Podcasts about Lewy

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.

We say it every year, but there is always a carnage round that sees many great teams copping bullets. This round unfortunately it was Lachie Whitfield, with many coaches not only copping the bullet but a captaincy bullet too! The PODPOD is here to help review the round that was and set you up to finish the bye rounds strong as we enter the final phase of the season!This week we have a full panel on deck as Holmesy, Lewy, Harmey and Sam discuss the key strategies for round 16, discuss a bunch of relevant trade targets and answer lots of listener questions! As the race for the hilux and the elusive top 100 hats heats up, this episode is not one that you want to miss!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

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!               

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

This week, the lads are celebrating 150 episodes of the PODPOD by bringing back the man that started it all. He has been known by many names over the years including but not limited to Buzz Dossyear, Dosby Lee-Steere and Dossy. That's right, Murdoch has given him a free pass as long as he hits his SuperCoach mentions quota. Fresh from tracking long effective kicks, contested possessions and spoils, Dossy makes his long anticipated return.On this episode Holmesy, Lewy, Harmey, Sam and Dosby review the first round of the multi-bye rounds, where many coaches found themselves hurting with only 18 or 19 players on field. They talk general bye strategy, look at players to target off the bye and answer a stack of listener questions. This one was fun!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

The PODPOD boys are flying. Lewy is on the verge of the top 100, Sam keeps climbing and Holmesy is fresh off a top 50 round rank. On the eve of the mid-season byes, the competition is heating up and cash gen is becoming as important as ever. It's all about discipline and attack now as we find out which coaches have been planning and which coaches will come unstuck.On this episode Holmesy, Lewy and Harmey get you prepped for the first round of best 18. They discuss key strategy, help guide you on launching into the bye round, talk about players of interest and answer your listener questions!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 the lead up to the 2025 State of Origin series kicking off on Wednesday, proud Queenslander Billy Moore and die-hard Blue Luke Lewis go head-to-head to preview game one.

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

He is back! We are almost at the bye rounds and there is no greater man in the AFL Fantasy game to talk about them than 5 top time 100 finisher The Statesman! This man built his fantasy career off the back of strategy during the bye rounds. His insight is invaluable!On this episode, Stato joins Holmesy, Harmey and Lewy as they discuss round nine and start to build towards a very interesting bye round period. They deep dive into strategy that has worked in the past, how we can learn and adapt inside a new 5 game system and look at players to target during the bye rounds. This episode is one for the old school listeners, new listeners and everyone chasing an elusive hat. Enjoy!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

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.

In the latest episode of The Keeper League AFL Fantasy podcast, Heff and Lewy dissect all the action from the recent AAMI Community Series preseason matches. They shed light on players who have emerged as potential standouts for AFL Fantasy keeper leagues, discussing standout performances, role changes, and unexpected value picks. Listeners are invited to join Heff and Lewy as they deliver the insights needed to ace upcoming drafts and stay ahead of the curve in scouting sleepers and 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.comCheck out SCRings: supercoachchampion.com

REDIFF - Le père d'Anne est atteint de la maladie d'Alzheimer et de la maladie de corps de Lewy. Elle vit ce que l'on appelle un deuil blanc. Bien qu'elle se soit préparée à cette éventualité, elle vit mal la situation. Chaque soir, en direct, Caroline Dublanche accueille les auditeurs pour 2h30 d'échanges et de confidences. Pour participer, contactez l'émission au 09 69 39 10 11 (prix d'un appel local) ou sur parlonsnous@rtl.fr

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

Join us for the first of our two-part special podcast shows, recorded live at the International Lewy Body Dementia Conference in Amsterdam! In this episode postdoc researcher Dr Josh Harvey (University of Exeter) is joined by three expert guests:

We're back with Part Two of our special highlights podcasts from the International Lewy Body Dementia Conference in Amsterdam! This time, host Dr Sterre de Boer (Alzheimer's Centre Amsterdam) leads the discussion with a fantastic panel of experts:

Hablamos con el presidente de Asinlewy, Enrique Niza. Es la primera asociación a nivel nacional contra la demencia por cuerpos de lewy. 

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. 

