Podcasts about Lewy

In this episode, editor in chief Joseph E. Safdieh, MD, FAAN, highlights articles about a promising blood test to distinguish Parkinson's disease from dementia with Lewy bodies, how CAR T-cell therapies are showing potential for patients with glioblastoma, and a new wireless electroencephalogram device that can even monitor young children with epilepsy.

Q-BANK: https://www.patreon.com/highyieldfamilymedicineIntro - (0:35),Normal aging (1:37),Mild cognitive impairment (2:37),Reversible causes of dementia (4:50),Vitamin B12 deficiency (5:09),Hypothyroidism (6:25),Pseudo-dementia (6:52),Normal pressure hydrocephalus (7:42),Neurosyphilis (8:57),HIV-associated dementia (10:05),Delerium (11:04),Alzheimer's disease (12:38),Vascular dementia (17:25),Lewy body dementia (18:58),Frontotemporal dementia (20:38),Huntington's disease (21:55),Creutzfeld-Jakob disease (22:54),Practice questions (24:03)

 Glen Lauder, Luke Lewis and John Gibbs discuss the move by Ivan Cleary to rest 16 players in their 28 to four loss against the Bulldogs last night.

Here at the PODPOD we would like to take one last opportunity to thank all of our amazing listeners for the 2025 season. From The Holmes Files, to the pre-season content and then all the way throughout season 2025, this show does not happen without the listeners and we are truly grateful for each and everyone of you. We have had an absolute blast and hope you have enjoyed coming along the journey with us!Follow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

Multiple system atrophy is a rare, sporadic, adult-onset, progressive, and fatal neurodegenerative disease. Accurate and early diagnosis remains challenging because it presents with a variable combination of symptoms across the autonomic, extrapyramidal, cerebellar, and pyramidal systems. Advances in brain imaging, molecular biomarker research, and efforts to develop disease-modifying agents have shown promise to improve diagnosis and treatment. In this episode, Casey Albin, MD speaks with Tao Xie, MD, PhD, author of the article “Multiple System Atrophy” in the Continuum® August 2025 Movement Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Xie is director of the Movement Disorder Program, chief of the Neurodegenerative Disease Section in the department of neurology at the University of Chicago Medicine in Chicago, Illinois. Additional Resources Read the article: Multiple System Atrophy Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Full episode transcript available here Dr. Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Albin: Hello everyone, this is Dr Casey Albin. Today I'm interviewing Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Xie: Thank you so much, Dr Albin. My name is Tao Xie, and sometimes people also call me Tao Z. I'm a mood disorder neurologist, professor of neurology at the University of Chicago. I'm also in charge of the mood disorder program here, and I'm the section chief in the neurodegenerative disease in the Department of Neurology at the University of Chicago Medicine. Thank you for having me, Dr Albin and Dr Okun and the American Academy of Neurology. This is a great honor and pleasure to be involved in this education session. Dr Albin: We are delighted to have you, and thank you so much for the thoughtful approach to the diagnosis and management. I really want to encourage our listeners to check out this article. You know, one of the things that you emphasize is multiple system atrophy is a fairly rare condition. And I suspect that clinicians and trainees who even have a fair amount of exposure to movement disorders may not have encountered that many cases. And so, I was hoping that you could just start us off and walk us through what defines multiple system atrophy, and then maybe a little bit about how it's different from some of the more commonly encountered movement disorders. Dr Xie: This is a really good question, Dr Albin. Indeed, MSA---multisystem atrophy----is a rare disease. It is sporadic, adult-onset, progressive, fatal neurodegenerative disease. By the name MSA, multisystem atrophy. Clinically, it will present with multiple symptoms and signs involving multiple systems, including symptoms of autonomic dysfunction and symptoms of parkinsonism, which is polyresponsive to the levodopa treatment; and the symptom of cerebellar ataxia, and symptom of spasticity and other motor and nonmotor symptoms. And you may be wondering, what is the cause- underlying cause of these symptoms? Anatomically, we can find the area in the basal ganglia striatonigral system, particularly in the putamen and also in the cerebellar pontine inferior, all of the nuclear area and the specific area involved in the autonomic system in the brain stem and spinal cord: all become smaller. We call it atrophy. Because of the atrophy in this area, they are responsible for the symptom of parkinsonism if it is involved in the putamen and the cerebral ataxia, if it's involved in the pons and cerebral peduncle and the cerebellum. And all other area, if it's involved in the autonomic system can cause autonomic symptoms as well. So that's why we call it multisystem atrophy. And then what's the underlying cellular and subcellular pathological, a hallmark that is in fact caused by misfolded alpha-synuclein aggregate in the oligodontia site known as GCI---glial cytoplasmic increasing bodies---in the cells, and sometimes it can also be found in the neuronal cell as well in those areas, as mentioned, which causes the symptom. But clinically, the patient may not present all the symptoms at the same time. So, based on the predominant clinical symptom, if it's mainly levodopa, polyresponsive parkinsonism, then we call it MSAP. If it's mainly cerebellar ataxia, then we call it MSAC. But whether we call it MSP or MSC, they all got to have autonomic dysfunction. And also as the disease progresses, they can also present both phenotypes together. We call that mixed cerebellar ataxia and parkinsonism in the advanced stage of the disease. So, it is really a complicated disease. The complexity and the similarity to other mood disorders, including parkinsonism and the cerebellar ataxia, make it really difficult sometimes, particularly at the early stages of disease, to differentiate one from the other. So, that was challenging not only for other professionals, general neurologists and even for some movement disorder specialists, that could be difficult particularly if you aim to make an accurate and early diagnosis. Dr Albin: Absolutely. That is such a wealth of knowledge here. And I'm going to distill it just a little bit just to make sure that I understand this right. There is alpha-synuclein depositions, and it's really more widespread than one would see maybe in just Parkinson's disease. And with this, you are having patients present with maybe one of two subtypes of their clinical manifestations, either with a Parkinson's-predominant movement disorder pattern or a cerebellar ataxia type movement disorder pattern. Or maybe even mixed, which really, you know, we have to make things quite complicated, but they are all unified and having this shared importance of autonomic features to the diagnosis. Have I got that all sort of correct? Dr Xie: Correct. You really summarize well. Dr Albin: Fantastic. I mean, this is quite a complicated disease. I would pose to you sort of a case, and I imagine this is quite common to what you see in your clinic. And let's say, you know, a seventy-year-old woman comes to your clinic because she has had rigidity and poor balance. And she's had several falls already, almost always from ground level. And her family tells you she's quite woozy whenever she gets up from the chair and she tends to kind of fall over. But they noticed that she's been stiff,and they've actually brought her to their primary care doctor and he thought that she had Parkinson's disease. So, she started levodopa, but they're coming to you because they think that she probably needs a higher dose. It's just not working out very well for her. So how would you sort of take that history and sort of comb through some of the features that might make you more concerned that the patient actually has undiagnosed multiple systems atrophy? Dr Xie: This is a great case, because we oftentimes can encounter similar cases like this in the clinic. First of all, based on the history you described, it sounds like an atypical parkinsonism based on the slowness, rigidity, stiffness; and particularly the early onset of falls, which is very unusual for typical Parkinson disease. It occurs too early. If its loss of balance, postural instability, and fall occurred within three years of disease onset---usually the motor symptom onset---then it raises a red flag to suspect this must be some atypical Parkinson disorders, including multiple system atrophy. Particularly, pou also mentioned that the patient is poorly responsive to their levodopa therapy, which is very unusual because for Parkinson disease, idiopathic Parkinson disease, we typically expect patients would have a great response to the levodopa, particularly in the first 5 to 7 years. So to put it all together, this could be atypical parkinsonism, and I could not rule out the possibility of MSA. Then I need to check more about other symptoms including autonomic dysfunction, such as orthostatic hypertension, which is a blood pressure drop when the patient stands up from a lying-down position, or other autonomic dysfunctions such as urinary incontinence or severe urinary retention. So, in the meantime, I also have to put the other atypical Parkinson disorder on the differential diagnosis, such as PSP---progressive supranuclear palsy---and the DLBD---dementia with Lewy body disease.---Bear this in mind. So, I want to get more history and more thorough bedside assessment to rule in or rule out my diagnosis and differential diagnosis. Dr Albin: That's super helpful. So, looking for early falls, the prominence of autonomic dysfunction, and then that poor levodopa responsiveness while continuing to sort of keep a very broad differential diagnosis? Dr Xie: Correct. Dr Albin: One of the things that I just have to ask, because I so taken by this, is that you say in the article that some of these patients actually have preservation of smell. In medical school, we always learn that our Parkinson's disease patients kind of had that early loss of smell. Do you find that to be clinically relevant? Is that- does that anecdotally help? Dr Xie: This is a very interesting point because we know that the loss of smelling function is a risk effect, a prodromal effect, for the future development of Parkinson disease. But it is not the case for MSA. Strange enough, based on the literature and the studies, it is not common for the patient with MSA to present with anosmia. Some of the patients may have mild to moderate hyposmia, but not to the degree of anosmia. So, this is why even in the more recent diagnosis criteria, the MDS criteria published 2022, it even put the presence of anosmia in the exclusion criteria. So, highlight the importance of the smell function, which is well-preserved for the majority in MSA, into that category. So, this is a really interesting point and very important for us, particularly clinicians, to know the difference in the hyposmia, anosmia between the- we call it the PD, and the dementia Lewy bodies versus MSA. Dr Albin: Fascinating. And just such a cool little tidbit to take with us. So, the family, you know, you're talking to them and they say, oh yes, she has had several fainting episodes and we keep taking her to the primary care doctor because she's had urinary incontinence, and they thought maybe she had urinary tract infections. We've been dealing with that. And you're sort of thinking, hm, this is all kind of coming together, but I imagine it is still quite difficult to make this diagnosis based on history and physical alone. Walk our listeners through sort of how you're using MRI and DAT scan and maybe even some other biomarkers to help sort of solidify that diagnosis. Dr Xie: Yeah, that's a wonderful question. Yeah. First of all, UTI is very common for patients with MSA because of urinary retention, which puts them into a high risk of developing frequent UTI. That, for some patients, could be the very initial presentation of symptoms. In this case, if we check, we say UTI is not present or UTI is present but we treat it, then we check the blood pressure and we do find also hypertension---according to new diagnosis criteria, starting drop is 20mm mercury, but that's- the blood pressure drop is ten within three minutes. And also, in the meantime the patients present persistent urinary incontinence even after UTI was treated. And then the suspicion for MS is really high right at this point. But if you want increased certainty and a comfortable level on your diagnosis, then we also need to look at the brain MRI mark. This is a required according to the most recent MDS diagnosis criteria. The presence of the MRI marker typical for MSA is needed for the diagnosis of clinically established MSA, which holds the highest specificity in the clinical diagnosis. So then, we have- we're back to your question. We do need to look at the brain MRI to see whether evidence suggestive of atrophy around the putamen area, around the cerebellar pontine inferior olive area, is present or not. Dr Albin: Absolutely. That's super helpful. And I think clinicians will really take that to sort of helping to build a case and maybe recognizing some of this atypical Parkinson's disease as a different disease entity. Are there any other biomarkers in the pipeline that you're excited about that may give us even more clarity on this diagnosis? Dr Xie: Oh, yeah. This is a very exciting area. In terms of biomarker for the brain imaging, particularly brain MRI, in fact, today there's a landmark paper just published in the Java Neurology using AI, artificial intelligence or machine learning aid, diagnoses a patient with parkinsonism including Parkinson's disease, MSA, and PSP, with very high diagnostic accuracy ranging from 96% to 98%. And some of the cases even were standard for autopsy, with pathological verification at a very high accurate rate of 93.9%. This is quite amazing and can really open new diagnosis tools for us to diagnose this difficult disease; not only in an area with a bunch of mood disorder experts, but also in the rural area, in the area really in need of mood disorder experts. They can provide tremendous help to provide accurate, early diagnosis. Dr Albin: That's fantastic and I love that, increasing the access to this accurate diagnosis. What can't artificial intelligence do for us? That's just incredible. Dr Xie: And also, you know, this is just one example of how the brain biomarker can help us. Theres other---a fluid biomarker, molecular diagnostic tools, is also available. Just to give you an example, one thing we know over the past couple years is skin biopsy. Through the immunofluorescent reaction, we can detect whether the hallmark of abnormally folded, misfolded, and the phosphorate, the alpha-synuclein aggregate can be found just by this little pinch of skin biopsy. Even more advanced, there's another diagnosis tool we call the SAA, we call the seizure amplification assay, that can even help us to differentiate MSA from other alpha-synucleinopathy, including Parkinson disease and dementia with Lewy bodies. If we get a little sample from CSF, spinal cerebral fluids, even though this is probably still at the early stage, a lot of developments still ongoing, but this, this really shows you how exciting this area is now. We're really in a fast forward-moving path now. Dr Albin: It's really incredible. So, lots coming down the track in, sort of, MRI, but also with CSF diagnosis and skin biopsies. Really hoping that we can hone in some of those tools as they become more and more validated to make this diagnosis. Is that right? Dr Xie: Correct. Dr Albin: Amazing. We can talk all day about how you manage these in the clinic, and I really am going to direct our listeners to go and read your fantastic article, because you do such an elegant job talking about how this takes place in a multidisciplinary setting, if at all possible. But as a neurointensivist, I was telling you, we have so much trouble in the hospital. We have A-lines, and we have the ability to get rapid KUBs to look at Ilias, and we can have many people as lots of diagnosis, and we still have a lot of trouble treating autonomiclike symptoms. Really, really difficult. And so, I just wanted to kind of pick your brain, and I'll start with just the one of orthostatic hypotension. What are some of the tips that you have for, you know, clinicians that are dealing with this? Because I imagine that this is quite difficult to do without patients. Dr Xie: Exactly. This is indeed a very difficult symptom to deal with, particularly at an outpatient setting. But nowadays with the availability of more medication---to give an example, to treat patients with orthostatic hypertension, we have not only midodrine for the cortisol, we also have droxidopa and several others as well. And so, we have more tools at hand to treat the patient with orthostatic hypertension. But I think the key thing here, particularly for us to the patient at the outpatient setting: we need to educate the patient's family well about the natural history of the disease course. And we also need to tell them what's the indication and the potential side effect profile of any medication we prescribe to them so that they can understand what to expect and what to watch for. And in the meantime, we also need to keep really effective and timely communication channels, make sure that the treating physician and our team can be reached at any time when the patient and family need us so that we can be closely monitoring, their response, and also monitoring potential side effects as well to keep up the quality of care in that way. Dr Albin: Yeah, I imagine that that open communication plays a huge role in just making sure that patients are adapting to their symptoms, understanding that they can reach out if they have refractory symptoms, and that- I imagine this takes a lot of fine tuning over time. Dr Xie: Correct. Dr Albin: Well, this has just been such a delight to get to talk to you. I really feel like we could dive even deeper, but I know for the sake of time we have to kind of close out. Are there any final points that you wanted to share with our listeners before we end the interview? Dr Xie: I think for the patients, I want them to know that nowadays with advances in science and technology, particularly given a sample of rapid development in the diagnostic tools and the multidisciplinary and multisystemic approach to treatment, nowadays we can make an early and accurate diagnosis of the MSA, and also, we can provide better treatment. Even though so far it is still symptomatically, mainly, but in the near future we hope we can also discover disease-modifying treatment which can slow down, even pause or prevent the disease from happening. And for the treating physician and care team professionals, I just want them to know that you can make a difference and greatly help the patient and the family through your dedicated care and also through your active learning and innovative research. You can make a difference. Dr Albin: That's amazing and lots of hope for these patients. Right now, you can provide really great care to take care of them, make an early and accurate diagnosis; but on the horizon, there are really several things that are going to move the field forward, which is just so exciting. Again today, I've been really greatly honored and privileged to be able to talk to Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes for this and other issues. And thank you again to our listeners for joining us today. Dr Xie: Thank you so much for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Send us a textLewy Body Dementia is different from Alzheimer's dementia and affects 1.4 million people in the U.S. The Lewy Body Dementia Association helps those living with Lewy Body Dementia and their care partners with online support groups, free materials, symptom checklists and treatment options. Got questions? Lewy line at: 1-800-539-9767 lbda.orgYouTube video:  lbdatv Support the show

