Podcasts about Amyloid

Amyloid-targeting monoclonal antibody treatments have ushered in a new era of Alzheimer's disease therapies after decades of research and clinical trials. A recent review published by Cochrane, a global, independent, non-profit network of researchers, professionals, patients and carers regarded as a gold standard for producing and promoting trusted, high-quality health information, has a different perspective on these therapies. The review found these treatments produce “little to no difference” in cognition and offer few benefits while increasing risks for adverse effects. Drs. Cynthia Carlsson, a clinical trialist, David Wolk, a clinician, and Henrik Zetterberg, a biomarker and disease biology expert, join the podcast to break down the review and their concerns, as well as highlight how this review could impact clinical care, research and public policy. Guests: Cynthia Carlsson, MD, MS, director, Wisconsin Alzheimer's Institute, Clinical Core leader, Wisconsin Alzheimer's Disease Research Center (ADRC), Louis A. Holland, Sr., Professor in Alzheimer's Disease, geriatrician, University of Wisconsin (UW) School of Medicine and Public Health; David Wolk, MD, director, Penn ADRC, co-director, Penn Memory Center, co-director, Penn Institute on Aging, professor of neurology, University of Pennsylvania Perelman School of Medicine; and Henrik Zetterberg, MD, PhD, professor of neurochemistry, University of Gothenburg, visiting professor, UW–Madison and University College London, Biomarker Core co-leader, Wisconsin ADRC Show Notes Read Cochrane's review, “Amyloid‐beta‐targeting monoclonal antibodies for people with mild cognitive impairment or mild dementia due to Alzheimer's disease,” on the Cochrane Library website. Learn more about Dr. Carlsson and Dr. Zetterberg at their profiles on the Wisconsin ADRC website and about Dr. Wolk at his profile on the Penn Memory Center website. Watch and listen to Dr. Carlsson's past episode, “A Closer Look at the Lecanemab Clinical Trials,” on our YouTube channel or on our website. Listen to Dr. Wolk's past episode, “LATE, Explained,” on our website. Listen to Dr. Zetterberg's past episode, “The Future of Fluid Biomarkers for Alzheimer's Disease and Related Dementias,” on our 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. Learn about Dr. Chin's book, When Memory Fades: What to Expect at Every Stage, from Early Signs to Full Support for Alzheimer's and Dementia, out June 2, 2026.

What if amyloid is only the match, tau is the brush fire, and neuroinflammation is the wildfire that causes the most damage in Alzheimer's disease?In this episode of Happy & Healthy with Amy, Amy explains why researchers are paying closer attention to neuroinflammation, what may be keeping the brain's immune system stuck in the “on” position, and why midlife is such an important window for protecting your brain.You'll learn how sleep, blood sugar, chronic stress, infections, oral health, and social connection may all influence the conditions that make the brain more—or less—flammable.What to Listen For[00:00] Why amyloid may be the match—but neuroinflammation is the wildfire. [02:30] What the Cochrane review found about anti-amyloid drugs. [04:30] Why timing matters in Alzheimer's disease. [07:00] Is neuroinflammation a side effect—or a driver? [09:00] Why inflammation itself is not the villain. [11:00] Meet microglia: the brain's immune cells. [14:00] Why gum disease matters for Alzheimer's risk.[18:00] The shingles vaccine and dementia risk. [22:00] Blood sugar, insulin resistance, stress, and sleep. [29:00] How to make your brain less “flammable.” Neuroinflammation may be one of the most important pieces of the Alzheimer's prevention puzzle because it connects so many things we often treat separately: sleep, stress, blood sugar, oral health, infections, diet, and connection.Listen to the full episode to understand what may be making your brain more “flammable,” then download the free RESTORED Protocol so you can choose one simple, evidence-based next step for protecting your brain.Mentioned in The EpisodeDownload the RESTORED ProtocolDownload The First Steps Guide for supporting a parent after Alzheimer's diagnosisRelated EpisodesAlzheimer's Prevention: What the Cochrane Review MeansAlzheimer's Drugs: Why Amyloid Removal May Not Be EnoughGum Disease, Menopause & Your Alzheimer's RiskSourcesRESOURCES:Book a FREE Discovery Call with AmyDownload After Mom's Alzheimer's Diagnosis: The First 8 Things to Know and learn how to support her with more calm, clarity, and confidence.Download the RESTORED Protocol: Eight Essential Protective Factors to Build an Alzheimer's-Resistant BrainSchedule your Breakthrough Roadmap session with AmyFollow Amy on Instagram @amylangcoaching  and on Facebook @amylangcoachingSubscribe to Amy's YouTube channel @happyandhealthywithamy