Anti-amyloid therapies provide the first FDA-approved option to alter AD pathology, but an understanding of overall utility and value to patients remains in its infancy. In this episode, Teshamae Monteith, MD, FAAN, speaks with David S. Geldmacher, MD, FACP, FANA, author of the article “Treatment of Alzheimer Disease” in the Continuum® December 2024 Dementia issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. Geldmacher is a professor and Warren Family Endowed Chair in Neurology and the director of the Division of Cognitive and Behavioral Neurology, Department of Neurology, Marnix E. Heersink School of Medicine at the University of Alabama at Birmingham in Birmingham, Alabama. Additional Resources Read the article: Treatment of Alzheimer Disease 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: @headacheMD Transcript Full interview transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Monteith: This is Dr Teshamae Monteith. Today, I'm interviewing Dr David Geldmacher about his article on treatment of Alzheimer's disease, which appears in the December 2024 Continuum issue on dementia. Welcome to our podcast, Dr Geldmacher. How are you?  Dr Geldmacher: I'm very well, thank you. It's a pleasure to be here.  Dr Monteith: Yeah. So, why don't you introduce yourself to our audience? Dr Geldmacher: Sure. I'm David Geldmacher. I'm a professor of neurology at the University of Alabama in Birmingham and I lead the division of Cognitive and Behavioral Neurology.  Dr Monteith: So, I'm really excited about this, to personally learn, and I know that or neurology community is also really excited about this interview. So, why don't we start off with your main objective.  Dr Geldmacher: So, my main goal in the article was to review the FDA-approved pharmacologic treatments for dementia. There's lots of ways of thinking about treatment of dementia; psychosocial, caregiver support, and so forth. But I really wanted to focus on the issues of drug treatment because that's what has been our backbone for a long time and now has recently expanded.  Dr Monteith: Why don't we talk a little bit about, first of all, the boom in the field? What's that been like?  Dr Geldmacher: So, the big change in the field is over the last several years, we've had treatments become available that actually attack the underlying Alzheimer pathology, and that's new and different. For decades, we've been able to treat the symptoms of the disease, but this is the first time we've really been able to get to the root of the pathology and look toward removing amyloid plaques from the brain.  Dr Monteith: Let's step back a little bit and talk about the framework of diagnosis and how that leads into the therapeutic potential. I know you're going to dive into some of the biologics, but we should probably talk about the kind of holistic approach to considering the diagnosis. Dr Geldmacher: Sure. So, you know, when someone comes to the clinic with memory complaints, our question we have to ask is, is this neurologic origin, a structural origin like Alzheimer's disease or vascular dementia? Are there complicating factors, the software issues of mood disorders and sleep disorders and pain that can all magnify those symptoms? The clinical reasoning is a critical part of that, but in Alzheimer's disease, typically the problems revolve around difficulty forming new memories of events and activities, the episodic memory. And then it's often accompanied by changes in word finding and semantic knowledge. And those are the things that we look for in the clinic to really point toward an AD diagnosis. And then we support it with exclusion of other causes through blood work and identification of patterns of brain atrophy on MRI. And then most recently in the last couple of years, we've been able to add to that molecular imaging for amyloid with PET scans as well as, most recently, blood-based biomarkers for Alzheimer's pathology. So, it's really been a revolution in the diagnosis over these last several years.  Dr Monteith: And when approaching patients or populations of individuals, there seems to be a real full spectrum with looking at the societal burden, the biological impact, of course, risk factors of primary prevention, and now this whole area of brain health and secondary prevention. How do you kind of tie all of this together when talking to patients and family members?  Dr Geldmacher: Sure. So, the approaches for brain health apply to everyone. In basically every clinic visited, our brain aging and memory clinic, we reviewed lifestyle approaches to brain health like regular physical exercise, healthy diet, cognitive and social stimulation. And those are fundamental to the approach to everyone, whether they have cognitive impairments that are measurable or not. These are all things that are good for our brain health. And then, you know, focusing on the vascular risk factors in particular and working with the patient and their primary care team to ensure that lipids and blood sugar and blood pressure are all in good healthy ranges and being appropriately treated.  Dr Monteith: You know, there's this kind of whole considerations of clinically meaningful endpoints and clinical trials, and even when we're talking to our patients. What would you say the field has kind of identified has the best endpoints in helping patients? Would you call it impaired daily function? Is that like the best hard endpoint? Obviously, there are other things such as caregiver burden, but you know, how do you approach assessing patients? Dr Geldmacher: Defining the endpoints is very difficult. Typically, if we talk to patients and their families, they would like to have better memory or improve memory. How that applies in everyday life actually is daily function. And so, we focus very much on daily function. And when I talk about our therapies, whether they're symptomatic therapies or the new disease-modifying therapies, I really talk about maintenance of function and delays and decline or slowing of decline, helping to foster the person's independence in the activities that they have and be able to sustain that over the longer term.  Dr Monteith: And when thinking about diagnosis- and we're going to get into treatments, but when thinking about the diagnosis, and of course, it's full-spectrum from mild cognitive impairment to moderate and severe forms of dementia, but who should have CSF testing and PET imaging? Obviously, these are invasive, somewhat invasive and expensive tests. Should all people that walk in the door that have memory complaints? How do you stratify who should have tests? Dr Geldmacher: I think about this in a big funnel, basically, and the starting point of the funnel, of course, is the person with memory complaints. Then there's that neurologic reasoning. Are these memory complaints consistent with what we expect from the anatomy of Alzheimer's disease, with atrophy in in the hippocampus and temporal lobe? Do they have episodic memory loss or not? That first step is really trying to characterize, do the clinical patterns act like those of Alzheimer's disease or not? And then we follow the Academy of Neurology guidelines, looking for reversible sources of cognitive decline, things like B12 deficiency and depression, sleep disorders and the like, and try to exclude those. We start with structural imaging with everyone, and MRI, typically, that will help us understand vascular burden and patterns of atrophy, looking for things like mesial temporal atrophy or precuneus atrophy that are characteristic of Alzheimer's disease. If those things are all pointing in the direction of AD as opposed to something else, then typically before moving on to CSF or PET scan, we will use blood-based biomarkers, which are one of the big changes in the field in the last year or so, and there are now multiple panels of these available. The downside is they are typically not covered by insurance. On the other hand, they can really help us identify who is likely to have a positive PET scan or positive findings on CSF. We start to provide that counseling and information to the patient before they get to those more definitive tests. We can push people in the other direction. We can say, your blood-based biomarkers are negative or do not indicate AD as the most likely source of your condition now, so let's treat other things. Let's see what else we can focus on. The blood-based biomarkers are now, in our clinic at least, the critical choke point between the routine workout that we've always done on everyone and then the more advanced workup of proving amyloid pathology with CSF or a PET scan. Dr Monteith: How sensitive are those blood biomarkers and how early are they positive?  Dr Geldmacher: The sensitivity is generally pretty good, in the ninety plus percent range on average and it depends on which panel. And as you point out, when in the course of symptoms that they're done, we know that they become positive and presymptomatic or asymptomatic people. We're using these kinds of markers to screen people for prevention trials. So, I think when someone is symptomatic, they're a good indicator of the presence or absence of AD pathology. Now that doesn't mean the AD pathology is the sole cause of their symptoms. And so, we still need to think about those other things like sleep and mood and so forth. But they do point us in the in the direction of Alzheimer's change.  Dr Monteith: So why don't we talk about some of the more standard older treatments, and it's also important to leave with kind of some rational approach to when we start and what should we be counseling our patients on. So why don't we start with the older, you know, choline esterase inhibitors and then some of the MDA- I guess there's only one modulator, SEPTA modulator. Dr Geldmacher: So, I've been really fortunate in my career span, the time from the first of those symptomatic agents reaching the market in 1993 to seeing the disease modifying drugs enter the market now. I think most neurologists actually have entered practice after those clinical trials of the colon esterase inhibitors were published. So, one of my goals in this article was to review that primary data and what can we expect from those symptomatic drugs. We know that they are inconsistently effective in mild cognitive impairment, and the Academy of Neurology guidelines says there is not strong evidence to use them in mild cognitive impairment. But in mild AD and beyond, the cholinesterase inhibitors provide meaningful benefits. They delay decline, they can delay nursing home placement. They reduce overall costs of care. So, I think they provide real value. So, in the article I have reviewed what the data looked like on those. My approach is to start with oral Donepezil at five milligrams and increase it to ten in everyone who tolerates the five. If for whatever reason the oral Donepezil is not well tolerated, I'll switch to transdermal rivastigmine to help improve tolerability. There are very few head to head comparisons, but nothing suggests that one of the cholinesterase inhibitors is superior to the other for clinical outcomes, and there's no evidence to support conjoint use of more than one at a time. Should someone be showing decline then on typical cholinesterase inhibitor therapy - and people will, it's often delayed, but the decline will reemerge - then I will add the NMDA receptor, a modulator memantine and titrate that up to full dosing, either 10 mg twice a day for the conventional release or 22 mg extended release. And at that point we're sort of on maximal pharmacologic therapy for Alzheimer's disease. These agents can provide some benefit in other conditions, they're off-label except for Lewy body disease where rivastigmine is labeled. But they can provide benefit across different conditions. And there's some preliminary data, for instance, of acetylcholinesterase inhibitors being helpful in vascular cognitive impairment. So, I will use them, but I expect the greatest response when someone really does follow the patterns of Alzheimer's disease.  Dr Monteith: And you have a great chart, by the way, and nice figures looking at some of the meta-analyses on cognitive outcomes as well as functional outcomes. So, thank you for that.  Dr Geldmacher: In general, all of those tables favor treatment over placebo in the domains of cognition, daily function, neuropsychiatric symptoms. And it's that consistency of result that lets me know that we really are seeing a drug effect, that it's not a class effect with those, that we really are helping our patients. It's not like some studies are positive and some are negative. They are very consistently positive. Small magnitude, but consistently positive.  Dr Monteith: And I know we have a lot of patients coming in where, at least, their caregivers are complaining about agitation, and sleep is also a problem for others. And so how do you help that patient? I know you have a good algorithm that also you included in your article, but why don't you summarize how we should approach these symptoms? Dr Geldmacher: Sure. So, for nonpsychotic agitation, you know, just restlessness, wandering, pacing and so forth, my first choice is an off-label use of citalopram. And there is good clinical trials evidence to support that. if someone has psychotic agitation that is with delusions or hallucinations and so forth, I think we do need to move to the antipsychotic drugs. And the one drug that is now approved for treatment of agitation and Alzheimer's disease does fall into that antipsychotic category, along with its various black box warnings - and that's brexpiprazole. For many of our patients, getting coverage for that agent is difficult. It's not on many formularies. So, it is something I progress toward rather than start with. Similarly, for sleep, there is one approved agent for sleep, that's a dual orexin agonist. And it shows effectiveness, but can have some negative cognitive effects, and so I tend not to start with that either. My first choice when sleep is the primary issue for our patients with dementia is trazodone, and there are some small, limited studies for it's off-label used to enhance sleep. It's safe, inexpensive, often effective, and therefore it's my first choice. Dr Monteith: So, now let's get into the big conversations that everyone is having. Let's talk about the newer disease modifying anti amyloid therapies. Give us a summary dating back 2021 probably, although we can hold the preclinical work, but let's talk about what is available to our patients. Dr Geldmacher: Sure. And the development of anti-amyloid therapies goes all the way back to 1999. So, it's a pretty long course to get us to where we are today.  Dr Monteith: Yeah, that's why we limited that.  Dr Geldmacher: With that first approved agent with aducanumab in 2021, it received a limited or accelerated approval in FDA parlance. These agents, the aducanumab, lecanemab and donanemab, all approved, are known to remove amyloid pathology from the brain as measured by CSF and/or BIPET. They are amyloid lowering therapies, often called disease-modifying therapies. And across the agents there's some variable results. But if we look at the two with full approval, lecanemab and donanemab, they slow clinical progression by 25% to 35% on average. And that's measured by either cognitive measures or global measures or composite measures, but it's pretty consistent in that range of about one-third slowing. That makes it really difficult to discern in an individual patient, though, because there's so much variability in the progression of the disease already that it can be difficult to tell in one person that these drugs are working. They're also complex to use, so there's a qualification process that involves MRI to exclude things like a high tendency toward hemorrhage. It includes genetic testing for papal E4 status to help us understand the risk for complication, and then once-monthly or twice-monthly infusions with standardized schedule for MRI scanning. So, there's a lot that goes into managing these agents. And they are expensive, and we don't yet know their cost effectiveness. The cost effectiveness of the cholinesterase inhibitors was questioned when they first came out back in the 1990s, and it took five or ten years to really understand that they provided benefit to society and to individuals in those domains of quality of life and return on investment. And we're still learning about that with the disease modifying therapies.  Dr Monteith: So, two questions. One, the case that you presented was an individual having symptoms and kind of voiced their desire to be on these therapies. So, people are going to be asking, coming to clinic asking and then of course, they're going to be people that you select out. So, how do you make that decision to recommend this treatment for patients given the potential risk? Dr Geldmacher: We've got some really good guidance from appropriate use recommendation papers for aducanumab and lecanemab, and I'm expecting one from donanemab fairly soon. But the key is to identify individualized risks, and that involves knowing their APOE4 status, knowing their- whether they've had microhemorrhages in the brain previously, and then documenting that they really do have amyloid pathology with something like PET scan to establish those baselines. I talk to people about the burden of twice-monthly infusions or, now with donanemab, once-monthly infusions. And for instance, for someone who's got a working caregiver, getting to an infusion center twice a month can be a significant burden. And then if there are complications, frequent MRI scans and so forth. So, we talk about the burden of entering into this therapeutic pathway. The reality is that people who are qualified generally want it. I have relatively few folks who have said, no, these risks are more than I'm willing to accept. For decades my patients have said, anything you can do to slow this down, I'm willing to try. And now we're seeing that translated to reality with people willing to accept high-risk, high-cost treatments with the chance of slowing their individual progression.  Dr Monteith: And how do you select between the two treatments? Dr Geldmacher: So far that's been easy because donanemab's not readily available.  Dr Monteith: Outside of clinical trials, right?  Dr Geldmacher: Exactly. For prescription use, it's coming in - the first cases have now been infused - but it's not generally available. Nonetheless, what I will do for patients in this is look at the risk tables. So donanemab appears to have in general some higher rates of the Aria complications, amyloid-related imaging anomalies, and some people are going to be more risk tolerant of that for the payoff of potentially faster response. The donanemab trials restructured that. They did their first assessment of effectiveness. I had amyloid removal at six months and a significant proportion of people were eligible to discontinue treatment at six months because their amyloid was below treatable thresholds. So higher risk, perhaps faster action and fewer infusions for donanemab. Lecanemab we have more direct experience with, and between the two of them, the eighteen month outcomes are pretty much the same and indistinguishable. So are we in it for a quick hit, or are we in it for the long race? And different patients and different families will have differing opinions on where they want to accept that risk and burden and so forth. But so far, the data don't indicate a lot of difference in their longer-term outcomes. We still have plenty to learn.  Dr Monteith: And so, it sounds like, as you mentioned, we're looking at eighteen months out for kind of a hard outcome, and that there is a lot of variability in response rate. How are you tracking patients- you know about the imaging, so just in terms of clinical outcomes and efficacy?  Dr Geldmacher: Sure. So, for Medicare to reimburse on these treatments, people need to be enrolled in a registry program - and there are several of these, CMS runs one of their own. But the requirement for that is, every six months, to do cognitive and functional outcomes through the first two years. Cognitive outcomes are up to the clinician, but things like the mini mental state exam, the MoCA, are appropriate. In our own program, we use something we developed locally called the Alabama Brief Cognitive Screener. As for the cognitive outcomes and then for functional, we use an instrument called the General Activities of Daily Living Scale, but there are many other ADL scales that could be used as well. CMS does not mandate specific tests. Since the progression of the disease is variable to begin with, we don't really know how to interpret these results in reference to whether the drug is working, but I can tell a patient or a family member, your scores are stable, or, you have a decline of three points in this test. That's typical for this duration of illness. But there isn't a good way to know whether the drug is working in this person at this time, at least with our current levels of data.  Dr Monteith: So, I think we have to talk about health equity, and it sounds like Medicare is reimbursing for some of us. We look at different socioeconomic backgrounds, educational backgrounds, race, ethnicity. Not everyone is aware of these treatments. So, how do we get more patients to become aware of these treatments? And how do we get them to more people to help people? Dr Geldmacher: Yeah, I mean, that's- it's a major, major issue of inequity in our population. We've done some work at UAB looking at the flow of members of minority communities into memory clinics. So, we know that the overall population of, and I'll choose, for an example, blacks and African Americans, that they are represented a much higher rate in our overall UAB treatment population than they are in our memory clinic population. So, they're not even getting to us in the specialty clinic at the same rates as other segments of our population. We also know that blacks and African Americans in our population are not receiving PET scans as often as the overall treatment population. So yes, there are real, real problems with access. There are cultural issues behind this as well. And in many communities, a change in cognition, a loss of memory is an expected part of the aging process rather than recognized as a disease. So, people who come to us from minority communities are often further along in the course of cognitive and functional decline and beyond the point where they might qualify for the disease-modifying therapies, where early AD is the sort of defining boundary. So, I think more awareness and more screening in primary care settings, perhaps more community outreach to let people know that changes in memory that affect daily function are not normal as part of the aging process and should be evaluated for intervention. So, there's lots of places in our healthcare community where we could foster better outreach, better knowledge to get more folks access to the medicines. And this is before we even get to cost. Dr Monteith: Yeah, yeah. And obviously, there's some stigma as well.  Dr Geldmacher: That's right.  Dr Monteith: Really recognizing what the issues are and diving and asking those questions and funding research that asks those questions, as you mentioned, is really important. And then you have also a nice area where, you know, looking on the impact of treatments on caregiver-related outcomes, and of course ultimately want to keep patients out of nursing homes and prevent death. And so, can you talk a little bit about that? And, you know, mainly the caregiver burden.  Dr Geldmacher: So, my research in that area goes back a long way now. But I learned early in the course of therapy that many times the outcome that the family is noticing for symptomatic therapies is not a change in the patient's memory per se, but that there is less work involved in the caregiving. Less time is spent in direct caregiving roles. The patient may shadow less and because they have better independent cognition. I remember one family member once told me, the medicine you started is a godsend because now I can go to the bathroom by myself and he's not pounding on the door saying where are you, where are you. He's able to recall long enough that I'm in the bathroom that I have that moment of privacy. That was very meaningful to me to hear that. So. Dr Monteith: Cool. So why don't you just help us wrap this up and just give us, like, three main takeaway points that we should be getting out of your article? Dr Geldmacher: The three points that I would emphasize from my article is that the symptomatic therapies provide meaningful benefits and measurable, consistent, meaningful benefits. The second is that those benefits extend beyond things like cognitive test scores and into things like caregiver well-being and maintenance of independence in the home environment. And the third is that the disease-modifying therapies are an exciting opportunity to modify the pathology, but we still are learning about their cost effectiveness and their long-term benefit both to individuals and to society. But the only way we're going to learn that is by using them. And that was the experience that we gained from the symptomatic therapies that took use in the community for years before we really began to understand their true value. Dr Monteith: Thank you. That was excellent. And I put you on the spot, too.  Dr Geldmacher: No problem.  Dr Monteith: Again, today I've been interviewing Dr David Geldmacher, whose article on treatment of Alzheimer's disease appears in the most recent issue of Continuum on Dementia. Be sure to check out Continuum audio episodes from this and other issues. 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 this 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 contentpub.com/AudioCME. Thank you for listening to Continuum Audio.