If you love our content and want to help support us for all of our years of work, please consider giving back by having your specific AFL Fantasy questions answered. At the link below, you have the option for a full team review, specific player / strategy questions and in-season trade and captain options. For a small fee you can have your questions answered whilst also supporting the PODPOD. All questions are greatly appreciated!Ask me a question to get a personalized audio response! - https://AskMeOnQu.com/podpodaflWant to join the PODPOD challenge and go up against this amazing community? We would love to have you! Join with the code below:HDPYPX6XThe winner will receive a custom AFL Fantasy ring courtesy of our friends at Supercoach Champion. Head over to supercoachchampion.com if you would like to enquire about custom rings or accessories for your own leagues!Like this episode? Follow us on spotify or subscribe on Apple Podcasts to make sure you are up to date for when new episodes are released!This episode was brought to you by Magic Sports. Magic Sports have a number of new products to help take your fantasy games to the next level:Slyder - https://www.slyder.team/loginAFL Fantasy Team Picker - https://picker.bolter.team/loginFollow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

Carol Weisman founded Board Builders, an international consultant firm focused on fundraising, philanthropy, and governance in 1994. She is the author of 11 books and is writing her 12th.  In 2020, her husband Frank Robbins was diagnosed with Lewy body dementia, Parkinson's disease, and spinal stenosis. Carol had to take a pause on her consultancy and speaking business to care for him.   Frank, sadly passed away in January of 2025. Carol is now returning to international work, grateful for the time she spent with Frank.  In Life After Loss, she speaks candidly about connecting with the world once again and how life is looking since losing Frank. “I started grieving the day that he was diagnosed. Because there was no medication. I knew there was no hope.  This was such a downward spiral, Frank died a little bit every day.”  Carol's endearing recollection brings her realistic vibe to a very painful experience.   As a listener, you are guaranteed a smile as well as a tear. “Following a loss, the biggest problem is loneliness especially if you were connected to a lot of people because of your spouse or your work.”  says Carol.  Carol has started internet dating, describing dating at 76 as really "bizarre”.  She ends encouragingly. “You recover at that point, it's a process. It's not an event. You don't all of a sudden wake up, go to a, some kind of meeting and you're okay.  Every death is different, every journey of healing, recovery, and repair is different.   You have got to find the pathway that works for you.”

If you love our content and want to help support us for all of our years of work, please consider giving back by having your specific AFL Fantasy questions answered. At the link below, you have the option for a full team review, specific player / strategy questions and in-season trade and captain options. For a small fee you can have your questions answered whilst also supporting the PODPOD. All questions are greatly appreciated!Ask me a question to get a personalized audio response! - https://AskMeOnQu.com/podpodaflWant to join the PODPOD challenge and go up against this amazing community? We would love to have you! Join with the code below:HDPYPX6XThe winner will receive a custom AFL Fantasy ring courtesy of our friends at Supercoach Champion. Head over to supercoachchampion.com if you would like to enquire about custom rings or accessories for your own leagues!Like this episode? Follow us on spotify or subscribe on Apple Podcasts to make sure you are up to date for when new episodes are released!This episode was brought to you by Magic Sports. Magic Sports have a number of new products to help take your fantasy games to the next level:Slyder - https://www.slyder.team/loginAFL Fantasy Team Picker - https://picker.bolter.team/loginFollow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

In this episode, we explore how nonprofit organizations like LBDA are working alongside industry partners to shape the evolving landscape of dementia biomarkers—bridging scientific innovation with real-world care. Featuring an engaging conversation with Dr. Sudhir Sivakumaran, Dr. Kathleen Poston, and Dr. Dustin Dunham on clinical utility, patient-centered research, and the road to broader adoption of biomarkers in Lewy body dementia, Alzheimer's disease and related disorders. This episode is sponsored by GE HealthCare

