Podcasts about Lewy

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

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

More than just Rugby!

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

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

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

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

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

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

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

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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

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

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.

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/

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.