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.

Welcome to the NeurologyLive® Mind Moments® podcast. Tune in to hear leaders in neurology sound off on topics that impact your clinical practice. In this episode, Russ Lebovitz, MD, PhD, chief executive officer and cofounder of Amprion, discussed the company's SAAmplify-aSYN biomarker test, a first-in-class qualitative laboratory developed test and the only seed amplification assay available to aid in the diagnosis of synucleinopathies such as Parkinson disease (PD) and multiple system atrophy (MSA). Lebovitz provided insight on the new technology and its remarkable accuracy in identifying underling a-synuclein pathology using fluorescence changes. He gave a complete overview of the notable study published in The Lancet Neurology that further tested and validated the assay among a heterogenous group of synucleinopathies. Furthermore, he provided clinical context on the feasibility of the assay, the potential for clinical use, and the continued validation needed.  Looking for more movement disorder discussion? Check out the NeurologyLive® Movement disorder clinical focus page. Episode Breakdown: 1:05 – Overviewing mechanistic function of SAAmplify-aSYN biomarker test, its purpose, and how it came about 7:50 – Results from the published study; ways the fluorescence-based amplification method could distinguish MSA from PD and Lewy body dementia 16:25 – Neurology News Minute 18:30 – Therapeutic feasibility of the assay in clinical settings and the next steps in validation The stories featured in this week's Neurology News Minute, which will give you quick updates on the following developments in neurology, are further detailed here: Axsome to Submit NDA for AXS-05 in Alzheimer Agitation Following Positive Phase 3 Trials FDA Clears IND for Trial Assessing Gene Therapy SGT-212 in Friedreich Ataxia FDA Grants Fast Track Designation to Anti-Tau Therapy Posdinemab Thanks for listening to the NeurologyLive® Mind Moments® podcast. To support the show, be sure to rate, review, and subscribe wherever you listen to podcasts. For more neurology news and expert-driven content, visit neurologylive.com.