If you love our content and want to help support us for all of our years of work, please consider giving back by having your specific AFL Fantasy questions answered. At the link below, you have the option for a full team review, specific player / strategy questions and in-season trade and captain options. For a small fee you can have your questions answered whilst also supporting the PODPOD. All questions are greatly appreciated!Ask me a question to get a personalized audio response! - https://AskMeOnQu.com/podpodaflWant to join the PODPOD challenge and go up against this amazing community? We would love to have you! Join with the code below:HDPYPX6XThe winner will receive a custom AFL Fantasy ring courtesy of our friends at Supercoach Champion. Head over to supercoachchampion.com if you would like to enquire about custom rings or accessories for your own leagues!Like this episode? Follow us on spotify or subscribe on Apple Podcasts to make sure you are up to date for when new episodes are released!This episode was brought to you by Magic Sports. Magic Sports have a number of new products to help take your fantasy games to the next level:Slyder - https://www.slyder.team/loginAFL Fantasy Team Picker - https://picker.bolter.team/loginFollow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Michael S. Okun, MD, FAAN, who served as the guest editor of the August 2025 Movement Disorders issue. They provide a preview of the issue, which publishes on August 1, 2025. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Okun is the director at Norman Fixel Institute for Neurological Diseases and distinguished professor of neurology at University of Florida in Gainesville, Florida. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @MichaelOkun Full episode transcript available here: Dr Jones: Our ability to move through the world is one of the essential functions of our nervous system. Gross movements like walking ranging down to fine movements with our eyes and our hands, our ability to create and coordinate movement is something many of us take for granted. So what do we do when those movements stop working as we intend? Today I have the opportunity to speak with one of the world's leading experts on movement disorders, Dr Michael Okun, about the latest issue of Continuum on Movement Disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Michael Okun, who is Continuum's guest editor for our latest issue on movement disorders. Dr Okun is the Adelaide Lackner Distinguished Professor of Neurology at the University of Florida in Gainesville, where he's also the director of the Norman Fixel Institute for Neurological Diseases. Dr Okun, welcome, and thank you for joining us today. Why don't you introduce yourselves to our listeners?  Dr Okun: It's great to be here today. And I'm a neurologist. Everybody who knows me knows I'm pretty simple. I believe the patient's the sun and we should always orbit around the person with disease, and so that's how I look at my practice. And I know we always participate in a lot of research, and I've got a research lab and all those things. But to me, it's always the patients and the families first. So, it'll be great to have that discussion today.  Dr Jones: Yeah, thank you for that, Dr Oaken. Obviously, movement disorders is a huge part of our field of neurology. There are many highly prevalent conditions that fit into this category that most of our listeners will be familiar with: idiopathic Parkinson's disease, essential tremor, tic disorders and so on. And having worked with trainees for a long time, it's one of the areas that I see a lot of trainees gravitate to movement disorders. And I think it's in part because of the prevalence; I think it's in part because of the diversity of the specialty with treatment options and DBS and Botox. But it's also the centrality of the neurologic exam, right? That's- the clinical examination of the patient is so fundamental. And we'll cover a lot of topics today with some questions that I have for you about biomarkers and new developments in the field. But is that your sense too, that people are drawn to just the old-fashioned, essential focus on the neurologic encounter and the neurologic exam? Dr Okun: I believe that is one of the draws to the field of movement. I think that you have neurologists from all over the world that are really interested and fascinated with what things look like. And when you see something that's a little bit, you know, off the normal road or off the normal beaten path… and we are always curious. And so, I got into movement disorders, I think, accidentally; I think even as a child, I was looking at people who had abnormal movements and tremors and I was very fascinated as to why those things happened and what's going on in the brain. And, you know, what are the symptoms and the signs. And then later on, even as my own career developed, that black bag was so great as a neurologist. I mean, it makes us so much more powerful than any of the other clinicians---at least in my biased opinion---out on the wards and out in the clinic. And, you know, knowing the signs and the symptoms, knowing how to do a neurological examination and really walking through the phenomenology, what people look like, you know, which is different than the geno- you know, the genotypes, what the genes are. What people look like is so much more important as clinicians. And so, I think that movement disorders is just the specialty for that, at least in my opinion. Dr Jones: And it helps bring it back to the patient. And that's something that I saw coming through the articles in this issue. And let's get right to it. You've had a chance to review all these articles on all these different topics across the entire field of movement disorders. As you look at that survey of the field, Dr Okun, what do you think is the most exciting recent development for patients with movement disorders?  Dr Okun: I think that when you look across all of the different specialties, what you're seeing is a shift. And the shift is that, you know, a lot of people used to talk in our generation about neurology being one of these “diagnose and adios” specialties. You make the diagnosis and there's nothing that you can do, you know, about these diseases. And boy, that has changed. I mean, we have really blown it out of the water. And when you look at the topics and what people are writing about now and the Continuum issue, and we compare that the last several Continuum issues on movement disorders, we just keep accumulating a knowledge base about what these things look like and how we can treat them. And when we start thinking about, you know, all of the emergence of the autoimmune disorders and identifying the right one and getting something that's quite treatable. Back in my day, and in your day, Lyle, we saw these things and we didn't know what they were. And now we have antibodies, now we can identify them, we can pin them down, and we can treat many of them and really change people's lives. And so, I'm really impressed at what I see in changes in identification of autoimmune disorders, of channelopathies and some of the more rare things, but I'm also impressed with just the fundamental principles of how we're teaching people to be better clinicians in diseases like Parkinson's, Huntington's, ataxia, and Tourette. And so, my enthusiasm for this issue of Continuum is both on, you know, the cutting edge of what we're seeing based on the identification on our exams, what we can do for these people, but also the emergence of how we're shifting and providing much better care across a continuum for folks with basal ganglia diseases. Dr Jones: Yeah, I appreciate that perspective, Dr Okun. One of the common themes that I saw in the issue was with these new developments, right, when you have new tools like new diagnostic biomarker tools, is the question of if and when and how to integrate those into daily clinical practice, right? So, we've had imaging biomarkers for a while, DAT scans, etc. For patients with idiopathic Parkinson disease, one of the things that I hear a lot of discussion and controversy about are the seed amplification assays as diagnostic biomarkers. What can you tell us about those? Are those ready for routine clinical use yet?  Dr Okun: I think the main bottom-line point for folks that are out there trying to practice neurology, either in general clinics or even in specialty clinics, is to know that there is this movement toward, can we biologically classify a disease? One of the things that has, you know, really accelerated that effort has been the development of these seed amplification assays, which---in short for people who are listening---are basically, we “shake and bake” these things. You know? We shake them for like 20 hours and we use these prionlike proteins, and we learn from diseases like prion disease how to kind of tag these things and then see, do they have degenerative properties? And in the case of Parkinson's disease, we're able to do this with synuclein. That is the idea of a seed amplification assay. We're able to use this to see, hey, is there synuclein present or not in this sample? And people are looking at things like cerebrospinal fluid, they're looking at things like blood and saliva, and they're finding it. The challenge here is that, remember- and one of the things that's great about this issue of Continuum is, remember, there are a whole bunch of different synucleinopathies. So, Dr Jones, it isn't just Parkinson's disease. So, you've got Parkinson's disease, you've got Lewy body, you know, and dementia with Lewy bodies. You've got, you know, multiple system atrophy is within that synucleinopathy, you know, group primary autonomic failure… so not just Parkinson's disease. And so, I think we have to tap the brakes as clinicians and just say, we are where we are. We are moving in that direction. And remember that a seed amplification assay gives you some information, but it doesn't give you all the information. It doesn't forgive you looking at a person over time, examining them in your clinic, seeing how they progress, seeing their response to dopamine- and by the way, several of these genes that are associated with Parkinson; and there's, you know, less than 20% of Parkinson is genetic, but several of these genes, in a solid third---and in some cases, in some series, even more---miss the synuclein assay, misses, you know, the presence of a disease like Parkinson's disease. And so, we have to be careful in how we interpret it. And I think we're more likely to see over time a gemish: we're going to smush together all this information. We're going to get better with MRIs. And so, we're actually doing much better with MRIs and AI-based intelligence. We've got DAT scans, we've got synuclein assays. But more than anything, everybody listening out there, you can still examine the person and examine them over time and see how they do over time and see how they do with dopamine. And that is still a really, really solid way to do this. The synuclein assays are probably going to be ready for prime time more in choosing and enriching clinical trials populations first. And you know, we're probably 5, 10 years behind where Alzheimer's is right now. So, we'll get there at some point, but it's not going to be a silver bullet. I think we're looking at these are going to be things that are going to be interpreted in the context for a clinician of our examination and in the context of where the field is and what you're trying to use the information for. Dr Jones: Thank you for that. And I think that's the general gestalt I got from the articles and what I hear from my colleagues. And I think we've seen this in other domains of neurology, right? We have the specificity and sensitivity issues with the biomarkers, but we also have the high prevalence of copathology, right? People can have multiple different neurodegenerative problems, and I think it gets back to that clinical context, like you said, following the patient longitudinally. That was a theme that came out in the idiopathic Parkinson disease article. And while we're on Parkinson disease, you know, the first description of that was what, more than two hundred years ago. And I think we're still thinking about the pathophysiology of that disorder. We understand risk factors, and I think many of our listeners would be familiar with those. But as far as the actual cause, you know, there's been discussion in recent years about, is there a role of the gut microbiome? Is this a prionopathic disorder? What's your take on all of that?  Dr Okun: Yeah, so it's a great question. It's a super-hot area right now of Parkinson. And I kind of take this, you know, apart in a couple of different ways. First of all, when we think about Parkinson disease, we have to think upstream. Like, what are the cause and causes? Okay? So, Parkinson is not one disease, okay? And even within the genes, there's a bunch of different genes that cause it. But then we have to look and say, well, if that's less than 20% depending on who's counting, then 80% don't have a single piece of DNA that's closely associated with this syndrome. And so, what are we missing with environment and other factors? We need to understand not what happens at the end of the process, not necessarily when synuclein is clumping- and by the way, there's a lot of synuclein in the brains normally, and there's a lot of Tau in people's brains who have Parkinson as well. We don't know what we don't know, Dr Jones. And so when we begin to think about this disease, we've got to look upstream. We've got to start to think, where do things really start? Okay? We've got to stop looking at it as probably a single disease or disorder, and it's a circuit disorder. And then as we begin to develop and follow people along that pathway and continuum, we're going to realize that it's not a one-size-fits-all equation when we're trying to look at Parkinson. By the way, for people listening, we only spend two to three cents out of every dollar on prevention. Wouldn't prevention be the best cure, right? Like, if we were thinking about this disease. And so that's something that we should be, you know, thinking about. And then the other is the Global Burden of Disease study. You know, when we wrote about this in a book called Ending Parkinson's Disease, it looked like Parkinson's was going to double by 2035. The new numbers tell us it's almost double to the level that we expected in 2035 in this last series of numbers. So, it's actually growing much faster. We have to ask why? Why is it growing faster? And then we have lots of folks, and even within these issues here within Continuum, people are beginning to talk about maybe these environmental things that might be blind spots. Is it starting in our nose? Is it starting in our gut? And then we get to the gut question. And the gut question is, if we look at the microbiomes of people with Parkinson, there does seem to be, in a group of folks with Parkinson, a Parkinson microbiome. Not in everyone, but if you look at it in composite, there seems to be some clues there. We see changes in Lactobacillus, we see some bacteria going up that are good, some bacteria going down, you know, that are bad. And we see flipping around, and that can change as we put people on probiotics and we try to do fecal microbiota transplantations- which, by the way, the data so far has not been positive in Parkinson's. Doesn't mean we might not get there at some point, but I think the main point here is that as we move into the AI generation, there are just millions and millions and millions of organisms within your gut. And it's going to take more than just our eyes and just our regular arithmetic. You and I probably know how to do arithmetic really well, but this is, like, going to be a much bigger problem for computers that are way smarter than our brains to start to look and say, well, we see the bacteria is up here. That's a good bacteria, that's a good thing or it's down with this bacteria or this phage or there's a relationship or proportion that's changing. And so, we're not quite there. And so, I always tell people---and you know, we talk about the sum in the issue---microbiomes aren't quite ready for prime time yet. And so be careful, because you could tweak the system and you might actually end up worse than before you started. So, we don't know what we don't know on this issue.  Dr Jones: And that's a great point. And one of the themes they're reading between the lines is, we will continue to work on understanding the bio-pathophysiology, but we can't wait until that day to start managing the risk factors and treating patients, which I think is a good point. And if we pivot to treatment here a little bit, you know, one of the exciting areas of movement disorders---and really neurology broadly, I think movement disorders has led the field in many ways---is bioelectronic therapy, or what one of my colleagues taught me is “electroceutical therapy”, which I think is a wonderful term. Dr Okun, when our listeners are hearing about the latest in deep brain stimulation in patients who have movement disorders, what should they know? What are the latest developments in that area with devices? Dr Okun: Yeah. So, they should know that things are moving rapidly in the field of putting electricity into the brain. And we're way past the era where we thought putting a little bit of electricity was snake oil. We know we can actually drive these circuits, and we know that many of these disorders---and actually, probably all of the disorders within this issue of Continuum---are all circuit disorders. And so, you can drive the circuit by modulating the circuit. And it's turned out to be quite robust with therapies like deep brain stimulation. Now, we're seeing uses of deep brain stimulation across multiple of these disorders now. So, for example, you may think of it in Parkinson's disease, but now we're also seeing people use it to help in cases where you need to palliate very severe and bothersome chorea and Huntington's disease, we're seeing it move along in Tourette syndrome. We of course have seen this for various hyperkinetic disorders and dystonias. And so, the main thing for clinicians to realize when dealing with neuromodulation is, take a deep breath because it can be overwhelming. We have a lot of different devices in the marketplace and no matter how many different devices we have in the marketplace, the most important thing is that we get the leads. You know, where we're stimulating into the right location. It's like real estate: location, location, location, whether you've got a lead that can steer left, right, up, down and do all of these things. Second, if you're feeling overwhelmed because there are so many devices and so many settings, especially as we put these leads in and they have all sorts of different, you know, nodes on them and you can steer this way and that way, you are not alone. Everybody is feeling that way now. And we're beginning to see AI solutions to that that are going to merge together with imaging, and then we're moving toward an era of, you know, should I say things like robotic programming, where it's going to be actually so complicated as we move forward that we're going to have to automate these systems. There's no way to get this and scale this for all of the locales within the United States, but within the entire world of people that need these types of devices and these therapies. And so, it's moving rapidly. It's overwhelming. The most important thing is choosing the right person. Okay? For this, with multidisciplinary teams, getting the lead in the right place. And then all these other little bells and whistles, they're like sculpting. So, if you think of a sculpture, you kind of get that sculpture almost there. You know, those little adds are helping to maybe make the eyes come out a little more or the facial expression a little bit better. There's little bits of sculpting. But if you're feeling overwhelmed by it, everybody is. And then also remember that we're starting to move towards some trials here that are in their early stages. And a lot of times when we start, we need more failures to get to our successes. So, we're seeing trials of people looking at, like, oligo therapies and protein therapies. We're seeing CRISPR gene therapies in the laboratory. And we should have a zero tolerance for errors with CRISPR, okay? we still have issues with CRISPR in the laboratory and which ones we apply it to and with animals. But it's still pretty exciting when we're starting to see some of these therapies move forward. We're going to see gene therapies, and then the other thing we're going to see are nano-therapies. And remember, smaller can be better. It can slip across the blood brain barrier, you have very good surface area-to-volume ratios, and we can uncage drugs by shining things like focused ultrasound beams or magnets or heat onto these particles to turn them on or off. And so, we're seeing a great change in the field there. And then also, I should mention: pumps are coming and they're here. We're getting pumps like we have for diabetes and neurology. It's very exciting. It's going to be overwhelming as everybody tries to learn how to do this. So again, if you're feeling overwhelmed, so am I. Okay? But you know, pumps underneath the skin for dopamine, pumps underneath the skin for apomorphine. And that may apply to other disorders and not just Parkinson as we move along, what we put into those therapies. So, we're seeing that age come forward. And then making lesions from outside the brain with focused ultrasound, we're starting to get better at that. Precision is less coming from outside the brain; complications are also less. And as we learn how to do that better, that also can provide more options for folks. So, a lot of things to read about in this issue of Continuum and a lot of really interesting and beyond, I would say, you know, the horizon as to where we're headed.  Dr Jones: Thank you for that. And it is a lot. It can be overwhelming, which I guess is maybe a good reason to read the issue, right? I think that's a great place to end and encourage our listeners to pick up the issue. And Dr Okun, I want to thank you for joining us today. Thank you for such a great discussion on movement disorders. I learned a lot. I'm sure our listeners will as well, given the importance of the topic, your leadership in the field over many years. I'm grateful that you have put this issue together. So, thank you. And you're a busy person. I don't know how we talked you into doing this, but I'm really glad that we did.  Dr Okun: Well, it's been my honor. And I just want to point out that the whole authorship panel that agreed to write these articles, they did all the work. I'm just a talking head here, you know, telling you what they did, but they're writing, and the people that are in the field are really, you know, leading and helping us to understand, and have really put it together in a way that's kind of helped us to be better clinicians and to impact more lives. So, I want to thank the group of authors, and thank you, Dr Jones. Dr Jones: Again, we've been speaking with Dr Michael Okun, guest editor of Continuum's most recent issue on movement disorders. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