Isaac Stoner, CEO of MindImmune Therapeutics, a drug discovery company pioneering a new class of medicines for Alzheimer's disease and other neurodegenerative conditions.Isaac has built his career moving between the founder seat and the investor seat. He was the founding CEO of Octagon Therapeutics, the first team member at liquid biopsy company Firefly BioWorks and has evaluated life science companies for investment at Slater Technology Fund, PureTech Health, KdT and Action Potential Venture Capital. At MindImmune Therapeutics, he is chasing one of the boldest ideas in neuroscience: that Alzheimer's may in fact be an autoimmune disease that presents in the brain.In this episode Isaac explains why the amyloid hypothesis that has dominated Alzheimer's research for 30 years has run its course, and why MindImmune is taking an immunology-first approach built on brain tissue donated by Alzheimer's patients. He breaks down the three biggest risk factors for the disease, how he pitched a 30 million dollar Series A on a condition where 99.9% of drugs have failed and what it would mean to develop a therapy bigger than the GLP-1 weight loss drugs.We also get into the founder-to-investor-to-founder journey, why a brilliant scientific founder is often the wrong person to sit in the CEO seat and the hard truths every aspiring biotech founder needs to hear before striking out on their own.Timestamps[00:02:50] Why a Career Investor Keeps Getting Pulled Back Into Building[00:05:25] Shutting Down Octagon Therapeutics and the Chip It Left Behind[00:07:10] Why MindImmune Treats Alzheimer's as an Autoimmune Disease[00:08:20] Why 30 Years of the Amyloid Hypothesis Has Run Its Course[00:10:05] The Three Biggest Risk Factors for Alzheimer's and What You Can Do[00:12:15] How He Raised a $30 Million Series A on the Hardest Disease in Medicine[00:15:30] Why 99.9% of Alzheimer's Drugs Fail and What Makes This Different[00:18:35] Why a Brilliant Scientific Founder Is Often the Wrong CEO[00:22:20] Where MindImmune Goes Next: AMD, ALS and Beyond[00:28:00] Final Advice: Get Into Biotech for the Right ReasonsConnect with Isaac - ⁠https://www.linkedin.com/in/isaacstoner/⁠Learn more about MindImmune Therapeutics - ⁠https://www.mindimmune.com/⁠Get in touch with Karandeep Badwal - ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.linkedin.com/in/karandeepbadwal/ ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Follow Karandeep on YouTube - ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.youtube.com/@KarandeepBadwal⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Medical device training courses delivered by Karandeep through Bywater - ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠https://www.bywater.co.uk/

If your parent was recently diagnosed with Alzheimer's, you may have heard about the latest Alzheimer's treatments - Kisunla and Lequembi - being described as breakthrough "disease-modifying" drugs.And yes, the science is promising in some ways.But here's the part most families are not told clearly: a drug may successfully remove amyloid from the brain and still not create a meaningful improvement in memory, thinking, reasoning, or day-to-day function.In this episode, Amy explains why.This is not medical advice. It is education designed to help you ask better questions, advocate more clearly, and make decisions with your eyes wide open.You'll learn what happens in the brain long before symptoms appear, why amyloid is only one part of the Alzheimer's disease process, and why tau, neuroinflammation, and neurodegeneration matter so much when you're trying to make informed decisions for someone you love.What to Listen For[00:00] Why amyloid removal may not translate into meaningful improvement. [02:00] What the Cochrane review found about anti-amyloid drugs. [04:30] Why memory problems are not the beginning of Alzheimer's. [07:00] The Alzheimer's disease timeline. [10:00] Why treating amyloid after symptoms appear may be too late. [12:30] What tau does in healthy brain cells. [14:00] What tracks closely with cognitive decline. [16:30] What ARIA is and why it matters. [18:00] The role of neuroinflammation in Alzheimer's.[22:00] Questions to ask the neurologist before deciding. Mentioned in the EpisodeAlzheimer's Prevention: What the Cochrane Review MeansCochrane Review: Anti-amyloid Alzheimer's drugs show no clinically meaningful effectListen now, subscribe to Happy & Healthy with Amy, and share this episode with someone who is trying to make sense of an Alzheimer's diagnosis in their family.RESOURCES:Book a FREE Discovery Call with AmyDownload After Mom's Alzheimer's Diagnosis: The First 8 Things to Know and learn how to support her with more calm, clarity, and confidence.Schedule your Breakthrough Roadmap session with AmyFollow Amy on Instagram @amylangcoaching  and on Facebook @amylangcoachingSubscribe to Amy's YouTube channel @happyandhealthywithamy