Recent progress in neurogenetics and molecular pathology has improved our understanding of the complex pathogenetic changes associated with neurodegenerative dementias. In this episode, Katie Grouse, MD, FAAN, speaks with Sonja W. Scholz, MD, PhD, FAAN, an author of the article “Genetics and Neuropathology of Neurodegenerative Dementias,” in the Continuum® December 2024 Dementia issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Scholz is a senior investigator at the National Institutes of Health in Bethesda, Maryland and an adjunct professor of neurology at Johns Hopkins University in Baltimore, Maryland. Additional Resources Read the article: Genetics and Neuropathology of Neurodegenerative Dementias 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 Full episode transcript available here:  Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Sonia Scholz about her article on genetics and neuropathy of neurodegenerative dementias, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast, and please introduce yourself to our audience.  Dr Scholz: Thank you so much for inviting me. My name is Sonia Scholz. I'm a neurologist working at the National Institutes of Health. My main focus of research and clinical work are neurodegenerative diseases, and I have a particular interest in using modern genomic tools to understand these diseases and potentially leverage it for new translational applications. Dr Grouse: Sonia, we're really excited to have you today and thanks for joining us.  Dr Scholz: I'm pleased to be here.  Dr Grouse: I'd like to start by asking what you think is the most important message or takeaway point from your article? Dr Scholz: So, this is an article that really captures a very broad and exciting field. So, one thing I wanted to really highlight is that there's a lot of heterogeneity, clinical, pathological, molecular heterogeneity in age-related neurodegenerative dementia syndromes. Our article was really aimed at providing a bird's eye view of the pertinent pathological characteristics, but also important genetic advances and insights and how we can leverage that, particularly in the new physician medicine era, hopefully come up with better treatments and better ways to counsel our patients.  Dr Grouse: What do you think is the most challenging aspect of understanding the genetics and neuropathologic basis of neurodegenerative dementias?  Dr. Scholz: That's a good question. There're many big and challenging questions, but I think one of the things we struggle the most with is really the heterogeneity. I see patients with one and the same Mendelian form of dementia. One patient is in their forties another patient is in their eighties, and the clinical manifestations can be very different from one patient to another. There's a lot of heterogeneity, also, on the pathological level. Not every patient has exactly the same distribution. And so, we're starting to slowly define what the underlying causes are, but it's still quite baffling and quite challenging to put them together and understand them. Dr Grouse: Do you feel that the genome-wide association studies has helped our understanding of these diseases, specifically the heterogeneity? And if so how?  Dr Scholz: That's a great question, but you're talking to a geneticist here. And I definitely would say genome-wide association studies have helped us a lot in identifying what the underlying disease pathways are and what the relationships between neurodegenerative disease entities are. It really also gave us a better understanding of apparently sporadic diseases where genetic factors are still playing a role. And we can leverage that type of knowledge increasingly to highlight high-risk groups, but also, we can increasingly use it to stratify patients for clinical trials, for example. And that's really exciting and there's still a lot of knowledge that we have to garner very quickly, especially in the non-Alzheimer dementia space.  Dr Grouse: You've mentioned, of course, the heterogeneity and these syndromes. And in your article, you go into a lot of the issue of the significant crossover between the genetic links and the neuropathological findings for the various types of neurodegenerative dementias. Do you think that this crossover has been more of a help or a hindrance in better understanding these diseases? Dr Scholz: Yeah, it can be a little bit, you know, challenging to wrap one 's mind around it. But by and large, I think it's actually good news because it highlights that there is a shared biology between many of the neurodegenerative disease entities. And by figuring out which the pathways are that are very often involved, we can prioritize certain targets for therapy development. But we can also be smarter about how we developed treatments. We could repurpose a drug that has been developed for Alzheimer's disease very easily for Lewy body dementia because we increasingly understand the overlap. And we can also leverage new clinical trials design, like basket trials. This is something that has been really transformative in the oncology sphere and now, increasingly, neurodegeneration. We're trying to apply that kind of thinking as well to our patient populations. Dr Grouse: What do you think our listeners will find to be most surprising when they read the article? Dr Scholz: We often present these diseases in our textbooks as these black-and-white entities, but the reality is that there's a lot of overlap. And we also see that co-pathologies are actually the norm and not the exception, and a lot of the molecular risk factors are shared. It's not really surprising. And I think that overlap and crosstalk between the various diseases is something that's a little bit strange to think about, but it actually makes increasingly sense now that we see the genetic risk profiles coming up. Dr Grouse: In reading your article, I was really struck by how many, or how much the prior studies have been lacking in inclusion of different ethno-racial backgrounds in the patients who've been studied. How can this be improved going forward?  Dr Scholz: Yeah, thank you. That's a really important and crucial question, and I think it really takes the collective effort of everybody in the healthcare research community to improve upon that. We need to talk to our patients about genetic testing, about brain donation programs, about referrals to clinical trials, and don't feel shy about reaching out to our colleagues and academic centers, even if you don't have the resources in a smaller institution. We also not only need to engage with the communities, we also need to build up a healthcare research community that has representatives from these various communities. So, it's really a collective effort that we build up and are proactive about building a more equitable healthcare system and research system that works for all of us and that really is going to provide us with the precision medicines that work for everybody. Dr Grouse: What do you think is the biggest debate or controversy related to the genetics and neuropathology of neurodegenerative dementias?  Dr Scholz: Yeah, there are loads of interesting debates, but I think in my field, in particular in the genetics is what to do with risk variance. What is it that I actually communicate to the patient? Obviously, I can learn a lot on the bench and I think I can use a lot of the genetic risk factors for molecular modeling, etc. But to which extent should I share that information? Because genetic information is something that we cannot alter and many of the risk factors are actually mild, that they may never result in disease. And so, communicating risk with patients is something that's very challenging and we used to just steer away from it. But now the discussion is starting to shift a little bit. You know, nowadays we are starting to offer, for example, testing for the APOE4 allele in individuals who are considering antiamyloid therapies. And this really, this is precision medicine in his earliest days because it allows us to stratify patients into those that are high-risk versus low-risk and those that need more frequent follow-up or may be advised not to pursue this treatment. And we're probably going to see more of those discussions and the ethics around it. And it's even harder in an aged population where you know, you may never manifest any of the symptoms despite carrying a lot of these risk deals. Dr Grouse: You mentioned, you know, that testing, APOE4 testing for certain populations when deciding to do the antiamyloid immunotherapies. Apart from that, which I think is a really good example of where genetic testing makes sense, what other scenarios do you think it makes sense at this point in time to recommend genetic testing for symptomatic patients who are concerned about neurodegenerative dementias? Dr Scholz: Yeah. So, I usually have a very frank discussion with patients in whom I suspect the genetic etiology. So those are individuals who have a strong family history, individuals from very early onset of the disease where genetic testing may allow us to establish a molecular diagnosis, individualize and refine our counseling, and potentially get them into targeted clinical trials that may be suitable for that. Those are always very nuanced discussions, but I usually start with those high-risk individuals. Increasingly patients are, even with the apparently sporadic forms, are asking me about it. And then I have a frank discussions about the pros and cons and offer it to the patients who really would like to pursue it.  Dr Grouse: That makes a lot of sense. What about in the case of patients who are asymptomatic but might have high risks because of, well, family members with certain types of neurodegenerative dementias? When would it make sense, if ever, to do genetic testing for them? Dr Scholz: Yeah, that's a that's a tough situation, to be honest. By and large, I would say I would like to understand what the motivation is to learn about the genetic status. If the motivation is something like family planning, future care planning, etc, then it may be a reasonable thing. But I also want to make it very clear upfront that knowing a genetic status, at least aside from APOE status, at least for now, doesn't actually change the clinical management. And I want to make sure patients understand if they are trying to lower their risk, knowing that genetic status is not going to lower their risk. There are other things, brain health habits, that are really important, that patients should double down on: avoiding vascular disease, avoiding traumatic brain injury, excessive alcohol use, etcetera. It's a discussion that really tries to understand the motivations behind the testing. But some patients are very frank and they want to have it. They may want to contribute to the research community, and so in those instances we may offer it, but I also really want to make them understand that knowing a genetic diagnosis may be acceptable to them, but family members who are related to them may not wish to know. And they can really cause a lot of psychological stress that extends beyond the individual. And then that's something to really consider before actually pursuing testing. Dr Grouse: I think that's a really good reminder, especially about how this can even affect people outside of the patient themselves. I think a lot of us don't even think about that. And certainly, our patients may not either. Taking it a step further, thinking about newly available biomarkers, imaging modalities, how should we incorporate the use of these for our patients when we're suspicious of things like Alzheimer's disease or dementia with the Lewy bodies? Dr Scholz: So by and large these biomarkers are used in in the research area, but we can, in a given patient where maybe the clinical presentation is somewhat atypical, we can use it to help with our diagnostic impression. It doesn't get rid of the clinical evaluation, but at least it gives us a little bit more certainty. Here are the you know, the molecular features, the abnormal amyloid tau deposits, for example, that we're there we're detecting supports diagnosis. May also sometimes help in patients where we suspect there could be even the co-pathology going on where we get a mixture of features, where we can counsel the patients and you know, detecting copathologies is something that is certainly challenging. We know that patients who have more pathologies on average are not doing as well as the ones who have relatively pure disease forms. But this is also an area of intense research and as long as it's used judiciously to help with the diagnostic compression, to reduce a diagnostic odyssey, I think there's a lot of potential there to improve the clinical evaluations nowadays. Dr Grouse: It is really exciting to see the options that are opening up as the years go by, which brings me to my next question. There is certainly, as we know, this new category of disease modifying therapies that are available in the form of the anti-amyloid immunotherapies. What else do you think's on the horizon for treatment and prevention, neurodegenerative dementias, going down the road five, ten, fifteen years down the line?  Dr Scholz: Yeah, I think we're entering the era of precision medicine already and we're, we're seeing it already with the anti-amyloid therapies. By and large, I think the standard of care is going to be a multidisciplinary individualized treatment plan that incorporates a more holistic view. It incorporates diet, lifestyle factors, symptomatic management, but also disease modification strategies and potentially even multitarget disease modifying strategies. I think there's a lot more work that we have to do, especially in in the non-Alzheimer's dementia field. But overall, we're becoming much better in refining our diagnostic impression and in treating some of the complications that arise in these very complex diseases.  Dr Grouse: I'm curious, with the future of dementia care and diagnosis being more of a precision medicine model, how do you think this will be possible in an aging population with already, I think, probably a limited access to neurologists even in current state? Dr Scholz: Yeah, this is- these are these are very challenging societal questions. Increasingly, you know, we can use modern technologies such as televisits for follow up, but also, you know, remote monitoring devices. We have to educate the next generation, we need more neurologists, we can't do it alone; but we also need to empower primary care doctors who are usually the first go-to person. And perhaps biomarker testing will become much more common even in the primary care setting. I think overall, you know, we can tackle it by educating the community, empowering participants in various clinical trials, and being flexible of embracing certain new technologies. Dr Grouse: Absolutely. I think that makes a lot of sense and hopefully this will be another call to arms to try to get the word out, get more access to neurology and more people interested and like you said, getting our other colleagues involved and being able to manage it as well.  Dr Scholz: Yeah.  Dr Grouse: I wanted to transition a little bit into learning more about you. How did you become interested in genetics of neurodegenerative dementias? Dr Scholz: Yeah, it's something, it's an interest that has grown gradually. I started out as a neuroscientist in in Austria, where I was fortunate to work with a group that was very strongly involved in Parkinson's disease care. And I was so thrilled to see patients, you know, treated with deep brain stimulation. But yet in the same clinic, I also saw the patients who were not eligible because they had atypical neurodegenerative diseases. And it's the realization that there is such a broad spectrum of diseases that we frankly don't understand very well, that we really need to work with, understand and hopefully develop the treatments with. That's really has resonated with me. And I've since then really built my entire career around it through different countries at the United Kingdom and the United States. And I'm very fortunate to work at the National Institutes of Health, where I can pursue a lot of these research passions and work with interesting patients and colleagues.  Dr Grouse: Well, I've learned a lot today, and I'm sure our listeners would agree. Thank you so much for joining us. It's really been a pleasure speaking with you.  Dr Scholz: Well, thank you so much for allowing me to contribute. And, you know, I hope the review article conveys a lot of the exciting developments in this really challenging field. But there's loads of hope that we will eventually get to the point to tackle these conditions.  Dr Grouse: I encourage all of our listeners to check out Dr Scholz 's article. It is a great overview of these conditions and the genetics and neuropathology underlining them. Again, thank you so much.  Dr Scholz: Thank you for having me. Dr Grouse: Again, today I've been interviewing Dr Sonia Scholz, whose article on genetics and neuropathology of neurodegenerative dementias appears in the most recent issue of Continuum on dementia. Be sure to check out Continuum audio episodes from this and other issues. 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 this 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.

It is widely known that a healthy diet can provide essential nutrients and lead to a multitude of benefits, but growing evidence has highlighted important links between diet, nutrition, and brain health, particularly related to neurodegenerative disease. In this episode, Dr. Puja Agarwal discusses her research investigating the role that diet and nutrition may play in Parkinson's disease and other neurodegenerative conditions. Evidence from her studies and the work of others suggests that certain diets, including the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet, are associated with brain health and may have the potential to delay the onset or slow progression of Parkinson's disease or other neurodegenerative conditions. We hear more about her ongoing MJFF-funded research project examining the role of diet in the progression of parkinsonian signs and its association with Lewy body pathologies, as well as future directions for this exciting line of research. Puja is an Assistant Professor in the Department of Internal Medicine at Rush University.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast at michaeljfox.org/podcasts. We're excited to announce that we will be merging our two podcasts in 2025, and we invite you to subscribe to our Michael J. Fox Foundation Parkinson's Podcast on Apple Podcasts or wherever you get your podcasts for future episodes featuring scientists, doctors and people with Parkinson's talking about different aspects of life with the disease as well as new research toward treatment breakthroughs.