Round 20 is done and dusted, and Heff and Lewy are here to break down all the key fantasy moments from the past week from a keeper league perspective. They'll dissect standout performances, important role changes, and highlight the players you need to have on your radar as fantasy finals come into focus.If you want to get ahead in your keeper leagues and discover those sneaky sleepers and hidden gems, this episode is packed with strategy, fresh names, and insights to help you set up for a strong finish to your season.Stick around for Listener Questions at the end of the show!Website: https://keeperleaguepod.com.au/Membership: https://keeperleaguepod.com.au/keeper-league-membership/Join our Discord server: https://discord.gg/APjqvT22zeJoin the Keeper Fantasy platform: https://keeperfantasy.com/FootyNumbers.com: https://footynumbers.comPlay FootyHeads: https://footyheads.comSubscribe on YouTube: https://www.youtube.com/@keeperleaguepod?sub_confirmation=1

If you love our content and want to help support us for all of our years of work, please consider giving back by having your specific AFL Fantasy questions answered. At the link below, you have the option for a full team review, specific player / strategy questions and in-season trade and captain options. For a small fee you can have your questions answered whilst also supporting the PODPOD. All questions are greatly appreciated!Ask me a question to get a personalized audio response! - https://AskMeOnQu.com/podpodaflWant to join the PODPOD challenge and go up against this amazing community? We would love to have you! Join with the code below:HDPYPX6XThe winner will receive a custom AFL Fantasy ring courtesy of our friends at Supercoach Champion. Head over to supercoachchampion.com if you would like to enquire about custom rings or accessories for your own leagues!Like this episode? Follow us on spotify or subscribe on Apple Podcasts to make sure you are up to date for when new episodes are released!This episode was brought to you by Magic Sports. Magic Sports have a number of new products to help take your fantasy games to the next level:Slyder - https://www.slyder.team/loginAFL Fantasy Team Picker - https://picker.bolter.team/loginFollow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

159 Innovative Tools for Dementia Care - An Interview with Angela Fairhurst of Geri-Gadgets In this episode of Hospice Explained, Marie Betcher interviews Angela Fairhurst, founder and CEO of Geri-Gadgets. Angela shares her journey of creating Geri-Gadgets, a company dedicated to enhancing the lives of individuals with dementia through safe and sensory tools. Highlighting the importance of meaningful connections, Angela discusses the products she developed inspired by her mother's battle with Lewy body dementia. She also elaborates on the profound impact these tools have on patients and caregivers alike, aiming to reduce the stigma around cognitive decline. Additionally, Angela emphasizes the rewarding nature of her work and the importance of proper care and touch in dementia treatment. Throughout the conversation, the significance of hospice care in easing end-of-life transitions is underscored. 00:00 Introduction to Hospice Explained 00:48 Understanding Pressure Injuries and Cloud Nine Care 01:25 Interview with Angela Fairhurst: Founder of Geri-Gadgets 02:35 Angela's Personal Journey with Dementia 03:01 Experiences with Hospice Care 06:28 Challenges of Dementia Diagnosis and Care 07:39 Angela's Mother's Final Years 10:58 The Impact of Dementia on Family Life 15:34 The Final Days and Hospice Support 16:23 Discovering the Need for Sensory Toys 17:04 Experimenting with Different Toys 17:59 Creating the Sensory Mat 18:44 Developing a Product Line 19:12 The Story of Jeremy 19:34 Designing for the Aging Eye 20:09 Product Features and Benefits 22:11 Market Reception and Reviews 22:30 Challenges and Future Plans 24:06 Global Interest and Expansion 28:39 The Importance of Connection 29:46 The Comfort of Geri-Gadgets 30:39 Making a Difference 31:13 Conclusion and Call to Action https://www.geri-gadgets.com/ Hospice Explained Affiliates & Contact Information Buying from these Affilite links will help support this Podcast.  Maire introduces a partnership with Suzanne Mayer RN inventor of the  cloud9caresystem.com,  When patients remain in the same position for extended periods, they are at high risk of developing pressure injuries, commonly known as bedsores. One of the biggest challenges caregivers face is the tendency for pillows and repositioning inserts to easily dislodge during care.(Suzanne is a former guest on Episode #119) When you order with Cloud 9 care system, please tell them you heard about them from Hospice Explained.(Thank You)  If you would, you can donate to help support Hospice Explained at the Buy me a Coffee link  https://www.buymeacoffee.com/Hospice Marie's Contact Marie@HospiceExplained.com www.HospiceExplained.com   Finding a Hospice Agency 1. You can use Medicare.gov to help find a hospice agency, 2. choose Find provider 3. Choose Hospice 4. then add your zip code This should be a list of Hospice Agencies local to you or your loved one.

In this episode of Talking Sleep, host Dr. Seema Khosla welcomes Dr. Luca Baldelli, a neurologist from the University of Bologna and Treasurer-Elect of the International REM Sleep Behavior Disorder Study Group, to discuss breakthrough research on predicting which RBD patients will develop neurodegenerative diseases. Building on the AASM's updated RBD guidelines, Dr. Baldelli presents compelling evidence for using simple autonomic reflex testing to identify patients at highest risk for phenoconversion to conditions like Parkinson's disease and dementia with Lewy bodies. His research demonstrates that objective autonomic testing, particularly orthostatic assessments, can reveal early neurogenic orthostatic hypotension that precedes overt neurodegeneration by years. The conversation explores practical clinical applications: How can sleep medicine practitioners implement these screening protocols? What constitutes abnormal autonomic function in RBD patients? How do we interpret changes over time, and when should patients be referred for neurological evaluation? Dr. Baldelli shares his longitudinal monitoring framework that could transform how we counsel RBD patients about their future risk. This episode addresses critical questions about biomarker development in prodromal neurodegeneration, the timeline of autonomic changes, and evidence-based approaches to patient discussions about prognosis. Dr. Baldelli also discusses current research initiatives and potential therapeutic interventions for high-risk patients. Whether you're a sleep medicine physician, neurologist, or researcher interested in neurodegenerative diseases, this episode provides essential insights into improving early detection and patient care in RBD. Join us for this informative discussion that bridges sleep medicine and neurology to enhance clinical decision-making and patient outcomes.

If you love our content and want to help support us for all of our years of work, please consider giving back by having your specific AFL Fantasy questions answered. At the link below, you have the option for a full team review, specific player / strategy questions and in-season trade and captain options. For a small fee you can have your questions answered whilst also supporting the PODPOD. All questions are greatly appreciated!Ask me a question to get a personalized audio response! - https://AskMeOnQu.com/podpodaflWant to join the PODPOD challenge and go up against this amazing community? We would love to have you! Join with the code below:HDPYPX6XThe winner will receive a custom AFL Fantasy ring courtesy of our friends at Supercoach Champion. Head over to supercoachchampion.com if you would like to enquire about custom rings or accessories for your own leagues!Like this episode? Follow us on spotify or subscribe on Apple Podcasts to make sure you are up to date for when new episodes are released!This episode was brought to you by Magic Sports. Magic Sports have a number of new products to help take your fantasy games to the next level:Slyder - https://www.slyder.team/loginAFL Fantasy Team Picker - https://picker.bolter.team/loginFollow us on X:The PODPOD: @podpodAFLHolmesy: @HolmesyheroesLewy: @LewyAFHarmey: @jonharmeyDos: @HKdosSam: @grillis03

More than just Rugby!

Mutations in LRRK2 are a common cause of familial and sporadic Parkinson's. Though clinical features resemble typical PD, about half of cases lack Lewy pathology. Doctors Hiroaki Sekiya and Nanna Møller Jensen discuss their recent studies on the neuropathology of LRRK2-PD patients. They dive into their methods and how proximity ligation assays may compare to alpha-synuclein seeding assays in identification of alpha-synuclein oligomers. Together they explain their surprising results on how alpha-synuclein oligomers may be a key early feature in LRRK2-PD. Read the first article. Read the second article.