Sleep and weight gain are directly connected. Poor sleep disrupts hormones, raises blood sugar, tanks testosterone and estrogen, causes fatty liver, and wrecks your gut. If you've been doing everything right and the scale won't move, your sleep could be the missing link. FEATURED PRODUCT Chill by MSW Nutrition is a powdered drink mix formulated to support your body's natural calming chemistry — exactly what's needed when chronic stress and cortisol overload are stealing your sleep. Featuring GABA, L-Theanine, myo-Inositol, Taurine, and Magnesium, Chill helps balance neurotransmitters, quiet the nervous system, and promote the deep, restorative sleep your hormones, metabolism, and weight depend on — all five mechanisms discussed in this episode.

In this episode, Dr. Allison Hennigan breaks down the science behind anti-amyloid agents and how they slow Alzheimer's progression by targeting harmful proteins in the brain. Discover practical lifestyle changes that can enhance treatment effectiveness and the importance of recognizing early signs of dementia. Tune in now for an enlightening discussion. Visit carle.org for further information.  Learn more about Allison Hennigan, MD 

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Development of a Predictive Tool in Patients With High Pretest Probability for Transthyretin Amyloid Cardiomyopathy.

Alzheimer's disease unfolds over many years through a complex interplay of amyloid, tau, genetics, lipid biology, and the brain's immune response. John Hardy, Ph.D., explains how rare inherited forms of Alzheimer's disease helped shape current thinking about how the disease begins, then connects those discoveries to broader questions about late onset disease and why it develops differently across people. Hardy shows that amyloid and tau are linked but not identical, and argues that problems with protein buildup and clearance both matter in understanding the disease. He also emphasizes that Alzheimer's is not a single event but a long process, which makes prediction, diagnosis, and treatment especially difficult. While current amyloid-targeting therapies can help and show measurable benefit, Hardy says they do not stop the disease, underscoring the need for earlier diagnosis, better treatments, and wider access to care Series: "Shiley Endowed Lecture" [Health and Medicine] [Show ID: 41250]

Alzheimer's disease unfolds over many years through a complex interplay of amyloid, tau, genetics, lipid biology, and the brain's immune response. John Hardy, Ph.D., explains how rare inherited forms of Alzheimer's disease helped shape current thinking about how the disease begins, then connects those discoveries to broader questions about late onset disease and why it develops differently across people. Hardy shows that amyloid and tau are linked but not identical, and argues that problems with protein buildup and clearance both matter in understanding the disease. He also emphasizes that Alzheimer's is not a single event but a long process, which makes prediction, diagnosis, and treatment especially difficult. While current amyloid-targeting therapies can help and show measurable benefit, Hardy says they do not stop the disease, underscoring the need for earlier diagnosis, better treatments, and wider access to care Series: "Shiley Endowed Lecture" [Health and Medicine] [Show ID: 41250]

Alzheimer's disease unfolds over many years through a complex interplay of amyloid, tau, genetics, lipid biology, and the brain's immune response. John Hardy, Ph.D., explains how rare inherited forms of Alzheimer's disease helped shape current thinking about how the disease begins, then connects those discoveries to broader questions about late onset disease and why it develops differently across people. Hardy shows that amyloid and tau are linked but not identical, and argues that problems with protein buildup and clearance both matter in understanding the disease. He also emphasizes that Alzheimer's is not a single event but a long process, which makes prediction, diagnosis, and treatment especially difficult. While current amyloid-targeting therapies can help and show measurable benefit, Hardy says they do not stop the disease, underscoring the need for earlier diagnosis, better treatments, and wider access to care Series: "Shiley Endowed Lecture" [Health and Medicine] [Show ID: 41250]