Although Alzheimer disease (AD) is the most common neurodegenerative cause of dementia, other etiologies can mimic the typical amnestic-predominant syndrome and medial temporal brain involvement. Neurologists should recognize potential mimics of AD for clinical decision-making and patient counseling. In this episode, Kait Nevel, MD, speaks with Vijay K. Ramanan, MD, PhD, an author of the article “LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy,” in the Continuum December 2024 Dementia issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Ramanan is a consultant and assistant professor of neurology in the Division of Behavioral Neurology at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy 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 Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: IUneurodocmom Guest: @vijaykramanan Full episode transcript available here Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum 's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum Journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Nevel: This is Dr Kait Nevel. Today I'm interviewing Dr Vijay Ramanan about his article he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast. Vijay, can you please introduce yourself to the audience? Dr Ramanan: Thanks so much, Kait. I'm delighted to be here. So, I am a cognitive neurologist and neuroscientist at the Mayo Clinic in Rochester, Minnesota. I have roles in practice, education and research, but amongst those I see patients with cognitive disorders in the clinic. I help direct our Alzheimer's disease treatment clinic and also do research, including clinical trial involvement and some observational research on genetics and biomarkers related to Alzheimer's and similar disorders. Dr Nevel: Great, thanks for that. So, I'd like to start off by talking about why is LATE hippocampal sclerosis, why is this important for the neurologist practicing in clinic to know about these things? Dr Ramanan: That's a great question. So, if we take a step back, we know that degenerative diseases of the brain are really, really common, and they get more and more common as we get older. I think all neurologists, and in fact most clinicians and large swaths of the general public, are well aware of Alzheimer's disease, which is the most common degenerative cause of cognitive impairment in the population. But there are non-Alzheimer's degenerative diseases which can produce cognitive difficulties as well. And it's important to be aware of those disorders, of their specific presentations and their implications, in part because it's always a healthy thing when we can be as precise and confident about diagnosis and expectation with our patients as possible. I'll look to the analogy of a patient presenting with a myelopathy. As neurologists, we would all find it critical to clarify, is that myelopathy the result of a compressive spondylotic change? The result of an inflammatory disorder, of a neoplastic disorder, of an infectious disorder? It's critical to guide the patient and choose appropriate management options based on the cause of their syndrome. It would potentially harm the patient if you treated an infectious myelopathy with steroids or other immune-suppressant drugs. So, a similar principle holds in cognitive neurology. I accept with humility that we can never be 100% crystal clear certain about things in medicine, just because when you think you got it all figured out there's a curveball. But I want to get as close to that 100% as possible. And recognizing that disorders like LATE or PART can mimic the symptoms, sometimes even the imaging features of Alzheimer's disease. I think it's critical to have heightened awareness of those disorders, how they look, to be able to apply appropriate counseling and management options to patients. I think this becomes particularly critical as we move into an era of disease-specific, and sometimes disease-modifying, therapies, where applying a choice of a treatment option could have significant consequences to a patient if the thing you're treating isn't the thing that the drug is trying to accomplish. So, having awareness and spreading awareness about some of these non-AD causes of cognitive difficulty, I think, is a big mission in the field.  Dr Nevel: Yeah, that makes total sense. And kind of leaning into this, you know, trying to differentiate between these different causes of late-life amnestic cognitive impairment. You know, I'll point out to the listeners today to please read your article, but in addition to reading your article, I'd like to note that there's a really nice table in your article, Table 6-1, where you kind of go through the different causes of amnestic cognitive impairment and the different features that better fit with diagnosis X, Y, or Z, because I think it's a really nice table to reference and really easy to look at and reference back to. But on that note, what is your typical approach when you're seeing a patient in clinic, have a new referral for an older patient presenting with a predominantly progressive amnestic-type features? Dr Ramanan: Excellent question. And this is one that I think has relevance not just in a subspecialty memory clinic, but to all the clinicians who help to diagnose and manage cognitive disorders, including in primary care and general neurology and others. One principle that I think it's helpful to keep in our minds is that in cognitive neurology, no one data point takes precedence over all the others. We have a variety of information that we can gather from history, from exam, from imaging, from fluid biomarkers. And really the fun, the challenge, the reward is in piercing together that information. It's almost like being a lawyer and compiling the evidence, having possibilities on your list and raising and lowering those possibilities to get as close to the truth as you can. So, for patients with a cognitive syndrome, I think the first plank is in defining that syndrome. As you mentioned, if I'm seeing someone with a progressive amnestic-predominant syndrome, I first want to make sure, are we talking about the same thing, the patient, the care partner, and I?  Can often be helpful to ask them for some examples of what they see, because sometimes what patients may report as memory troubles may in fact reflect cognitive difficult in other parts of our mental functioning. For example, executive functioning or naming of objects. And so helpful to clarify that in the history to get a sense of the intensity and the pace of change over time, and then to pair that with a good general neurologic exam and some type of standardized assessment of their cognitive functioning. At the Mayo Clinic, where partial to the short test of mental status. There are other ways to accomplish that, such as with an MMSE or a MoCA. If I understand that the syndrome is a progressive amnestic disorder, Alzheimer's disease is the most common cause of that presentation in older adults, it deserves to be on my differential diagnosis. But there might be some other features in the story that could raise or lower those mimics on my list. So, in patients who are, say, older than the age of seventy five, disorders like LATE or PART start to rise higher on the likelihood for me, in particular if I know that their clinical course has been more slow brewing, gradually evolving. And again, most degenerative disorders we expect to evolve not over days or weeks, but over many months to many years. But in comparison with Alzheimer's disease, patients with LATE or with PART would be expected to have a little more slow change where maybe year over year they or their care partners really aren't noticing big declines. Their daily function is relatively spare. There might not be as much involvement into other non-memory cognitive domains. So, these are some of the pieces of the story that can help to perhaps isolate those other non-AD disorders on the list as being more likely and then integrating, as a next level, diagnostic testing, which helps you to rule in and rule out or support those different causes. So, for example, with LATE there can be often out of proportion to the clinical picture, out of proportion to what you see on the rest of their imaging or other profiles, very predominant hippocampal and medial temporal volume loss. And so that can be a clue in the right setting that you may not be dealing with Alzheimer's disease or pure Alzheimer's disease, but that this other entity is there. So, in the big picture, I would say being systematic, recognizing that multiple data points being put together helps you get to that confident cause or etiology of the syndrome. And in particular, taking a step back and thinking about big picture factors like age and course to help you order those elements of the differential, whether AD or otherwise. Dr Nevel: Great, thanks. In your article, you talk about different imaging modalities that can be used, as you mentioned, you know, just another piece of the puzzle, if you will, to try and put together what may be going on with the patient, and recognizing that some of these imaging techniques are imaging is special imaging, not available in a lot of places.  You know, and maybe other diagnostic type tests that could be helpful in differentiating between these different disorders may not be available, you know, for the general neurologist practicing in the community. So, what do you suggest to the general neurologist maybe practicing somewhere where they don't have access to some of these ancillary tests that could assist with a diagnosis?  Dr Ramanan: Critical question. And here I think there's not likely to be one single answer. As with most things, awareness and recognition is a good place to start. So, some of those clues that I mentioned earlier about the clinical course, about the age, the- we're talking about clinical setting there. So, comfort with and understanding that the clinical setting can help you to be more confident about, for example, LATE or PART being present in contrast to AD. That's important information. It deserves to be part of the discussion. It doesn't necessarily need other tests to have value on its own. A second piece is that tests help, in some cases, to rule in and rule out causes for cognitive difficulty. As part of a standard cognitive evaluation, we would all be interested in getting some blood tests to look for thyroid dysfunction or vitamin deficiencies. Some type of structural head imaging to rule out big strokes, tumors, bleeds. Head CT can accomplish some of that perspective. It's ideal if a brain MRI can be obtained, but again, keeping in mind, what's the primary goal of that assessment? It's to assess structure. Occasionally you can get even deeper clues into a syndrome from the MRI. For example, that very profound hippocampal or medial temporal atrophy. So, increasing awareness amongst clinicians throughout our communities to be able to recognize that change and put it in the context of what they see in other brain regions that can be affected by Alzheimer's or related disorders. For example, the parietal regions can be helpful. And recall that MRI can also be helpful in assessing for chronic cerebrovascular disease changes. This is another mimic that shows up in that table that you mentioned. And so multiple purposes can be satisfied by single tests. Now, you're absolutely right that there are additional test modalities that, perhaps in a subspecialty clinic at an academic medical center, we're very used to relying on and finding great value on; for example, glucose PET scans or sometimes fluid biomarkers from the blood or from the spinal fluid. And these are not always as widely available throughout our communities. Part of the challenge for all of us as a field is therefore to take the expertise that we have gathered in more subspecialty settings and tertiary care settings and translate and disseminate that out into our communities where we need to take care of patients. That's part of the challenge. The other challenge is in continued tool and technological development. There's a lot of optimism in our field that the availability of blood-based biomarkers relevant for Alzheimer's disease may play a part in helping to address some of the disparities in resource and access to care. You can imagine that doing a blood test to give you some high-quality information, there are going to be less barriers to doing that in many settings compared to thinking about a lumbar puncture or a PET scan, both in terms of cost to the patient as well as infrastructure to the clinicians and the care team. So I'm optimistic about a lot of those changes. In the meantime, I think there are, through both clinical evaluation and some basic testing including structural head imaging, there are clues that can help navigate these possibilities. Dr Nevel: So, let's say you have your patient in clinic, you've done your evaluation, maybe gotten some ancillary testing, and you highly suspect either LATE or PART. How do you counsel those patients and their families? How do you manage those patients moving forward who you really suspect don't have, you know, some sort of co-pathology? Dr Ramanan: So, it's- I think it's helpful to remember when patients are coming to see us, either they or the people around them have noticed an issue. And very likely it's an issue that's been brewing for a little while. I think it can be very valuable, very helpful for patients to have answers. What's the cause for the issue? Once you have answers, even if sometimes those answers are not the most welcome things or the things that you'd be looking forward to, answers give you an opportunity to grab hold of what's going on, to define a game plan. So, understanding there is a degenerative disease there, it sheds light on why that individual had had memory symptoms over the years. And it gives them a general expectation that over time on an individualized basis, but generally expecting gradually over many months to many years, there may be some worsening in some of those symptoms helps them to plan and helps them to make the adaptations that are a-ok and great to make to just help you to do the things you want to do. As much as I can, I try to put the focus here closer to how we would view things like high blood pressure or high cholesterol. Those are also chronic issues that tend to be more common as we get older, tend to get more troublesome as we get older. The goal is, know what you're dealing with and take the combination of lifestyle modifications, adaptations in your day-to-day and maybe medications to keep them as mild and as slow-changing as possible. With something like LATE, we don't have specific medication therapies to help support cognitive functioning at this time. There's a lot of hope that with additional research we will have those therapies. But even so, I think it's an important moment to emphasize some of those good healthy lifestyle habits. Staying mentally, socially and physically active, getting a good night's sleep, eating a healthy, balanced diet, keeping good control of vascular risk factors, all of that is critical to keeping the brain healthy, keeping the degenerative disease as mild and slow-brewing as possible. And understanding what some of the symptoms to expect could be. So, with LATE the syndrome tends to be very memory-predominant. There may be some trouble with maybe naming of objects or perhaps recall of emotionally salient historical knowledge, world events, but you're not expecting, at least over the short to medium term, huge intervening on other cognitive functioning. And so that can be helpful for patients to understand. So, the hope is once you know what what you're dealing with, you understand that the disease can look different from person to person. Having a general map of what to expect and what you can do to keep it in check, I think, is the goal. Dr Nevel: I agree with you 100% that it really can be helpful even if we can't, quote unquote, fix it, that for people, family, the patient have a name for what they have and kind of have some sort of idea of what to expect in the future. And they may come in thinking that they have Alzheimer's or something like that. And then, so, to get that information that this is going to be a little different, we expect this to go a little bit differently then it would if you had a diagnosis of Alzheimer's, I can see how that would be really helpful for people.  Dr Ramanan: I completely agree. And here's another challenge for us in the field when most patients have heard about Alzheimer's disease and many have perhaps even heard of dementia with Lewy bodies or frontotemporal dementia, but may not have heard of things like LATE. And they're not always easy to go online or find books that talk about these things. Having a name for it and being able to pair that with patient-friendly information is really critical. I see our appointments where we're sharing those diagnosis and making initial game plans as an initial foray into that process.  Dr Nevel: Yeah, absolutely. What is the greatest inequity or disparity that you see in taking care of patients with progressive amnestic cognitive impairment? Dr Ramanan: Yeah, great question. I think two big things come to mind. The first, you hinted at very well earlier that there are disparities in access to care, access to diagnostic testing, access to specialists and expertise throughout our communities. If we want diagnostics and therapeutics to be broadly applicable, they do need to be broadly available. And that's a big challenge for us as a field to work to address those disparities. There's not going to be one single cause or contributor to those iniquities, but as a field, I'm heartened to see thought and investment into trying to better address those. Another big weakness, and this is not just limited to cognitive neurology, it's a challenge throughout neurology, is that too many of our research studies are lacking in diversity. And that impacts our biological and pathophysiological understanding of these disorders. It also impacts our counseling and management. Again, if we want a new drug treatment to be broadly applicable throughout all of the patients that we take care of, we need to have data which guides how we apply those treatments. And so again, I'm heartened. This is a big challenge. It's a long standing challenge. It will take deep and long standing committed efforts to reverse. But I'm heartened that there are efforts in the field to broaden clinical trial enrollment, broaden observational research enrollment, and again, broaden access to tools and expertise. As a neurologist, I got into this field because I want to help people, use my expertise and my training to help people. These are steps that we can take to make sure that that help is broadly applicable throughout everybody in our communities. Dr Nevel: Yeah, absolutely. So, kind of segueing from you mentioning research and how we can better include patients in research. What do you think the next breakthrough is going to be? What do you think the next big thing is going to be in these disorders? What do we still need to learn? Dr Ramanan: There's a lot. I think for LATE and PART, the development of specific biomarkers would be top of the agenda. Now, biomarkers are by their nature imperfect. Even with Alzheimer's disease, where in comparison, we know quite a lot. We have a variety of imaging and fluid biomarkers that we can use to support or rule out a diagnosis. There are nuances in how you interpret those biomarkers. Patients can have signs of amyloid plaques in their brain and have completely normal cognition. They may be at risk for developing cognitive trouble due to Alzheimer's disease in the future, but it's one piece of the puzzle. Patients can have the changes of Alzheimer's disease amyloid plaques and tau tangles in the brain. We can confirm that through biomarkers. But at the end of the day, their cognitive syndrome might be driven by something else. Maybe it's Lewy body disease, maybe it's LATE, maybe it's a combination of factors. So, integrating and interpreting those biomarkers is challenging. But I do think, again, from the standpoint of giving patients answers with a diagnosis, having those biomarkers is really critical to just kind of closing the loop. It will also be critical to have those biomarkers as we're assessing for treatment response. So, for example, patients who may have coexistent Alzheimer's disease and LATE, I don't think we know the answer fully as to how likely they are to benefit from, say, newer antiamyloid monoclonal antibodies for Alzheimer's disease in the setting of that second pathology. So, wouldn't it be great if, similar to an oncologic setting where you engage in a treatment and then you're tracking two or three or four plasma measures and you're tracking tumor size with imaging, if we had this multimodal ability to track neurodegenerative pathology through biomarkers? I think that'll be a critical next step. And so, filling out that for non-Alzheimer's diseases, including LATE and PART, I think is item number one on the agenda. Dr Nevel: Wonderful, thank you so much. I really appreciate you taking the time to chat with me today about your article. I really enjoyed our conversation, certainly learned a lot. Dr Ramanan: Thank you so much, Kait. Love talking with you. And again, it was an honor to write this article. I hope it's helpful to many out in the field who take care of patients with cognitive issues.  Dr Nevel: Yeah, I think it will be. So again, today I'm interviewing Dr Vijay Ramanan about his article that he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the most recent issue of Continuum on dementia. Be sure to check out Continuum audio episodes from this and other issues. And thank you, Vijay, and thank you to our listeners for joining us 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 this 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.