Jane Stelboum, a yoga instructor and Certified Brain Longevity® Specialist, with a background in advertising, shares her insights on brain longevity and Alzheimer's prevention. Drawing from personal experience with her mother's Alzheimer's and Lewy body dementia, Jane emphasizes the importance of lifestyle choices in maintaining brain health. She highlights the four pillars of Alzheimer's prevention: stress management, diet, exercise, and spiritual fitness. Stress management involves techniques like yoga and breathing exercises to reduce cortisol levels. A Mediterranean diet, rich in fruits, vegetables, and lean proteins, is recommended for its potential to lower Alzheimer's risk. Exercise, both physical and mental, is crucial for brain health, with yoga offering unique benefits through poses that stimulate brain activity. Spiritual fitness, encompassing connections to community and nature, combats isolation and loneliness. Jane also underscores the significance of quality sleep for cognitive health. Through her company, Sarasvate, she offers workshops and one-on-one coaching to share these tools, aiming to enhance the quality of life for individuals and caregivers alike.https://sarasvate.com/Recording https://www.retirementlivingsourcebook.com/videos/finding-joy-and-meaning-appreciative-inquiry-for-life-and-death-with-jill-greenbaum-8052

Lewy body dementia affects over a million people in the United States, but many people don't know much about it. It's difficult to diagnose and often misdiagnosed. A new documentary called “Facing the Wind” shines a light on Lewy body dementia, both living with it and caring for someone who has the disease. Racquel Williams talks with Philadelphia filmmaker Tony Heriza and Linda Szypula, who lives in Plymouth Meeting and whose journey caring for her husband is featured in the film. Scribe Video Center is hosting a screening of “Facing the Wind” on September 18. Listen to Linda's podcast, “Lewy Body Roller Coaster”, here. Then, on Shara in the City, we visit one of Fairmount Park's oldest buildings - the Ohio House, which dates back to the centennial World's Fair in 1876. Shara Dae Howard takes a tour and learns about the building's deep history. To learn more about listener data and our privacy practices visit: https://www.audacyinc.com/privacy-policy Learn more about your ad choices. Visit https://podcastchoices.com/adchoices

Presidential advisor and former News Hour contributor David Gergen died at 83 after being diagnosed with Lewy body dementia. Throughout his career, Gergen served four presidents, both Democrats and Republicans, and he spent many Friday nights offering his insights and analysis here on the MacNeil/Lehrer NewsHour. Geoff Bennett has this remembrance. PBS News is supported by - https://www.pbs.org/newshour/about/funders

Presidential advisor and former News Hour contributor David Gergen died at 83 after being diagnosed with Lewy body dementia. Throughout his career, Gergen served four presidents, both Democrats and Republicans, and he spent many Friday nights offering his insights and analysis here on the MacNeil/Lehrer NewsHour. Geoff Bennett has this remembrance. PBS News is supported by - https://www.pbs.org/newshour/about/funders

Normal pressure hydrocephalus (NPH) is a clinical syndrome characterized by the triad of gait apraxia, cognitive impairment, and bladder dysfunction in the radiographic context of ventriculomegaly and normal intracranial pressure. Accurate diagnosis requires consideration of clinical and imaging signs, complemented by tests to exclude common mimics. In this episode, Lyell Jones, MD, FAAN speaks with Abhay R. Moghekar, MBBS, author of the article “Clinical Features and Diagnosis of Normal Pressure Hydrocephalus” in the Continuum® June 2025 Disorders of CSF Dynamics issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Moghekar is an associate professor of neurology at Johns Hopkins University School of Medicine in Baltimore, Maryland. Additional Resources Read the article: Clinical Features and Diagnosis of Normal Pressure Hydrocephalus Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today I'm interviewing Dr Abhay Moghekar, who recently authored an article on the clinical features and diagnosis of normal pressure hydrocephalus for our first-ever issue of Continuum dedicated to disorders of CSF dynamics. Dr Moghekar is an associate professor of neurology and the research director of the Cerebrospinal Fluid Center at Johns Hopkins University in Baltimore, Maryland. Dr Moghekar, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Moghekar: Thank you, Dr Jones. I'm Abhay Moghekar. I'm a neurologist at Hopkins, and I specialize in seeing patients with CSF disorders, of which normal pressure hydrocephalus happens to be the most common. Dr Jones: And let's get right to it. I think most of our listeners who are neurologists in practice have encountered normal pressure hydrocephalus, or NPH; and it's a challenging disorder for all the reasons that you outline in your really outstanding article. If you were going to think of one single most important message to our listeners about recognizing patients with NPH, what would that be? Dr Moghekar: I think I would say there are two important messages. One is that the triad is not sufficient to make the diagnosis, and the triad is not necessary to make the diagnosis. You know these three elements of the triad: cognitive problems, gait problems, bladder control problems are so common in the elderly that if you pick 10 people out in the community that have this triad, it's unlikely that even one of them has true NPH. On the other hand, you don't need all three elements of the triad to make the diagnosis because the order of symptoms matters. Often patients develop gait dysfunction first, then cognitive dysfunction, and then urinary incontinence. If you wait for all three elements of the triad to be present, it may be too late to offer them any clear benefit. And hence, you know, it's neither sufficient nor necessary to make the diagnosis. Dr Jones: That's a really great point. I think most of our listeners are familiar with the fact that, you know, we're taught these classic triads or pentads or whatever, and they're rarely all present. In a way, it's maybe a useful prompt, but it could be distracting or misleading, even in a way, in terms of recognizing the patient. So what clues do you use, Dr Moghekar, to really think that a patient may have NPH? Dr Moghekar: So, there are two important aspects about gait dysfunction. Say somebody comes in with all three elements of the triad. You want to know two things. Which came first? If gate impairment precedes cognitive impairment, it's still very likely that NPH is in the differential. And of the two, which are more- relatively more affected? So, if somebody has very severe dementia and they have a little bit of gait problems, NPH is not as likely. So, is gait affected earlier than cognitive dysfunction, and is it affected to a more severe degree than cognitive dysfunction? And those two things clue me in to the possibility of NPH. You still obviously need to get imaging to make sure that they have large ventricles. One of the problems with imaging is large ventricles are present in so many different patients. Normal aging causes large ventricles. Obviously, many neurodegenerative disorders because of cerebral atrophy will cause large ventricles. And there's an often-used metric called as the events index, which is the ratio of the bitemporal horns- of the frontal horns of the lateral ventricles compared to the maximum diameter of the skull at that level. And if that ratio is more than 0.3, it's often used as a de facto measure of ventriculomegaly. What we've increasingly realized is that this ratio changes with age. And there's an excellent study that used the ADNI database that looked at how this ratio changes by age and sex. So, in fact, we now know that an 85-year-old woman who has an events index of 0.37 which would be considered ventriculomegaly is actually normal for age and sex. So, we need to start adopting these more modern age- and sex-appropriate age cutoffs of ventriculomegaly so as not to overcall everybody with big ventricles as having possible NPH. Dr Jones: That's very helpful. And I do want to come back to this challenge that we've seen in our field of overdiagnosis and underdiagnosis. But I think most of us are familiar with the concept of how hydrocephalus could cause neurologic deficits. But what's the latest on the mechanism of NPH? Why do some patients get this and others don't? Dr Moghekar: Very good question. I don't think we know for sure. And it for a long time we thought it was a plumbing issue. Right? And that's why shunts work. People thought it was impaired CSF absorption, but multiple studies have shown that not to be true. It's likely a combination of impaired cerebral blood flow, biomechanical factors like compliance, and even congenital factors that play a role in the pathogenesis of NPH. And yes, while putting in shunts likely drains CSF, putting in a shunt also definitely changes the compliance of the brain and affects blood flow to the subcortical regions of the brain. So, there are likely multiple mechanisms by which shunts benefit, and hence it's very likely that there's no single explanation for the pathogenesis of NPH. Dr Jones: We explored this in a recent Continuum issue on dementia. Many patients who have cognitive impairment have co-pathologies, multiple different causes. I was interested to read in your article about the genetic risk profile for NPH. It's not something I'd ever really considered in a disorder that is predominantly seen in older patients. Tell us a little more about those genetic risks. Dr Moghekar: Yeah, everyone is aware of the role genetics plays in congenital hydrocephalus, but until recently we were not aware that certain genetic factors may also be relevant to adult-onset normal pressure hydrocephalus. We've suspected this for a long time because nearly half of our patients who come to us to see us in clinic with NPH have head circumferences that are more than 90th percentile for height. And you know, that clearly indicates that this started shortly at the time after birth or soon afterwards. So, we've suspected for a long time that genetic factors play a role, but for a long time there were not enough large studies or well-conducted studies. But recently studies out of Japan and the US have shown mutations in genes like CF43 and CWH43 are disproportionately increased in patients with NPH. So, we are discovering increasingly that there are genetic factors that underlie even adult onset in patients. There are many more waiting to be discovered. Dr Jones: Really fascinating. And obviously getting more insight into the risk and mechanisms would be helpful in identifying these patients potentially earlier. And another thing that I learned in your article that I thought was really interesting, and maybe you can tell us more about it, is the association between normal pressure hydrocephalus and the observation of cervical spinal stenosis, many of whom require decompression. What's behind that association, do you think? Dr Moghekar: That's a very interesting study that was actually done at your institution, at Mayo Clinic, that showed this association. You know, as we all get older, you know, the incidence of cervical stenosis due to osteoarthritis goes up, but the incidence of significant, clinically significant cervical stenosis in the NPH population was much higher than what we would have expected. Whether this is merely an association in a vulnerable population or is it actually causal is not known and will need further study. Dr Jones: It's interesting to speculate, does that stenosis affect the flow of CSF and somehow predispose to a- again, maybe a partial degree for some patients? Dr Moghekar: Yeah, which goes back to the possible hydrodynamic theory of normal pressure hydrocephalus; you know, if it's obstructing normal CSF flow, you know, are the hydrodynamics affected in the brain that in turn could lead to the development of hydrocephalus. Dr Jones: One of the things I really enjoyed about your article, Abhay, was the very strong clinical focus, right? We can't just take an isolated biomarker or radiographic feature and rely on that, right? We really do need to have clinical suspicion, clinical judgment. And I think most of our listeners who've been in practice are familiar with the use and the importance of the large-volume lumbar puncture to determine who may have, and by exclusion not have, NPH, and then who might respond to CSF diversion. And I think those of us who have been in this situation are also familiar with the scenario where you think someone may have NPH and you do a large-volume lumbar puncture and they feel better, but you can't objectively see a difference. How do you make that test useful and objective in your practice? What do you do? Dr Moghekar: Yeah, it's a huge challenge in getting this objective assessment done carefully because you have to remember, you know, subconsciously you're telling the patients, I think you have NPH. I'm going to do this spinal tap, and if you walk better afterwards, you're going to get a shunt and you're going to be cured. And you can imagine the huge placebo response that can elicit in our subjects. So, we always like to see, definitely, did the patient subjectively feel better? Because yes, that's an important metric to consider because we want them to feel better. But we also wanted to be grounded in objective truths. And for that, we need to do different tests of speed, balance and endurance. Not everyone has the resources to do this, but I think it's important to test different domains. Just like for cognition, you know, we just don't test memory, right? We test executive function, language, visuospatial function. Similarly, walking is not just walking, right? It's gait speed, it's balance, and it's endurance. So, you need to ideally test at least most of these different domains for gait and you need to have some kind of clear criteria as to how are you going to define improvement. You know, is a 5% improvement, is a 10% improvement in gait, enough? Is 20%? Where is that cutoff? And as a field, we've not done a great job of coming up with standardized criteria for this. And it varies currently, the practice varies quite significantly from center to center at the current time. Dr Jones: So, one of the nice things you had in your article was helpful tips to be objective if you're in a lower-resource setting. For you, this isn't a common scenario that someone encounters in their practice as opposed to a center that maybe does a large volume of these. What are some relatively straightforward objective measures that a neurologist or someone else might use to determine if someone is improving after a large-volume LP? Dr Moghekar: Yeah, excellent question, Dr Jones, and very practically relevant too. So, you need to at least assess two of the domains that are most affected. One is speed and one is balance. You know, these patients fall ultimately, right, if you don't treat them correctly. In terms of speed, there are two very simple tests that anybody can do within a couple of minutes. One is the timed “up-and-go” test. It's a test that's even recommended by the CDC. It correlates very well with faults and disability and it can be done in any clinic. You just need about ten feet of space and a chair and a stopwatch, and it takes about a minute or slightly more to do that test. And there are objective age-associated norms for the timed up-and-go test, so it's easy to know if your patient is normal or not. The same thing goes for the 10-meter walk test. You do need a slightly longer walkway, but it's a fairly easy and well-standardized test. So, you can do one of those two; you don't need to do both of them. And for balance, you can do the 30-second “sit-to-stand”; and it's literally, again, 30 seconds. You need a chair, and you need somebody to watch the patient and see how many times they can sit up and stand up from a seated position. Then again, good normative data for that. If you want to be a little more sophisticated, you can do the 4-stage balance test. So, I think these are tests that don't add too much time to your daily assessment and can be done with even trained medical assistants in any clinic. And you don't need a trained physical therapist to do these assessments. Dr Jones: Very practical. And again, something that is pretty easily deployed, something we do before and then after the LP. I did see you mentioned in your article the dual timed up-and-go test where it's a simultaneous gait and executive function test. And I've got to be honest with you, Dr Moghekar, I was a little worried if I would pass that test, but that may be beyond the scope of our time today. Actually, how do you do that? How do you do the simultaneous cognitive assessment? Dr Moghekar: So, we asked them to count back from 100, subtracting 3. And we do it particularly in patients who are mildly impaired right? So, if they're already walking really good, but then you give them a cognitive stressor, you know, that will slow them down. So, we reserve it for patients who are high-performing. Dr Jones: That's fantastic. I'm probably aging myself a little here. I have noticed in my career, a little bit of a pendulum swing in terms of the recognition or acceptance of the prevalence of normal pressure hydrocephalus. I recall when I was a resident, many, many people that we saw in clinic had normal pressure hydrocephalus. Then it seemed for a while that it really faded into the background and was much less discussed and much less recognized and diagnosed, and less treated. And now that pendulum seems to have swung back the other way. What's behind that from your perspective? Dr Moghekar: It's an interesting backstory to all of this. When the first article about NPH was published in the Newman Journal of Medicine, it was actually a combined article with both neurologists and neurosurgeons on it. They did describe it as a treatable dementia. And what that did is it opened up the floodgates so that everybody with any kind of dementia started getting shunts left, right, and center. And back then, shunts were not programmable. There were no antibiotic impregnated catheters. So, the incidence of subdural hematomas and shunt-related infections was very high. In fact, one of our esteemed neurologists back then, Houston Merritt, wrote a scathing editorial that Victor and Adam should lose their professorships for writing such an article because the outcomes of these patients were so bad. So, for a very long period of time, neurologists stopped seeing these patients and stopped believing in NPH as a separate entity. And it became the domain of neurosurgeons for over two or three decades, until more recently when randomized trials started being done early on out of Europe. And now there's a big NIH study going on in the US, and these studies showed, in fact, that NPH exists as a true, distinct entity. And finally, neurologists have started getting more interested in the science and understanding the pathophysiology and taking care of these patients compared to the past. Dr Jones: That's really helpful context. And I guess that maybe isn't rare when you have a disorder that doesn't have a simple, straightforward biomarker and is complex in terms of the tests you need to do to support the diagnosis, and the treatment itself is somewhat invasive. So, when you talk to your patients, Dr Moghekar, and you've established the diagnosis and have recommended them for CSF diversion, what do you tell them? And the reason I ask is that you mentioned before we started recording, you had a patient who had a shunt placed and responded well, but continued to respond over time. Tell us a little bit more about what our patients can expect if they do have CSF diversion? Dr Moghekar: When we do the spinal tap and they meet our criteria for improvement and they go on to have a shunt, we tell them that we expect gait improvement definitely, but cognitive improvement may not happen in everyone depending on what time, you know, they showed up for their assessment and intervention. But we definitely expect gait improvement. And we tell them that the minimum gait improvement we can expect is the same degree of improvement they had after their large-volume lumbar puncture, but it can be even more. And as the brain remodels, as the hydrodynamics adapt to these shunts… so, we have patients who continue to improve one year, two years, and even three years into the course of the intervention. So, we're, you know, hopeful. At the same time, we want to be realistic. This is the same population that's at risk for developing neurodegenerative disorders related to aging. So not a small fraction of our patients will also have Alzheimer's disease, for example, or go on to develop Lewy body dementia. And it's the role of the neurologist to pick up on these comorbid conditions. And that's why it's important for us to keep following these patients and not leave them just to the neurosurgeon to follow up. Dr Jones: And what a great note to end on, Dr Moghekar. And again, I want to thank you for joining us, and thank you for such a wonderful discussion and such a fantastic article on the clinical diagnosis of normal pressure hydrocephalus. I learned a lot reading the article, and I learned a lot more today just in the conversation with you. So, thank you for being with us. Dr Moghekar: Happy to do that, Dr Jones. It was a pleasure. Dr Jones: Again, we've been speaking with Dr Abhay Moghekar, author of a wonderful article on the clinical features and diagnosis of NPH in Continuum's first-ever issue dedicated to disorders of CSF dynamics. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Lyssna på två fullmatade avsnitt av Tutto Balutto, helt utan reklam, på Podme. Signa upp dig på podme.com – de första 14 dagarna är gratis. Ladda sedan ner Podme-appen i Appstore eller Google Play. EXKLUSIVT NordVPN-erbjudande ➼ https://nordvpn.com/tuttobalutto. Prova riskfritt med 30 dagars återbetalningsgaranti!