Alzheimer's disease unfolds over many years through a complex interplay of amyloid, tau, genetics, lipid biology, and the brain's immune response. John Hardy, Ph.D., explains how rare inherited forms of Alzheimer's disease helped shape current thinking about how the disease begins, then connects those discoveries to broader questions about late onset disease and why it develops differently across people. Hardy shows that amyloid and tau are linked but not identical, and argues that problems with protein buildup and clearance both matter in understanding the disease. He also emphasizes that Alzheimer's is not a single event but a long process, which makes prediction, diagnosis, and treatment especially difficult. While current amyloid-targeting therapies can help and show measurable benefit, Hardy says they do not stop the disease, underscoring the need for earlier diagnosis, better treatments, and wider access to care Series: "Shiley Endowed Lecture" [Health and Medicine] [Show ID: 41250]

Alzheimer's disease unfolds over many years through a complex interplay of amyloid, tau, genetics, lipid biology, and the brain's immune response. John Hardy, Ph.D., explains how rare inherited forms of Alzheimer's disease helped shape current thinking about how the disease begins, then connects those discoveries to broader questions about late onset disease and why it develops differently across people. Hardy shows that amyloid and tau are linked but not identical, and argues that problems with protein buildup and clearance both matter in understanding the disease. He also emphasizes that Alzheimer's is not a single event but a long process, which makes prediction, diagnosis, and treatment especially difficult. While current amyloid-targeting therapies can help and show measurable benefit, Hardy says they do not stop the disease, underscoring the need for earlier diagnosis, better treatments, and wider access to care Series: "Shiley Endowed Lecture" [Health and Medicine] [Show ID: 41250]