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?

Send us a textIn this episode, Jason talks with Ellen Patnaude, author, coach, and dementia educator, about her journey as a caregiver for her mother with Lewy body dementia. Ellen shares her experiences navigating family dynamics, systemic gaps in elder care, and the importance of planning for the future. With honesty and humor, this conversation offers practical insights and support for anyone dealing with caregiving challenges or aging parents.“Plan. Talk to your loved ones, an attorney, and put something in writing. Don't leave the burden of guessing to your family.”Ellen Patnaude has always been fascinated by how a person's nature and lived experiences cause them to interact with others. She is a Detroit native and graduated from Alma College with a BA in Biology & French. She thought she wanted to be Jacques Cousteau, but her first few science-based jobs pointed clearly towards working with people. She worked for several years as a community organizer in Indiana and Ohio. Returning to Michigan in 2005, her reputation followed her for challenging people to see and be a better version of themselves, and the phone started ringing. Since then, Ellen has built an internationally recognized company supporting teams and their leaders in improving everyday interactions.Ellen is the author of two books, “I Thought You Knew… Confessions of a Chronic Assumer (and How to Stop Guessing Your Way Through Important Interactions)” and “You're Not Doing It Right: Loving My Mother Through An Unpredictable Caregiving Journey.”https://patnaudecoaching.com/Free ResourceGet better-quality, faster results from your teams with these coaching methodologies here. Connect with Jason If you enjoyed listening, then please take a second to rate the show on iTunes. Every podcaster will tell you that iTunes reviews drive listeners to our shows, so please let me know what you think and make sure you subscribe using your favorite podcast player. It means a lot to me and the guests.https://www.jasonfrazell.comhttps://www.jasonfrazell.com/podcastshttps://www.instagram.com/jasontfrazellhttps://www.https://www.linkedin.com/in/jasonfrazell/