Episode 70. I denne episoden intervjuer vi professor og nevrolog Ole-Bjørn Tysnes ved Universitetet i Bergen og Haukeland universitetssykehus. Han forklarer oss hva som kjennetegner de ulike atypiske parkinsonistiske syndromene: MSA (multisystem atrofi), PSP (progressiv supranukleær parese), CBD (cortikobasal degenerasjon) og demens med Lewy-legemer.  Lise Elveseter og Jeanette Koht intervjuer. Redaksjon: Karoline Haslum Kongsvik (lege i spesialisering), Anna Bjerkreim (lege i spesialisering), Lise Elveseter (nevrolog) og Jeanette Koht (nevrolog, ph.d).  Jingle: Christoffer E. Hørbo og Are Brean Klipp og lyd: Lise Elveseter Logo: Tilde Rasmussen   Følg oss på Facebook og Instagram!               

Alexander Pantelyat, MD, FAAN is an associate professor of Neurology at the Johns Hopkins University School of Medicine. He is the founder and director of the Johns Hopkins Atypical Parkinsonism Center, and the co-Founder and Director of the Johns Hopkins Center for Music and Medicine. Dr. Pantelyat's research is focused on the diagnosis and treatment of atypical parkinsonian disorders, such as dementia with Lewy bodies, progressive supranuclear palsy, corticobasal syndrome/degeneration and multiple system atrophy; cognitive aspects of movement disorders; and music-based rehabilitation of neurodegenerative diseaseshttps://www.seniorcareauthorit...

It can be hard to tell the difference between depression (feeling sad) and apathy (loss of interest in things). In this episode, learn what causes apathy in people living with dementia and how to deal with it.Interested in one of my caregiver studies? Email the team atCURBIT@uab.edu Have a question? Want more information about my programs?Email me: dr.rita.jablonski@gmail.com#frontotemporal #alzheimers #dementia #caregiving #behaviors  #dementiabitch #Lewy body #Parkinsons#vascular #apathy #depression #strategies

In part two of this two-part series, Dr. Jeff Ratliff and Dr. Per Borghammer explore the subcategories of Lewy body disease, focusing on the body-first subtype Show reference: https://www.nature.com/articles/s41593-025-01910-9 

Dr. Jeff Ratliff talks with Dr. Per Borghammer about the classification of Lewy body disease into brain-first and body-first subtypes, with a focus on the newly identified parasympathetic and sympathetic subtypes within the body-first category.  Read the related article in Nature.  Disclosures can be found at Neurology.org. 

Dr Ben Underwood is Assistant Professor in Applied and Translational Old Age Psychiatry at the University of Cambridge and an Honorary Consultant Old Age Psychiatrist. His interests are in translational medicine in dementia, where he has been principal investigator (PI) for academic and pharma led clinical trials.Today we discuss:Trajectories of Common Mental Health Problems into Older Age, how mental health issues such as depression or psychosis evolve as people age.Dementia and Its Different Types, including Alzheimer's disease, vascular dementia, Lewy body dementia, and frontotemporal dementia.Dementia Prevention,  strategies for reducing risk and managing symptoms, including lifestyle interventions and early detection.How Dementia is Treated, including pharmacological and non-pharmacological approaches. The Advent of AI in Psychiatric Research, exploring how artificial intelligence is transforming diagnosis, treatment prediction, and mental health monitoring.Interviewed by Dr. Alex Curmi. Dr. Alex is a consultant psychiatrist and a UKCP registered psychotherapist in-training.If you would like to invite Alex to speak at your organisation please email alexcurmitherapy@gmail.com with "Speaking Enquiry" in the subject line.Alex is not currently taking on new psychotherapy clients, if you are interested in working with Alex for focused behaviour change coaching , you can email - alexcurmitherapy@gmail.com with "Coaching" in the subject line.Give feedback here - thinkingmindpodcast@gmail.com - Follow us here: Twitter @thinkingmindpod Instagram @thinkingmindpodcast Tiktok - @thinking.mind.podcast 

In the latest episode of The Keeper League AFL Fantasy podcast, Heff and Lewy dissect all the action from Round 9. They shed light on players who have emerged as potential standouts for AFL Fantasy keeper leagues, discussing standout performances, role changes, and value picks. Listen as they deliver the insights needed to stay ahead of the curve in scouting hidden gems for keeper league teams.Website: https://keeperleaguepod.com.au/Membership: https://keeperleaguepod.com.au/keeper-league-membership/Join our Discord server: https://discord.gg/APjqvT22zeJoin the Keeper Fantasy platform: https://keeperfantasy.com/FootyNumbers.com: https://footynumbers.comPlay FootyHeads: https://footyheads.comSubscribe to our YouTube Channel: https://www.youtube.com/@keeperleaguepod?sub_confirmation=1

Au cœur de la nuit, les auditeurs se livrent en toute liberté aux oreilles attentives et bienveillantes de Valérie Darmon. Pas de jugements ni de tabous, une conversation franche, mais aussi des réponses aux questions que les auditeurs se posent. Un moment d'échange et de partage propice à la confidence pour repartir le cœur plus léger. Distribué par Audiomeans. Visitez audiomeans.fr/politique-de-confidentialite pour plus d'informations.

Having a relative or loved one receive a dementia diagnosis can be challenging for families, especially for families with children. How can parents, guardians and other adults explain these complex memory and thinking changes to children in a way they'll understand? One possible way – children's books. Dr. Tomás León joins the podcast to discuss his collection of children's books focused on different kinds of dementia, including Alzheimer's disease, frontotemporal dementia, Lewy body dementia and vascular dementia. He discusses his inspiration for the four stories, the writing and translation process, and the importance of helping children understand what's happening to their loved ones, as well as shares advice on how to address these difficult conversations. Guest: Tomás León, MD, psychiatrist, Memory and Neuropsychiatry Clinic, Hospital del Salvador, Atlantic Fellow for Equity in Brain Health, Global Brain Health Institute (GBHI) Show Notes Read more about Dr. León's children's books and download copies of the Here's Grandma! collection for free in English and Spanish on the Global Brain Health Institute's website. Learn more about Dr. León through his profile on the Global Brain Health Institute's website. Connect with us Find transcripts and more at our website. Email Dementia Matters: dementiamatters@medicine.wisc.edu Follow us on Facebook and Twitter. Subscribe to the Wisconsin Alzheimer's Disease Research Center's e-newsletter. Enjoy Dementia Matters? Consider making a gift to the Dementia Matters fund through the UW Initiative to End Alzheimer's. All donations go toward outreach and production.