The research and real talk keep rolling in! Join Jenny and John yet again as they dive into some new revelations on vitamin D, Alzheimer's disease, and ultra-processed foods. Then, John brings the heat with an enthralling round of “Real Talk? Or Bro-Science?”Guest Name/ Guest Company / Guest or Company websiteJohn Bauer, Lionel UniversityInterview Date11/20/25Episode Title and Subtitle (i.e. Ep.0: Meet Your Hosts, Meet your co-hosts Jenny Scott and Dan Duran!)Research & Real Talk Episode 20 with GUEST John Bauer (he's baaaack!!)Episode Description- For website and podcast platformsThe research and real talk keep rolling in! Join Jenny and John yet again as they dive into some new revelations on vitamin D, Alzheimer's disease, and ultra-processed foods. Then, John brings the heat with an enthralling round of “Real Talk? Or Bro-Science?”Notes: (Links, websites, references etc) for show notesLighting Fitness Facts1. Which Fat-soluble vitamin is being researched for its anti-aging properties on a DNA level?A: Vitamin D!A new review out of Augusta University in the US is shedding light on how vitamin D—the so-called “sunshine vitamin”—may do more than just build strong bones. Researchers found that taking 2,000 IU of vitamin D daily helped preserve telomeres, the protective caps at the ends of our chromosomes that act like the plastic tips on shoelaces, keeping our DNA from fraying each time cells divide. Shorter telomeres are tied to aging and diseases like cancer and heart disease, so keeping them intact could mean healthier aging.In a five-year study of more than 1,000 adults, those who took vitamin D maintained their telomeres by about 140 base pairs more than those on a placebo—potentially slowing cellular aging. Scientists think vitamin D's anti-inflammatory effects may be key here, since inflammation accelerates telomere damage.That said, researchers caution that we still don't know the perfect dosage or whether longer telomeres always equal better health. The takeaway? Vitamin D might be one helpful piece of the healthy aging puzzle, but the best telomere protection still comes from the basics—good nutrition, regular exercise, quality sleep, and managing stress.2. As it relates to the diet, what are researchers homing in on as a primary cause of chronic systemic inflammation possibly leading to chronic health issues?A: high ultra-processed food consumptionNew research from Florida Atlantic University is sounding the alarm on ultra-processed foods—things like chips, soda, frozen meals, and processed meats that make up nearly 60% of the average adult's calories in the U.S. and almost 70% of kids' diets. These foods are packed with additives, low in nutrients, and designed to keep you eating more. The study found that people who consumed the highest amounts of ultra-processed foods had significantly higher levels of high-sensitivity C-reactive protein, or hs-CRP—a key marker of inflammation and a strong predictor of heart disease.Researchers analyzed data from over 9,000 adults across the U.S. and discovered that those getting 60 to 79% of their calories from ultra-processed foods had about an 11% higher likelihood of elevated inflammation compared to people eating the least. Even moderate consumers saw higher risk. The link was especially strong among people aged 50 to 59, those with obesity, and smokers.Inflammation is at the root of many chronic diseases—from heart problems to cancer—and the study's authors say this growing reliance on ultra-processed foods could be playing a major role. They even compare the situation to early warnings about tobacco use, predicting that it may take time and policy change before the food industry shifts. For now, the takeaway is clear: the closer your food is to its natural form—fruits, vegetables, lean proteins, and whole grains—the better for your long-term health.3. Alzheimer's research is constantly advancing and scientists think they have identified something that may be contributing to the development and progression of the disease. What do you think that may be? HINT- it is the buildup of something that is causing issues.A: Fat in the brain!Researchers at Purdue University have uncovered a surprising new clue in the fight against Alzheimer's disease—fat buildup inside the brain's immune cells may be a key driver of the disease's progression. Published in the journal Immunity, the study reveals that microglia, the brain's cleanup crew responsible for clearing toxic proteins like amyloid beta, become overloaded with fat and lose their ability to protect the brain.The team found that these fat-stuffed microglia, clustered around amyloid plaques, clear about 40% less amyloid than healthy cells. The culprit appears to be an enzyme called DGAT2, which gets stuck in overdrive and turns useful fatty acids into stored fat, clogging the microglia. When researchers blocked or degraded this enzyme in animal models, the microglia regained their function and began clearing out harmful debris again—restoring the brain's balance.This discovery marks a shift from the traditional focus on protein plaques and tangles to what scientists are calling a “lipid model” of Alzheimer's, where the buildup of certain fats—not just misfolded proteins—plays a central role in neurodegeneration. The findings open the door to a new class of therapies that target fat metabolism in the brain, potentially helping immune cells fight back against Alzheimer's and related diseases.References:1. Haidong Zhu, JoAnn E Manson, Nancy R Cook, Bayu B Bekele, Li Chen, Kevin J Kane, Ying Huang, Wenjun Li, William Christen, I-Min Lee, Yanbin Dong. Vitamin D3 and marine ω-3 fatty acids supplementation and leukocyte telomere length: 4-year findings from the VITamin D and OmegA-3 TriaL (VITAL) randomized controlled trial. The American Journal of Clinical Nutrition, 2025; 122 (1): 39 DOI: 10.1016/j.ajcnut.2025.05.0032. Kevin Sajan, Nishi Anthireddy, Alexandra Matarazzo, Caio Furtado, Charles H. Hennekens, Allison Ferris. Ultra-processed foods and increased high sensitivity C-reactive protein. The American Journal of Medicine, 2025; DOI: 10.1016/j.amjmed.2025.08.0163. Salt, Sugar, Fat by Micahel Moss4. Priya Prakash, Palak Manchanda, Evi Paouri, Kanchan Bisht, Kaushik Sharma, Jitika Rajpoot, Victoria Wendt, Ahad Hossain, Prageeth R. Wijewardhane, Caitlin E. Randolph, Yihao Chen, Sarah Stanko, Nadia Gasmi, Anxhela Gjojdeshi, Sophie Card, Jonathan Fine, Krupal P. Jethava, Matthew G. Clark, Bin Dong, Seohee Ma, Alexis Crockett, Elizabeth A. Thayer, Marlo Nicolas, Ryann Davis, Dhruv Hardikar, Daniela Allende, Richard A. Prayson, Chi Zhang, Dimitrios Davalos, Gaurav Chopra. Amyloid-β induces lipid droplet-mediated microglial dysfunction via the enzyme DGAT2 in Alzheimer's disease. Immunity, 2025; 58 (6): 1536 DOI: 10.1016/j.immuni.2025.04.0295. Kevin A. Guttenplan, Maya K. Weigel, Priya Prakash, Prageeth R. Wijewardhane, Philip Hasel, Uriel Rufen-Blanchette, Alexandra E. Münch, Jacob A. Blum, Jonathan Fine, Mikaela C. Neal, Kimberley D. Bruce, Aaron D. Gitler, Gaurav Chopra, Shane A. Liddelow, Ben A. Barres. Neurotoxic reactive astrocytes induce cell death via saturated lipids. Nature, 2021; 599 (7883): 102 DOI: 10.1038/s41586-021-03960-y6. China N. Byrns, Alexandra E. Perlegos, Karl N. Miller, Zhecheng Jin, Faith R. Carranza, Palak Manchandra, Connor H. Beveridge, Caitlin E. Randolph, V. Sai Chaluvadi, Shirley L. Zhang, Ananth R. Srinivasan, F. C. Bennett, Amita Sehgal, Peter D. Adams, Gaurav Chopra, Nancy M. Bonini. Senescent glia link mitochondrial dysfunction and lipid accumulation. Nature, 2024; 630 (8016): 475 DOI: 10.1038/s41586-024-07516-8