Lewy body dementia is a common cause of cognitive impairment in older adults but is often subject to significant delays in diagnosis and treatment, increasing the burden on patients and family caregivers. Understanding key features of the disease and use of biomarkers will improve recognition. In this episode, Allison Weathers, MD, FAAN, speaks with James E. Galvin, MD, MPH, author of the article “Lewy Body Dementia,” in the Continuum December 2024 Dementia issue. Dr. Weathers is a Continuum® Audio interviewer associate chief medical information officer at the Cleveland Clinic in Cleveland, Ohio. Dr. Galvin is a professor of neurology at the University of Miami Miller School of Medicine in Miami, Florida. Additional Resources Read the article: Lewy Body Dementia 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 Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Weathers: This is Dr Allison Weathers. Today I'm interviewing Dr James Galvin, author of Lewy body dementias from the December 2024 Continuum issue on dementia. Welcome to the podcast, Dr Galvin. Please introduce yourself to our audience.  Dr Galvin: Thank you, Allison. My name is Jim Galvin. I'm a neurologist, a professor of neurology at the University of Miami Miller School of Medicine. Dr Weathers: We're so happy to have you with me today. Thanks, Jim, for your time. And as you highlight right from the start in your really outstanding and comprehensive overview of this really complex topic, even though Lewy body dementia is the second most common cause of neurodegenerative dementia, it often goes unrecognized in clinical practice, resulting in really potentially lengthy diagnostic delays. So, this is a really important article for a neurologist and an important topic for our listeners. So, I'm thrilled we're having this conversation today. While I traditionally start by asking the authors what they feel is the most important clinical message of their article, I would love to actually start a step earlier in this conversation with you. Can you start us off by explaining what's actually meant when we say Lewy body dementia? Dr Galvin: Great. So, you know, I think this is a, this is an interesting concept. So, we're really talking about two diseases that have a shared common pathology. So, Parkinson's sees dementia and dementia with Lewy bodies. So, their shared pathology is a Lewy body and that's why they're often grouped together as the Lewy body dementias. And then there's arguments back and forth as to whether these are distinct diseases or sort of two ends of the same candle burning in different directions. So, Parkinson's dementia is a lot like what it sounds like. So, if someone has Parkinson's disease, then at some point later they develop a dementia. And so back in the 1800's when Parkinson's disease was like first described as an entity, we basically felt that cognition wasn't affected. But we now know that's not true. And so most patients with Parkinson's do have some cognitive symptoms and a large proportion of them will eventually develop dementia. Perhaps up to 80% of Parkinson's patients will develop a dementia. The flip side is the dementia with Lewy body picture. And these are people who present primarily with a cognitive behavioral syndrome that may or may not have parkinsonism. So, they will sometimes have bradykinesia. They rarely have a rest tremor. And so, these are the people that are very much in the delayed diagnosis group. The Parkinson's dementia is more whether the clinician is checking their cognition as part of their annual visit. The flip side is that the people with DLB are often misdiagnosed early on, but together, this is Lewy body dementia, which is the most common disease that many people have never heard of. Dr Weathers: That's a great tagline, I think, for the whole article and for this concept. So now that that we're all on the same page about what's meant when we use that the term, what would you want our listeners to walk away with as their one key takeaway from our conversation today? Dr Galvin: Well, I think the article makes several key points, but I think if I put those all together into a single key point, it would really be that the Lewy body dementias are underrecognized, they're underdiagnosed, yet it is very possible to make the diagnosis using the standardized clinical criteria. They're very, very, very specific. They lack a little bit in sensitivity. So, because other diseases sometimes can look like this, but they're really quite specific. So, if you're confident clinically that the person has Lewy body dementia, you're probably going to be right. And in today's world, we have tests available to help confirm our diagnosis. The world is changing. We can make these diagnosed with much more confidence and we have confirmatory diagnosis laboratory tests that can help us. Dr Weathers: I want to talk more about the diagnosis in one minute, but first, how common actually are dementia with Lewy bodies and Parkinson's disease dementia? Dr Galvin: That's a great question. I think one of the challenges, of course, we really don't know how many people have any disease because it's going to largely rely on how well people code the diseases in the medical record. So, if you look at the most common cause of dementia in the United States, it's really dementia not otherwise specified, right? But we believe it to be the second most common cause of dementia. The Lewy Body Dementia Association, about a decade ago, started to try to develop some estimates. So, we have an estimate about how many people roughly have Parkinson's disease and that about 80% of those individuals would go on to develop dementia. And we know from the dementia population that about 40% of those individuals coming to autopsy have Lewy bodies. So, when you start to put that all together, you can get a reasonable estimate of how many people likely have the disease. And then that can be expanded on an annual basis, just like the Alzheimer's Association uses, by extrapolating those estimates onto the census data. So, we estimate right now there are about 1.4 to 1.6 million Americans who are living with Lewy body dementia. That's less than the 6.8 million people who have Alzheimer's disease, but more than a lot of other common diseases. So, if you think about, again, I said before, it's the most common disease no one's ever heard of. You know, there are about a million people who have multiple sclerosis. There are about eight hundred thousand people who have a stroke. There are about seven hundred thousand people who have a brain tumor. There are two hundred and fifty thousand people who have muscular dystrophy. There are twelve thousand people who have ALS. But I think if you stopped clinicians or people in the street and say have you ever heard of ALS or muscular dystrophy, they would say yes. If you ask them if they've heard of Lewy body dementia, they would say no.  Dr Weathers: That's an excellent point. And I know over the years I think there's been some increased awareness. I think sadly with some of the celebrities that have been impacted, I think that did a lot to raise awareness. But I think you're right that it's still so less commonly recognized by the lay public, by non-neurologists, than so many other diseases that you mentioned. And I think that leads back well into my next question into something that we've already mentioned just a few times already in our short conversation, this unfortunate and very common delay in the diagnosis. Why? And you mentioned earlier that there are these, you know, clinical criteria, these now ancillary tests. So, what makes the diagnosis so challenging? What aspects in particular do you think that neurologists find to be the most challenging in diagnosing patients? What trips us up?  Dr Galvin: So, there's an old analogy, right, that, you know, if you'll be three blind men to an elephant and each of them are touching a different part of the elephant, they'll each think it's something different. So because Lewy body dementia has so many different diverse kind of symptoms, it would really depend on who's seeing the patient first. So, if a person presents predominantly with a memory cognitive disorder and they go see someone who specializes in memory disorders, they're highly likely to be called Alzheimer's disease. If they present predominantly with the movement problem, they're going to see a movement disorder person and be called Parkinson's disease. If they present with a behavioral disorder, they're going to go see a psychiatrist. Then they'll get diagnoses like, you know, geriatric schizophrenia or bipolar disease or major depressive disorder. If they present with the constitutional symptoms, which are very common and drive patients absolutely batty. So chronic constipation, REM sleep disorder, runny nose, you know, heat intolerance, urinary frequency, obstipation, and you know, they're going to be called all sorts of things. So, if you start thinking about this, who do you show up with first is going to guide how fast you can get a diagnosis. So, we interviewed at point over a thousand caregivers and what we found was there was about an eighteen month delay after seeing five to six doctors for the majority of patients, of which Lewy body dementia was misdiagnosed about 75% of the time for the initial diagnosis.  Dr Weathers: Wow, what a sobering statistic. And you spoke about the criteria and some of the ancillary tests. What can really help, do you think, kind of mitigate or prevent this misdiagnosis? What is your approach in your own patients?  Dr Galvin: Well, I think like every good clinician, not starting off with a preconceived notion of what the person has and trying to collect all the valuable information. So, one of the things I highlighted in the article was, while there are diagnostic criteria and people can follow diagnostic criteria, the truth is at your fingertips. You don't always sit and think about whether someone meets diagnostic criteria. So, in the first table in the article, we tried to really then put all the different common symptoms into buckets, right? Because people present like that. They say, well, I have this and I have this and I have this and I have this. Well, then you can start to think about, well, they have a cognitive symptom that's predominantly executive attention or visual perceptual in nature. And gee, they have constipation and heat intolerance and they say they can't smell quite as well as they once did, right, and they're having some disturbance in their sleep with excessive daytime sleepiness. Now you can start to say, well, even though that didn't fit the core and suggestive criteria, the fact is that spectrum of symptoms makes it much easier to begin to make a diagnosis. And so, it's investigative work. A lot of neurology is still investigative work. The old days, they used to say, we knew everything but could do nothing, but now we know everything and can do something about it. And so, I think it's really important that we try to apply this information in clinically useful ways. That was part of the gist of putting this Continuum article together was to try to present it not just as listing the diagnostic criteria, because you can get that anywhere, but how do you actually apply it in clinical practice? Dr Weathers: That's a great point. And that table that you referenced was really fantastic. And I know I say this a lot, but they're true. So, you know, many of the tables, the reference to Continuum, one I will certainly kind of come back to again, again, as an excellent point of care tool. So, I know in, in preparing for today and reading more about, about you and your areas of research that one of your particular areas of focus and expertise is in healthcare disparities, especially in the early detection of neurodegenerative dementias. What is the greatest inequity or disparity that you see in the diagnosis and treatment of patients with Lewy body dementia?  Dr Galvin: So, there's a couple things that are that are really interesting. So first, unlike Alzheimer's disease, which tends to be a little bit more female predominant, the Lewy body dementias are male predominant. It's about 1.6 men for everyone woman. So, it's going to be a different presentation. It's going to be largely men and their caregivers are largely going to be their spouses. So, you're going to see sort of a different person looking, you know, staring on the other side of the table to you. It's going to be largely a male. And the other thing that's really interesting is that almost all of the series, case series, case reports, clinical papers are in predominantly white populations. So, this lends to some interesting things. So, you know, is the disease less common in African Americans and other minority populations or are we just really bad at ascertaining the disease? You know, many of the case reports in Alzheimer's disease include African Americans. In fact, we know that African Americans may be at a twofold increased risk of developing Alzheimer's disease compared to nonHispanic whites, probably due to vascular risk factors. But in case series of Lewy body dementia, almost all the patients are non-Hispanic white. There also seems to be a higher risk in Asian populations, and in fact, some of the very earliest case reports were from Japan. Is this a case ascertainment problem or is this really a disparity in how the disease presents? And I think those are really important questions that still need to be asked. I know as researchers, we struggle to try to develop cohorts that could help us understand that. I would say in my twenty five years of seeing these patients, I would say the large percentage of them, and I've seen a lot of them, have been no-Hispanic white.  Dr Weathers: So, so definitely more research needed in this very important area. So, moving on to somewhat of a personal question, I always, this is such an honor. I always talk about that I get to have this time to sit down with the authors of these outstanding articles and learn not only more about their subjects, but about them as people. I had shared during my last interview that my paternal grandmother had Alzheimer's disease, and unfortunately also my maternal grandmother actually did as well. In preparing for this, I had listened to one of your previous interviews and learned that you also have a personal connection that led you to this subspecialty with several family members impacted. How has this connection inspired your research and your interactions with your patients?  Dr Galvin: Yeah, I mean, so my personal connection was that my maternal grandfather had Lewy body dementia. So, I grew up in a two family home in New Jersey. My grandparents lived on the second floor. We lived on the first floor. I wass very close to my grandparents. I'm still close to my grandmother, who's a hundred and three years old. But when I was a high junior in high school, my grandfather was driving me home from a swimming practice. I was thinner, fitter and more athletic at that point in my life, and he made the world 's slowest left hand turn and we were broadsided. So luckily no one was hurt. But I remember because I was sixteen at the time and just learning how to drive us, Grandpa, what happened? And he's like, oh, the car didn't react. Or, you know, he was blaming the car. And I didn't think much of it because, you know, I was sixteen years old. Sometime after that he was at work, and he was a greaser. So, he would climb through the machines at Colgate Palmolive and keep them all moving. And so, he was at work and he fell off a ladder and then broke his ribs. And in the emergency room, when my grandmother went to pick him up, the ER doctor turned to her and said, how long has your husband had Parkinson's disease? And she's like, what are you talking about? And then that was the first time that all of us had noticed his rest tremor. And the reason he turned the wheel so slow is because he was Bradykinetic. And so then over the next few years, he progressed in his motor symptoms. And then as I got into college, he developed the cognitive symptoms. And so, by the time I had finished medical school that was doing my residency, he was no longer oriented to time. So that even though I had finished medical school, I was in my neurology residency, I was married and with children, I was still in college at that time for him. So, he would always ask me, you know, have I heard anything from getting to medical school and the like. So, I got to watch this person who I grew up with go through all of the different stages of disease. And then eventually he developed lots of hallucinations. And although he was relatively immobile, he experienced a hallucination and jumped out of his chair, fell down, and broke his hip. And so, he underwent a hip replacement, being rather severely demented, and then passed away in the rehab hospital. As I was living this with my grandparents, the one thing that my grandfather, while he could still communicate, and that my grandmother continued to say to me, you know, up until fairly recently was, you know, what are you going to do about this? You know, we're counting on you to make a difference. And so, a lot of my research is really focused on how I can make a difference for people. One, to make sure they get diagnosed properly. Two that we would have something to offer the patient and the family. And three, we can provide hope that we are actually going to come away with effective treatments to make a difference in their lives. Dr Weathers: Well, that is really inspiring. And I think you have really done that in your work. I always like to end these conversations on a hopeful note. So, what are the developments that are on the horizon in terms of diagnosis and treatment of Lewy body dementia that you are most excited about?  Dr Galvin: Well, I think there are three things that are of great interest right now. I mean, there's lots of things, but I think three things of great interest are, one, on the diagnostic side is that we now have assays that allow us to assess synuclein in body fluids and body tissues. So, we can measure synuclein seeding assays in the spinal fluid and we can visualize Lewy bodies through skin biopsies. And that's a tremendous advance because we were really, really limited otherwise to using indirect evidence, and the only indirect evidence we had was abnormalities on DAT scanning. So, we're looking at dopamine deficiencies. But as I mentioned earlier, that's very abnormal in Parkinson's disease. But in dementia with Lewy bodies, it's a little more subtle. So, the extent of dopamine degeneration in- particularly in early DLB is limited. So, you have to look very carefully. If we're not doing quantitative DAT scan imaging, then you may miss those subtle changes. So, I think that being able to directly visualize either synuclein seeding or synuclein aggregation has really changed the game. Plasma assays, blood-based biomarkers are probably a little farther away because they're- the red blood cells have a lot of synuclein and so it interferes with the ability to get a good sensitive assay. But I do think in the next couple of years we will see PET ligands that also bind  synnuclein. So, I think diagnostically we're going to be able to provide better, earlier, and more precise diagnoses. From a treatment perspective, traditionally we've just borrowed medicines from other fields to treat symptoms, but there are a number of disease-modifying trials that are ongoing. I was fortunate to be the academic PI on two very large NIH grants where we test tested disease modifying medicines. Both of those studies are fully recruited and we should get a readout toward the end of 2024 or the beginning of 2025. So very, very excited about that. I also am fortunate to be MPI an NIH grant where we're just going to be testing the first inhuman synuclein vaccine. So very, very excited about the potential to offer disease-modifying medicines and to fulfill the promise that I made to my grandma and grandpa twenty years ago. And I think the third thing is that right now there's a little bit of like an emerging controversy about developing some integrated staging paradigms between the movement disorder world and the cognitive world. And so, while those paradigms are currently published, you know, not everybody agrees with them. But I think whether I like that staging paradigm now or not, the fact that we're coming together and trying to develop some unified staging paradigms, I think, is going to make a big difference in increasing the ability for clinicians to make early diagnoses that are more precise so that we can either get people into clinical trials or into clinical treatment protocols at the earliest possible time. And that's going to make all the difference in the world for the patients and their families.  Dr Weathers: I think that was a fantastic answer. Really, all really exciting things that I think are all, I normally, I say on the horizon. I'm thinking, you know, pretty far ahead. And I think the really wonderful thing is that all of these are either here now or very, very close to being here. So, definitely a very positive way to end this discussion. Well, Jim, thank you so much for taking the time to speak with me today. Dr Galvin: Thank you. This was wonderful. I hope the listeners found this enjoyable and interesting and read the Continuum issue. I think it's going to be the latest and greatest on what we know about the dementias.  Dr Weathers: Again, thank you again, Dr Galvin, for joining me on Continuum Audio. Again, today I've been reviewing Dr James Galvin, his article on the Lewy body dementias, dementia with Lewy bodies, and Parkinson's disease dementia appears in the December 2024 Continuum issue on dementia. Be sure to check out Continuum Audio episodes from this and other issues. 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 this 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.

