in decline since he made the decision to retire from touring back in 2019. Prioritizing his health and ensuring he can commit to performaning at Back To The Beginning seems to be his main focus. That being said, fans shouldn't expect Osbourne or Black Sabbath to perform a full 90 minute set. In other recent interviews Osbourne has clearly stated, 'I'm not planning on doing a set with Black Sabbath but I am doing little bits and pieces with them. 'I am doing what I can, where I feel comfortable.' From the looks of it, Back To The Beginning seems to be promoting itself more as a celebration of Ozzy Osbourne and Black Sabbath's legacy, rather than a reunion show. Sure, it is a reunion of the original Black Sabbath lineup, however, the litany of legendary acts billed, namely Metallica, Guns N' Roses, TOOL, and Pantera seems to be the main draw, in addition to the guest musicians booked for the one day festival as well. In fact, it wouldn't be surprising if the plan was for some of these guest musicians to accompany Osbourne and Black Sabbath during each of their sets. It could be a great way for these iconic metal and rock musicians to show much they've been inspired by Ozzy Osbourne and Black Sabbath, which seems to be essentially what Back To The Beginning is all about – honoring heavy metal's founders.
NDTV
a day ago
- Health
- NDTV
Sleeping Disorders May Signal Risk Of Parkinson's Disease, Dementia: Study
New Delhi: Sleeping disorders may act as an early indicator of neurodegenerative diseases like Parkinson's disease and Lewy body dementia (LBD) -- a type of dementia, according to a study. The study focused on patients with Rapid eye movement behaviour disorder -- a sleep disorder where individuals physically act out their dreams during the rapid eye movement (REM) stage of sleep. "Normally, when we're asleep and dreaming, our muscles are paralysed, but around age 50, some people become very agitated during sleep and start punching, kicking and screaming," said Shady Rahayel, a medical professor at Université de Montréal in Canada. Unlike sleepwalking, which occurs during slow-wave sleep, RBD occurs during rapid eye movement (REM) sleep, he added, and it affects people of middle age. In the study, published in the journal eBioMedicine, the researchers said that nearly 90 per cent of people with the disorder will go on to develop either Parkinson's disease or LBD. "RBD is an early warning sign that certain mechanisms in the brain are no longer working as they should," said the team. "The people with RBD who come to see us are in good health... but of those who subsequently develop a disease, half will have Parkinson's and the other half LBD." Rahayel explained that with LBD, the second most common form of dementia after Alzheimer's, "patients are no longer able to function in everyday life". In addition to dementia, "they will have Parkinson's-like symptoms, vivid visual hallucinations, fluctuating attention and other symptoms." For the study, the team used data from 1,276 MRI scans of people at risk of, or with, Parkinson's disease or LBD, and also of healthy people. Using machine learning and computational models, the researchers identified two trajectories of brain atrophy progression. LBD seems to be associated with brain atrophy that begins in the cortex and then spreads to the interior of the brain, while in Parkinson's the atrophy progresses from the interior to the exterior of the brain. The team next aims to investigate the factors that lead to this deterioration in the cortex, such as vascular lesions, the effects of drugs, and of lifestyle choices. "Now that we have identified these new progression patterns, our goal is to be able to determine from an MRI whether a person has one of them so that we can provide the best possible care," said Rahayel.