In this powerful and science-forward episode of the Tick Boot Camp Podcast, host Matt Sabatello sits down with Amy Proal, PhD, a leading microbiologist whose work is reshaping how the medical community understands chronic Lyme disease, post-treatment Lyme disease (PTLD), ME/CFS, and Long COVID. Dr. Proal brings a rare combination of deep scientific expertise, lived experience with chronic illness, and real-world clinical integration, offering listeners clarity on why so many patients remain sick long after standard treatment ends — and what science is finally doing about it.

What if Alzheimer's, multiple sclerosis, chronic fatigue, and even psychiatric symptoms are not random but driven by hidden infections? In this episode of Integrative Lyme Solutions, Dr. K sits down with research scientist and Lyme survivor Nikki Schultek to explore the infection hypothesis behind chronic disease. After battling years of misdiagnosed symptoms including asthma flares, interstitial cystitis, arrhythmias, neurological decline, and suspected MS, Nikki uncovered a complex web of infections including Borrelia, Bartonella, Babesia, Chlamydia pneumoniae, Epstein-Barr virus, and more. Now founder of the Alzheimer's Pathobiome Initiative, Nikki is leading a global consortium investigating how stealth pathogens may trigger neurodegeneration, immune dysfunction, and dementia. This conversation dives into intracellular infections, the Herxheimer reaction, amyloid as an antimicrobial response, sterile brain autopsies, precision medicine, and why federal health agencies are finally acknowledging Lyme disease as a serious public health crisis. If you or someone you love is dealing with chronic Lyme, long COVID, autoimmune illness, or cognitive decline, this episode may change how you see disease. Key Takeaways: 0:00 Introduction 3:15 Asthma, air hunger, and early misdiagnoses 8:40 From interstitial cystitis to suspected multiple sclerosis 14:30 Discovering intracellular infections and Chlamydia pneumoniae 18:45 Lyme, Bartonella, Babesia and the whack-a-mole effect 24:10 The Pathobiome concept and microbial imbalance 27:30 Alzheimer's disease and the infection hypothesis 32:00 Sterile brain autopsies and spinal fluid research 35:20 Amyloid plaque as an antimicrobial defense mechanism 41:00 APOE4, genetics, and infection susceptibility 44:30 Federal recognition of Lyme disease and future funding Resources Mentioned: Alzheimer's Pathobiome Initiative - https://alzheimerspathobiome.org ILADS - https://www.ilads.org ILADS Education Foundation - https://www.iladef.org Philadelphia College of Osteopathic Medicine - https://www.pcom.edu Medical Disclaimer: This content is for educational purposes only and is not intended to diagnose, treat, cure, or replace professional medical advice. Always consult your physician or qualified healthcare provider regarding any medical condition or treatment decisions. _______________________________The Karlfeldt Center offers the most cutting-edge and comprehensive Lyme therapies. To schedule a Free 15-Minute Discovery Call with a Lyme Literate Naturopathic Doctor at The Karlfeldt Center, call 208-338-8902 or email info@TheKarlfeldtCenter.comCheck out Dr. K's Ebook: Breaking Free From Lyme: A Comprehensive Guide to Healing and Recovery here: https://store.thekarlfeldtcenter.com/products/breaking-free-from-lymeUse the code LYMEPODCAST for a 100% off discount!