Dr. Vikram Karnik and Dr. Kate Wyman-Chick discuss distinguishing prodromal dementia with Lewy bodies from prodromal Alzheimer disease and the implications for clinical practice. Show reference: https://www.neurology.org/doi/10.1212/CPJ.0000000000200380 

Dr. Vikram Karnik talks with Dr. Kate Wyman-Chick about distinguishing prodromal dementia with Lewy bodies from prodromal Alzheimer disease, the importance of early diagnosis, and the implications for clinical practice. Read the related article in Neurology: Clinical Practice. Disclosures can be found at Neurology.org.

Ladies and gentlemen, with honesty, tenderness and, yes, sometimes humor, the film Facing the Wind invites viewers into the lives of people with Lewy body dementia and their caregivers…real people in real time.  FACING THE WIND, a sixty-minute documentary film, reveals how a mutual support community can be an antidote to despair, letting people know they are not alone.  You will follow their journey, laughing and crying with them, while taking an unflinching look at dementia care with its overwhelming and isolating aspects. The struggle is real, but so is the love. Lewy body dementia is not a rare disease. It affects more than 1.4 million people in America. It is the second most common form of dementia, but it still being misdiagnosed. Alzheimer's disease is the gradual decline of memory as Lewy body dementia is the roller coaster ride with ups and downs. One moment the patient can be fully present and lucid and the next be completely lost or deal with hallucinations from mild to severe. There is no cure, but this very powerful film documentary is not for those suffering with Lewy body dementia, but for the people who care for them. Many spouses and family members are thrust into being a caregiver and navigating the vast ocean of the unknown. FACING THE WIND is a starting place for caregivers and to know that it's ok to not be ok. Head over to LewyBodyResourceCenter.org for more information. If your loved one was diagnosed with Lewy body dementia, you are not alone and there are resources right now that can help you. Facing the Wind is the latest collaboration of award-winning director Deedra Fishel and producer Tony Heriza. Their groundbreaking film Care, funded by the Ford and MacArthur Foundations, shed light on America's broken eldercare system. Deerdra and Tony both have family members with dementia and share deep empathy for those with the disease and their caregivers. Deerdra Fishel has been writing and directing documentaries and dramas for 25 years now. Her life's goal is to create complex, realistic portraits that challenge mainstream stereotypes and work to improve lives. She started her career at WNYC-TV where she produced a half-hour program on women community organizers working to save the South Bronx. She went on to write/direct RISK, a dramatic feature, which premiered in competition at Sundance and was broadcast in 35 countries. Tony Heriza's award-winning films and videos have addressed a broad range of social issues, including gentrification, immigration, racism, gender equity, sexuality, criminal justice, and peace-building. His New Day film, Care, produced with Deerdra Fishel, is an intimate exploration of home-based elder care from the POV of both workers and their clients. #lewybodydementia #lewybody #dementia #alzheimersdisease #alzheimers #parkinsonsdisease #film #filmdocumentary #documentary #mentalhealth #memory #brainhealth #medicine #wellness

Ladies and gentlemen, with honesty, tenderness and, yes, sometimes humor, the film Facing the Wind invites viewers into the lives of people with Lewy body dementia and their caregivers…real people in real time.  FACING THE WIND, a sixty-minute documentary film, reveals how a mutual support community can be an antidote to despair, letting people know they are not alone.  You will follow their journey, laughing and crying with them, while taking an unflinching look at dementia care with its overwhelming and isolating aspects. The struggle is real, but so is the love. Ladies and gentlemen, Lewy body dementia is not a rare disease. It affects more than 1.4 million people in America. It is the second most common form of dementia, but it still being misdiagnosed. Alzheimer's disease is the gradual decline of memory as Lewy body dementia is the roller coaster ride with ups and downs. One moment the patient can be fully present and lucid and the next be completely lost or deal with hallucinations from mild to severe. There is no cure, but this very powerful film documentary is not for those suffering with Lewy body dementia, but for the people who care for them. Many spouses and family members are thrust into being a caregiver and navigating the vast ocean of the unknown. FACING THE WIND is a starting place for caregivers and to know that it's ok to not be ok. Head over to LewyBodyResourceCenter.org for more information. If your loved one was diagnosed with Lewy body dementia, you are not alone and there are resources right now that can help you. Mary Lou Falcone, author of the book, “I Didn't See It Coming: Scenes of Love, Loss and Lewy Body Dementia”. Mary Lou Falcone, author of I DIDN'T SEE IT COMING: Scenes of Love, Loss, and Lewy Body Dementia, is internationally known as a classical music publicist/strategist who for 50 years has helped guide the careers of celebrated artists – Van Cliburn, Gustavo Dudamel, Renée Fleming, Sir Georg Solti, James Taylor – and advised many institutions including Carnegie Hall, Chicago Symphony, Los Angeles Philharmonic, Philadelphia Orchestra, New York Philharmonic, Vienna Philharmonic.  Combining communication skills with her background as a performer and educator, she now adds another layer: advocate for Lewy body dementia (LBD) awareness.  Her late husband, the illustrator/painter Nicky Zann who died from LBD in 2020, was the catalyst for her book.  She is also an Executive Producer of a new documentary film about LBD entitled Facing the Wind, a love story about people with Lewy body dementia, the spouses who care for them, and the remarkable community where they find sustenance and support. #lewybodydementia #lewybody #dementia #alzheimersdisease #alzheimers #parkinsonsdisease #brainhealth #medicine #filmdocumentary #documentary #health #wellness #caregiving #caregivers 

My guest today is the founder and executive director of the Lewy body Resource Center. Norma's knowledge and experience with Lewy body dementia began with the personal care of her mother, Lillian, who had LBD for many years. Norma has been facilitating the only New York Metro area LBD caregivers support groups since 2008.  She also leads a national group for people living with LBD which has been lauded.  She served on the board of directors of the Lewy Body Dementia Association for three years before launching the LBD Resource Center in 2016 to provide much needed support and resources on more personal and connective levels. Norma worked as executive assistant to the CFO at The New York Times Company for over 20 years. While there, she served as chairperson of the work/life committee of The New York Times' women's affinity group and initiated and ran their eldercare support group. Her expertise working with the top executives at The Times, as well as her managerial experience as executive director and a co-founder of What BETTER Looks Like, a nonprofit organization which partners with communities to help individuals imagine, articulate, and create visions for a better world, has prepared her to lead the LBD Resource Center which is very dear to her heart. Ladies and gentlemen, Lewy body dementia (LBD) is the second most common form of progressive dementia, affecting more than 1.4 million Americans. Because LBD comes with a host of physical, cognitive and behavioral symptoms, it often mimics Alzheimer's disease, Parkinson's disease or a psychiatric disorder. As a result, it is widely misdiagnosed. Even as diagnoses increase, resources for people with LBD and their families still remain extremely limited. Citing this lack of resources and assistance, the Lewy Body Dementia Resource Center was founded to provide much needed services and support for people with LBD and their loved ones. Go to LewybodyResourceCenter.org or LDBNY.org for more information. #lewybodydementia #lewybody #dementia #brainhealth #mentalhealth #resourcecenter #facingthewind #LBD #misdiagnosis #Alzheimers #AlzheimersDisease #ParkinsonsDisease #medicine #wellness #psychiatricdisorders