When the unexpected diagnosis of Lewy body dementia struck Carla Preyers's husband, she found herself thrust into a role she never anticipated. "The journey chose me," she explains, recounting the four-year battle for a proper diagnosis and the profound challenges that followed. This conversation reveals the often-invisible struggles caregivers face when supporting loved ones with dementia.The emotional heart of this episode lies in Carla's honest discussion of caregiver self-preservation. Her commitment to morning prayers, positive environments, and regular exercise wasn't just about wellness—it was survival. "I had to manage my energy," she shares, explaining how negativity directed at someone with dementia "comes back to you triple." Her story has now found wider resonance through the documentary "Facing the Wind," executive produced by Yo-Yo Ma, Yolanda Wong, and David Hyde Pierce, which chronicles the journey of dementia caregivers across America.Are you caring for someone with cognitive decline or concerned about a loved one showing symptoms? Reach out to Carla through the links on our show page to learn how you might bring the "Facing the Wind" documentary to your community and join the growing advocacy movement for better dementia care and caregiver support.Carla's Story My husband, Patrick Preyer, was diagnosed with Lewy Body Dementia in 2018. For eight years, I walked alongside him as his caregiver until his peaceful transition in January 2023. Through heartbreak and healing, I learned how vital faith, community, and support are—especially for caregivers who often feel invisible.That journey is now told in the documentary Facing the Wind, which candidly captures our experience with dementia, caregiving, and the importance of self-care. This film was born out of connection—sparked by the Lewy Body Spouses Support Group on Facebook—and nurtured into a message of hope and resilience.I'm proud to share that Facing the Wind premiered at DOC NYC, one of the nation's leading documentary festivals, and was recently featured on People.com. The film is executive produced by Renée Fleming, Yo-Yo Ma, and David Hyde Pierce.As a caregiver self-care coach, I now dedicate my life to supporting those who give so much of themselves. While organizations like Voices Inclusive Research focus on providing a voice in clinical research to the community, my passion is to amplify the voices of the women caring behind the scenes—quiet heroes who need to be seen, supported, and sustained.Clips and Media Documentary ClipPeople Magazine FeatureFacebook Page We hope you have enjoyed this episode. Please like, comment, subscribe, and share the podcast.To find out more about Lynnis and what is going on in the V.I.B.E. Living World please go to https://link.tr.ee/LynnisJoin the V.I.B.E. Wellness Woman Network, where active participation fuels the collective journey toward health and vitality. Subscribe, engage, and embark on this adventure toward proactive well-being together. Go to https://www.vibewellnesswomannetwork.com to join. We have wonderful events, courses, challenges, guides, blogs and more all designed for the midlife woman who wants to keep her V.I.B.E. and remain Vibrant, Intuitive, Beautiful, and Empowered after 40+. Interested in an AI platform that meets all your needs? Click here

Lynn & Carl are joined by Chef Liz from Tenacious Eats to discuss the May the Fourth Brunch featuring Spaceballs. Also, they are having Adult Summer Camp featuring food & film. Next they speak to director Lize Lewy and star & playwright Summer Baer about the new show Scream Echo Scream. Plus Carl is enjoying his new job at KTRS.

U2 released a part-live, part studio album in October 1988 called Rattle and Hum.  This album accompanied a filmed “Rockumentary” of the band which was filmed in Denver and Arizona.  Originally intended to be entitled  “U2 in the Americas,” the album and film instead take their name from lyrics in the song “Bullet the Blue Sky' from their album “The Joshua Tree.” Studio sessions for Rattle and Hum included time at Sun Studio in Memphis, and include collaborations with other musicians including Bob Dylan and B.B. King.  The intent of Rattle and Hum was to explore more American blues rock, and folk, and roots music of the 50's and 60's, and includes both original and cover songs.  Critics were divided on the album at the time of its release.  Some felt that U2 was not celebrating blues rock and artists as much as they were attempting to insert themselves into higher echelons of rock celebrity.  Over time the criticisms of egotism would fade, as U2 has indeed proven to be a major force in the Rock pantheon.  In retrospect, both Bono and The Edge have found Rattle and Hum to be a bit of a side excursion for the band, more of a “scrapbook” than a true direction.  The new direction of U2 would be set beginning with their next studio album, “Achtung Baby” in 1991.  Regardless, Rattle and Hum is a great album, well worth a listen.  The collaboration with other artists is worth special attention, as is its examination of the way that modern rock finds its roots in the delta blues.Friend of the show Greg Lyon sits in for Wayne, while Rob brings us this hybrid album for today's podcast.Angel of HarlemThe second single from the album is an original studio release which was written as an homage to Billie Holiday.  Songwriting took place during the tour for ”The Joshua Tree,” and the lyrics take inspiration form various landmarks around New York City.  The track reached number 14 on the Billboard Hot 100 and number 9 on the UK Singles chart.  When Love Comes to TownRecorded in Sun Studios, this U2 original song features collaboration with blues guitarist B.B. King. Live performances included B.B. King and his band during the “Lovetown Tour” in 1989.  U2 would discontinue playing the song in concert over time, but revived it in 2015 as a tribute to B.B. King after his death.  King plays lead on this song written by The Edge, who takes on rhythm guitar for this track.All Along the WatchtowerThis live cover is of a song written by Bob Dylan and made famous by Jimi Hendrix.  The lyrics are of a conversation between a joker and a thief, and several lines echo lines of scripture from the book of Isaiah in the Bible.  U2 performed this live cover in San Francisco at the “Save The Yuppie Free Concert.”  Some of the lyrics were altered, which irritated Dylan. Pride (In the Name of Love)A live version of the studio song from the 1984 album The Unforgettable Fire, this was recorded in Denver.  The popularity of this song can be heard in the audience call-and-response.  The lyrics were inspired by elements of the civil rights movement, particularly the assassination of Martin Luther King, Jr. ENTERTAINMENT TRACK:Iko Iko by The Belle Stars (from the motion picture “Rain Man”)Tom Cruise and Dustin Hoffman turned in stellar performances in this dramatic film exploring autism. STAFF PICKS:Kiss by Art of Noise featuring Tom JonesBruce leads off the staff picks with a cover of a Prince song performed by an unusual pairing of art rock group the Art of Noise with Vegas crooner Tom Jones.  This became the biggest hit for the Art of Noise to that point, reaching number 5 on the UK charts and number 31 on the Billboard Hot 100.  She Drives Me Crazy by Fine Young CannibalsLynch brings us the most successful single from the British pop trio, off their second and final album, “The Raw & the Cooked.” The band formed from two previous bands, one Ska, and one Punk.  The track was composed at Prince's Paisley Park Studios in Minneapolis.Once Bitten, Twice Shy by Great WhiteGreg features a rocker.  Great White covered a song originally written and performed by Ian Hunter in 1975.  This song went to number 5 on the Billboard Hot 100.  Great White had a more blues-oriented sound than many of the hair metal bands of the late 80's.  Lead singer Jack Russell passed after a battle with Lewy body dementia in August 2024.What I Am by Edie Brickell & New BohemiansRob closes out the staff picks with the signature song off Edie Brickell & New Bohemians' debut album, "Shooting Rubberbands at the Stars."  The inspiration for the song was Brickell's frustration with the dogma exhibited in a world religions class in college.  Brickell would meet her husband and fellow musician, Paul Simon, when she performed this song on Saturday Night Live. INSTRUMENTAL TRACK:Sunset Road by Bela Fleck & the FlecktonesThis jazz fusion piece with an unusual banjo lead was on the group's debut album, and takes us out for this episode. Thanks for listening to “What the Riff?!?” NOTE: To adjust the loudness of the music or voices, you may adjust the balance on your device. VOICES are stronger in the LEFT channel, and MUSIC is stronger on the RIGHT channel.Please follow us on Facebook https://www.facebook.com/whattheriffpodcast/, and message or email us with what you'd like to hear, what you think of the show, and any rock-worthy memes we can share.Of course we'd love for you to rate the show in your podcast platform!**NOTE: What the Riff?!? does not own the rights to any of these songs and we neither sell, nor profit from them. We share them so you can learn about them and purchase them for your own collections.

Dr. Michele Matarazzo interviews Prof. Irena Rektorová about her recent study on early changes in the locus coeruleus in mild cognitive impairment with Lewy bodies. Using neuromelanin-sensitive MRI, the study reveals selective vulnerability of the caudal locus coeruleus and its association with specific cognitive and other nonmotor features. The conversation explores the implications for early diagnosis, the “body-first” hypothesis, and the potential role of NM-MRI as a biomarker. Read the article.

Description:In this powerful episode of When the Moment Chooses You, Coach Charlene sits down with the remarkable Carla Preyer—caregiver, advocate, and featured voice in the upcoming documentary Facing the Wind. Carla shares her deeply moving journey of caring for her husband through an 8-year battle with Lewy body dementia. What started as subtle signs turned into a life-changing calling—one filled with heartbreak, strength, grace, and sacred moments of connection.From leaving her successful salon business to becoming a full-time caregiver, Carla's story reveals the emotional toll and soul-deep courage required to love someone through decline. She opens up about the challenges of receiving a diagnosis, the importance of support groups, and why representation in caregiving matters—especially for women of color.✨ This episode is a love letter to every caregiver who has ever felt invisible while holding everything together.

Hello Rank Squad!It's time for this week's second Champions League Takeaway - looking back at Wednesday's Quarter Final first legs, where PSG roared back from 1-0 down to beat Aston Villa 3-1 and Barcelona romped to yet another astounding win, routinely dismantling a discombobulated Dortmund 4-0. We start with PSG and wonder if anybody could have held up against the power of their attacking might last night - looking at the emergence of Desire Doué as a bona-fide starter and wonderkid, as well as the devastating directness of Kvicha Kvaratskhelia - before going a bit deeper into a discussion of how Luis Enrique has moulded this club to one in his own image - where the team comes first, but individual brilliance is actively encouraged as well. Then in Part Two it's time to head to Catalunya, to take a deep dive into how Barcelona pretty much killed this tie stone dead in the first leg, breaking a host of records in the process. All three of the front line of Raphinha (controversially), Lamine Yamal, and Robert Lewandowski were on the scoresheet - with Lewy making it 29 goals in 28 games against Dortmund since leaving them in 2014. Ouch. It's Ranks! And remember, if you'd like more from the Rank Squad, including extra podcasts every Monday and Friday (including our weekly Postbox taking a look at the whole weekend of football) and access to our brilliant Discord community, then why not join us here on Patreon?

Le Barça s'est imposé facilement face à Dortmund hier soir 4 à 0. Les hommes d'Hansi Flick ont géré leur match aller de quart de finale de Ligue des champions avec beaucoup de tranquillité. Raphinha, Yamal et un doublé de Robert Lewandowski permettent au Barça d'aborder le retour avec beaucoup de sérénité. La saison de l'attaquant polonais est-elle sous-cotée ? Pourquoi parle-t-on peu des performances de Lewy ? En Ligue Europa, Lyon reçoit Manchester United ce soir en quart de finale aller au Groupama Stadium. Comment aborder cette rencontre ? L'OL est-il favori face aux Red Devils ? La jeunesse incarnée par Almada et Mikautadze prend-elle le pouvoir ?