In this episode, I sit down with neuroscientist Dr. Louisa Nicola to unpack what women actually need to know about Alzheimer's risk, cognitive decline, and long term brain protection. We break down APOE genetics, advanced blood biomarkers that can now detect amyloid and tau with remarkable accuracy, and why brain health is inseparable from metabolic health. Louisa explains how muscle acts as a metabolic sink for glucose, why resistance training and high intensity intervals stimulate BDNF, and how sleep drives the glymphatic system to clear amyloid from the brain. If you want practical tools to assess your personal risk, understand your labs, and build a proactive prevention plan decades before symptoms appear, this conversation is for you. → Leave Us A Voice Message!  Topics Discussed: → What does APOE4 mean for Alzheimer's risk? → Can exercise prevent cognitive decline? → Do blood tests detect early Alzheimer's? → How does perimenopause affect brain health? → Does hormone therapy reduce dementia risk? Sponsored By:  → Timeline | Support your cells and how you age with Mitopure® Gummies from Timeline. Visit https://timeline.com/KELLY and save up to 39% off your Mitopure® Gummies. → Be Well By Kelly Protein Powder & Essentials | Get $10 off your order with PODCAST10 at https://bewellbykelly.com. → Cozy Earth |  Head to https://cozyearth.com and use code BEWELL for up to 20% off. And if you get a post-purchase survey, make sure you tell them you heard about Cozy Earth right here at the Be Well by Kelly podcast.  → LMNT | Get a free 8-count Sample Pack of LMNT's most popular drink mix flavors with any purchase at https://drinklmnt.com/Kelly. Find your favorite LMNT flavor, or share with a friend. Timestamps:  → 00:00:00 - Introduction → 00:01:27 - Mission to end Alzheimer's  → 00:03:28 - Women's rate of Alzheimer's  → 00:04:11 - Alzheimer's overview  → 00:07:44 - Education level & health  → 00:09:57 - Anatomy  → 00:14:16 - Neuroplasticity & glucose  → 00:19:38 - Amyloid-beta → 00:26:41 - LDL Cholesterol → 00:28:36 - Preparing for menopause  → 00:31:30 - Blood testing recommendations  → 00:34:26 - Lifestyle interventions  → 00:39:05 - Nutrition & the MIND diet  → 00:42:19 - Zone 2 vs zone 5 training  → 00:44:36 - Lactic acid  → 00:47:58 - HRT is protective → 00:50:19 - When to test for HRT → 00:51:56 - Testosterone + brain health  → 00:53:40 - Cognitive reserve  → 00:57:12 - Hot flashes  → 00:58:13 - Quick fixes  → 01:00:01 - Brain surgery  → 01:05:38 - The brain code  Show Links: → Function | Own your health for $365 a year. That's a dollar a day. Learn more and join using my link. Visit https://www.functionhealth.com/bewellbykelly and use gift code BEWELL25 for a $25 credit toward your membership Further Listening: → How to Take Control of Your Health in a Toxic Food Landscape | Max Lugavere  Check Out Louisa:  → Instagram  → The Brain Code Check Out Kelly: → Instagram → Youtube → Facebook

On today's Good Day Health Show - ON DEMAND…Host Doug Stephan and Dr. Ken Kronhaus of Lake Cardiology (352-735-1400) cover a number of topics affecting our health. First up, Doug and Dr. Ken begin with the brain, specifically how it can be enhanced and how it can be damaged. There's a new study about a silent brain disease, Amyloid protein buildup in the brain being a hallmark of Alzheimer's disease and other neurodegenerative conditions, and a massive review on how to best help your brain through depression. Moving on to AI diagnostics, the latest in medical technology involves an AI system capable of interpreting MRIs in seconds, flagging strokes or hemorrhages, and drastically cutting down the time to treatment in ER settings.Then, a focus on men's cardiovascular health showing an increase in cardiovascular disease risk, starting at age 35, much earlier than women, suggesting the preventative screening needs to begin by mid-30s. Lastly, a recent scientific review as provided reassuring data for pregnant women that there is no increased-risk of autism , ADHD, or any intellectual disability in children. It's important to remember to follow dosage guidelines when it comes to acetaminophen (Tylenol).  Website: GoodDayHealthShow.com Social Media: @GoodDayNetworks

Host: Holly M. Brothers, PhD Guest: Niklas Mattsson-Carlgren, MD, PhD The prevalence of dementia is projected to almost double every 20 years.1 Alzheimer's disease (AD) is the most common cause of dementia,2 making early diagnosis and management increasingly important. Based on our current understanding of its pathology, AD is an amyloid driven tauopathy3 with biomarker changes occurring years before clinical symptoms appear.4 Learn more with this webinar featuring Dr Niklas Mattsson-Carlgren, Associate Professor at Lund University as he explores the relationship between amyloid beta and tau, the correlation between pathology and clinical symptoms, and biomarker progression across the AD continuum. To learn more about tau in Alzheimer's disease, explore the Know Tau medical education platform. Know Tau is created and funded by Biogen and is intended for healthcare professionals only. References: Alzheimer's Disease International. Numbers of people with dementia worldwide. Available from: https://www.alzint.org/resource/numbers-of-people-with-dementia-worldwide/ (Accessed June 2025) Alzheimer's Association. Alzheimer's disease facts and figures. Available from: https://www.alz.org/alzheimers-dementia/facts-figures (Accessed June 2025) Aksman LM, et al. Brain 2023;146:4935–4948 Jack CR Jr, et al. Alzheimers Dement 2018;14:535–562

In this deep-dive episode, Dr. Jill Carnahan and Dr. O'Bryan explore why LPS is far more than a gut issue—and how it silently fuels systemic inflammation for decades before symptoms like Alzheimer's, dementia, Parkinson's, or autoimmune disease appear.