Send us a textKristy Russell takes us on a deeply personal and professional journey through the world of Alzheimer's disease and related dementias (ADRD). As Utah's sole specialist covering the entire state, Kristy shares how her grandmother's Lewy body dementia diagnosis transformed her perspective on memory care after initially swearing off working with dementia patients due to challenging experiences.The conversation tackles misconceptions head-on. Memory loss is just one symptom — thinking, behavior, and problem-solving abilities are equally affected. Kristy reveals a startling reality: only half of people with Alzheimer's are diagnosed, and of those, merely 30% share their diagnosis with loved ones, often fearing loss of independence.Communication emerges as the cornerstone challenge for caregivers. Through vivid examples, Kristy explains why arguing with someone with dementia about recent events is futile. Her "filing cabinet" metaphor brilliantly illustrates how memory works — newest files disappear first — helping caregivers understand why their loved ones can't simply "try harder" to remember.For overwhelmed caregivers, Kristy offers practical wisdom about delegation and self-care. "The energy you put out is the energy you're going to get back from the person with dementia," she notes, emphasizing that seeking help isn't failure but excellence in caregiving. She explains respite options and encourages caregivers to maintain their own health appointments and activities.Looking forward, Kristy shares hope about new medications like aducanumab that can remove brain plaques in early stages, signaling a positive trajectory in treatment development. Her powerful closing message resonates deeply: "You're doing a good job and you're not alone."Whether you're caring for someone with dementia, working in healthcare, or simply seeking to understand these conditions better, this episode provides invaluable insights, practical strategies, and heartfelt encouragement for the journey ahead.• Kristy's journey from swearing off dementia care to becoming Utah's statewide ADRD specialist• Only about half of people with Alzheimer's disease are diagnosed, and of those, only 30% share their diagnosis with family and friends• Early diagnosis allows for better planning and less crisis management as the disease progresses• Communication challenges require meeting people with dementia in their reality rather than constantly correcting them• The "filing cabinet" memory metaphor explains why recent memories disappear first• Self-care for caregivers includes delegating tasks and utilizing respite services• New medications like aducanumab can help in early stages by removing brain plaques• The Utah government's WISE initiative focuses on helping seniors age in place independentlySupport the show

Lisa Ricciardi, CEO, and Dr. Tony Caggiano, Chief Medical Officer at Cognition Therapeutics, are developing effective treatments for neurological disorders, particularly Alzheimer's disease and dementia with Lewy bodies (DLB). While DLB is related to Parkinson's, sharing symptoms include hallucinations, sleep disorders, and cognitive dysfunction, there are no good diagnostics to identify DLB and effective treatments. Cognition Therapeutics' lead drug candidate, an oral treatment, has shown promise in protecting neurons from the toxic effects of the pathological proteins involved in Alzheimer's and DLB. Lisa explains, "This company started in 2007, so we've had a long number of years to burnish our mission. One of the things we say is we're the beginning of the end of neurologic disorders and the start of hope for an improved future for patients. So Alzheimer's disease, in particular, has been long studied with little success, and in the last few years, we've seen some successes with monoclonal antibodies. There are a number of other approaches in clinical trials, but we have recently generated very positive data in two different trials with an oral once-a-day drug." Tony elaborates, "Lewy body dementia or dementia with Lewy bodies is a disease very much related to Parkinson's disease that's believed to be, in part, caused by pathological levels of a certain protein called alpha synuclein and particularly small oligomers of misfolded alpha synuclein." "And in Alzheimer's disease, this is largely a cognitive memory disorder as it presents. So, those two diseases are very different. Now, the idea of treating them with a single drug is somewhat unique to what we have here at Cognition Therapeutics. So our company started around the idea of developing therapies for Alzheimer's disease, and our lead molecule CT1812 or zervimesine was developed out of a screening assay where we were looking for molecules that could protect neurons or brain cells from the toxicities of this pathological amyloid protein. So, we identified CT1812 and have been developing it."  #CognitionTherapeutics #BrainHealth #DementiaCare #LewyStrong #Livingwithlewy #Alzheimers #EndAlz #Alzheimersdisease #DLBAwareness #NeurodegenerativeDisease #Dementia #DementiaWithLewyBodies  cogrx.com Download the transcript here

Lisa Ricciardi, CEO, and Dr. Tony Caggiano, Chief Medical Officer at Cognition Therapeutics, are developing effective treatments for neurological disorders, particularly Alzheimer's disease and dementia with Lewy bodies (DLB). While DLB is related to Parkinson's, sharing symptoms include hallucinations, sleep disorders, and cognitive dysfunction, there are no good diagnostics to identify DLB and effective treatments. Cognition Therapeutics' lead drug candidate, an oral treatment, has shown promise in protecting neurons from the toxic effects of the pathological proteins involved in Alzheimer's and DLB. Lisa explains, "This company started in 2007, so we've had a long number of years to burnish our mission. One of the things we say is we're the beginning of the end of neurologic disorders and the start of hope for an improved future for patients. So Alzheimer's disease, in particular, has been long studied with little success, and in the last few years, we've seen some successes with monoclonal antibodies. There are a number of other approaches in clinical trials, but we have recently generated very positive data in two different trials with an oral once-a-day drug." Tony elaborates, "Lewy body dementia or dementia with Lewy bodies is a disease very much related to Parkinson's disease that's believed to be, in part, caused by pathological levels of a certain protein called alpha synuclein and particularly small oligomers of misfolded alpha synuclein." "And in Alzheimer's disease, this is largely a cognitive memory disorder as it presents. So, those two diseases are very different. Now, the idea of treating them with a single drug is somewhat unique to what we have here at Cognition Therapeutics. So our company started around the idea of developing therapies for Alzheimer's disease, and our lead molecule CT1812 or zervimesine was developed out of a screening assay where we were looking for molecules that could protect neurons or brain cells from the toxicities of this pathological amyloid protein. So, we identified CT1812 and have been developing it."  #CognitionTherapeutics #BrainHealth #DementiaCare #LewyStrong #Livingwithlewy #Alzheimers #EndAlz #Alzheimersdisease #DLBAwareness #NeurodegenerativeDisease #Dementia #DementiaWithLewyBodies  cogrx.com Listen to the podcast here

There is an important role for cost-effective clinical biomarkers in the diagnosis of Parkinson's disease. Dr. Eduardo de Pablo-Fernández and Dr. Cecilia Tremblay discuss how accurate hyposmia and REM sleep behavior disorder can predict Lewy pathology in a non-selected population using data from the Arizona clinicopathological study on Aging and Neurodegeneration. Read the article.

Send us a textSam, Rik and Toni talk about Barca's important, if not overly impressive, win over Alaves which helped them get back in the title race after Real Madrid slipped up big time at Espanyol.Support the showFor bonus content, including additional podcasts, Q&As, special collections and Discord access to join the discussion with other Barça fans, join our Patreon: patreon.com/siemprepod

All Home Care Matters and our host, Lance A. Slatton were honored to welcome Julia Wood, MOT, OTR/L the Director of Professional & Community Education for the Lewy Body Dementia Association (LBDA).   About Julia Wood, MOT, OTR/L:   Julia Wood, MOT, OTR/L is an occupational therapist and international educator specializing in assessment and treatment of people with Parkinson's disease and related dementias. Julia joined the Lewy Body Dementia Association (LBDA) as director of Professional & Community Education in 2021.   She co-authored the first American Occupational Therapy Association Practice Guideline for Adults with Parkinson's Disease in 2022 and serves on the Comprehensive Care Subcommittee for the World Parkinson's Congress (WPC).   About the Lewy Body Dementia Association (LBDA):   The Lewy Body Dementia Association (LBDA) is the leading national organization dedicated to improving the lives of Lewy body dementia (LBD) families.   The Lewy Body Association (LBDA) Mission:   To optimize the quality of life for those affected by Lewy body dementia, we accelerate awareness, advance research for early diagnosis and improved care, and provide comprehensive education and compassionate support.   Program Provision Highlights:   Support:    LBDA offers a wide variety of compassionate and confidential support services for those who are symptomatic or diagnosed, their families and current or former care partners, including but not limited to: • Virtual and in-person support groups • Connecting to Lewy Buddies, lived-experience volunteers who share their time and experience with individuals and families • Opportunity to connect directly with one of LBDA's licensed social workers through the Lewy Line, a toll-free number, Monday - Friday • Assistance in identifying additional external programs or local resources   (LBDA does not promote any doctor, medical center, allied healthcare provider, medication, product or treatment, nor direct referrals for residential facilities or home care agencies).    Education:   LBDA provides free resources and educational programming throughout the year on a wide variety of LBD topics.   • 2024 Community Webinar Series: Empowerment through Education is designed to provide strategies for self-advocacy, exploration of the complex symptoms of LBD, and skills and resources to enhance quality of life.   o Available to watch on LBDAtv or Mediflix   • 2025 Community Webinar Series: Mastering Lewy Body Dementia Together will focus on building mastery of understanding on the complex symptoms of (LBD), continuation of providing strategies for self-advocacy and resources for support, and tactics for enhancing quality of life.   o Begins January 15    • The Lewy Learning Center is a free online platform for sharing education LBD with the community and health care professionals. A go to place for on-demand learning, courses are available to watch at any time, share with friends and family members, with unlimited viewing options.  • LBDA offers complimentary educational materials for individuals and families as well as healthcare provides which can be requested via lbda.org (US only)   Research:   LBDA facilitates, promotes and assists in the development of LBD clinical trials and research studies.   • The Lewy Trial Tracker is a tool for individuals to receive information on new and currently recruiting clinical trials and studies. It is a single source of information that highlights study topics, procedures, locations and study site contact information. Registrants receive quarterly emails, and the information collected is confidential.   • LBDA's Research Centers of Excellence is a network of 25 of the nation's leading academic medical research institutions connecting individuals and their families with highly-specialized physicians providing advanced diagnosis and treatment, as well as conducting LBDA research. 

While there are many kinds of dementia, like Alzheimer's disease and Lewy body dementia, there's one that researchers have only recently identified. LATE, or Limbic-predominant Age-related TDP-43 Encephalopathy, is a newly-characterized type of dementia associated with abnormal clumps of a protein called TDP-43. So, what exactly do we know about LATE? Dr. David Wolk joins the podcast to share what key features of LATE are, how it compares to Alzheimer's disease and impacts treatment, and what next steps are needed to better understand this neurodegenerative disease. Guest: David Wolk, MD, director, Penn Alzheimer's Disease Research Center, co-director, Penn Memory Center, co-director, Penn Institute on Aging, chief, Division of Cognitive Neurology, professor of neurology, University of Pennsylvania Perelman School of Medicine Show Notes Learn more about LATE on the National Institute on Aging's website and on Penn Memory Center's website. Read Dr. Wolk's article, "Clinical criteria for limbic-predominant age-related TDP-43 encephalopathy," on the journal Alzheimer's & Dementia's website. Learn more about Dr. Wolk in his profile on the Penn Memory Center website. Connect with us Find transcripts and more at our website. Email Dementia Matters: dementiamatters@medicine.wisc.edu Follow us on Facebook and Twitter. Subscribe to the Wisconsin Alzheimer's Disease Research Center's e-newsletter. Enjoy Dementia Matters? Consider making a gift to the Dementia Matters fund through the UW Initiative to End Alzheimer's. All donations go toward outreach and production.

Hello Rank Squad!On today's episode we thought it would be a good time to take a look at the players currently leading the way in the scoring charts across Europe, and cast our thoughts ahead to who looks like they have a good chance of taking home the award at the end of the season. We skim across some of the players who have set out their stalls early in the summer leagues of Europe, before diving deeper into the contenders from the big five and beyond, based on current form and our expectations of minutes and consistency going forward. Before that, there's time for Things We Love, where Dean goes a bit off beat to criticise some of the decisions coming from Sir Jim Ratcliffe regarding his staff at Manchester United, and Jack waxes lyrical about Atletico Madrid's dramatic win over Sevilla at the weekend and the potential of a genuine three-way title race in Spain. It's Ranks!  And remember, if you'd like more from the Rank Squad, including extra podcasts every Monday and Friday (including our weekly Postbox taking a look at the whole weekend of football) and access to our brilliant Discord community, then why not join us here on Patreon?