In this episode, we get an update on Anti-Amyloid therapies and ARIA, along with the new POC tool to help physicians navigate these therapeutics and how they may impact patients in the emergency department. We talk with Dr. Christina Shenvi who introduced us to ARIA earlier in the year and now we have more evidence and a POC tool. Supported by Eli Lilly, USA

As little as 3000 steps per day can slow progression to Alzheimer's Disease; Self-reports of memory impairment soaring among young people; New study vindicates unprocessed red meat—and even often-vilified processed red meat—for cancer and overall health. Prostate artery embolization (PAE) offers new non-invasive option for men's age-related urinary problems; Targeting the mitochondria and the microbiome for Parkinson's Disease; Popular prostate and hair loss prevention drugs linked to depression and suicide—while Cialis for urinary symptoms may stave off cardiovascular disease; Discovery that a safe, cheap medication may increase survival after breast cancer surgery. 

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Early Access to Tafamidis for Patients With Transthyretin Amyloid Cardiomyopathy.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/NCPD information, and to apply for credit, please visit us at PeerView.com/CXX865. CME/NCPD credit will be available until September 18, 2026.Preparing Your Practice for Amyloid-Directed Therapies in Alzheimer's Disease: Key Strategies to Enhance Early Diagnosis and Optimize Management In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant by Eisai Inc.Disclosure information is available at the beginning of the video presentation.

Australia has just approved a second amyloid-targeting therapy for patients with incipient Alzheimer's dementia. Lecanemab (Leqembi) now joins donanemab (Kisunla) on the Australian Registry of Therapeutic Goods but the impact of both has been modest in Phase III trials to date. After 18 months of therapy they delay progression of disease, as quantified on neurocognitive tests, by around 5 months on average.  For some, the prolonged independence and dignity will justify the $60,000 to $80,000 a year price tag for the drugs. But for the Pharmaceutical Benefits Advisory Committee “the high burden of [donanemab] treatment on both patients and the health system, combined with the risks and modest clinical impact, makes the drug unsuitable for PBS subsidy”. This burden includes specialist consults, gene screening, multiple MRI and PET brain scans, and delivery of monthly or fortnightly infusions, adding up to another $20,000 in costs. Even before considering these logistical requirements, Australian memory clinics don't have anywhere near the capacity to address the 245,000 new cases of early dementia or mild cognitive impairment every year. Advocates see these disease-modifying therapies as a turning point for dementia research and argue for further investment in the systems infrastructure needed to roll them out. Sceptics argue that the available evidence instead questions the importance of amyloidosis in the Alzheimer's disease cascade.GuestsProfessor Michael Woodward AM FRACP FANZSGM FAAG FAWMA (Austin Health, Melbourne; University of Melbourne) Dr Chrysanth Pulle FRACP (Prince Charles Hospital, Brisbane)  Chapters 13:16 Time Saved16:18 Costs of treatment 26:44 IMJ paper on resourcing 39:10 Scepticism and stagingProductionProduced by Mic Cavazzini DPhil. Music licenced from Epidemic Sound ‘RGBA' and ‘Pulse Voyage' by Chill Cole, ‘A Forest Melody' by Tellsonic, ‘Axon Terminal' by Out to the World, ‘Organic Textures 2' by Johannes Bornlof and ‘Fugent' by Lupus Nocte. Image courtesy of Wikimedia Commons and University of Pittsburgh. Editorial feedback kindly provided by physicians of the podcast editorial group Ronaldo Piovezan, Aidan Tan, Hugh Murray, Joseph Lee, Rahul Barmanray, Simeon Wong and Sebastian Lambooy. Thanks also to Profs Bruce Campbell, Mike Parsons and Amy Brodtmann and registrars Jamie Bellinge and Karan Singh for additional insights into research methods. Please visit the Pomegranate Health web page for a transcript and supporting references. Login to MyCPD to record listening and reading as a prefilled learning activity. Subscribe to new episode email alerts or search for ‘Pomegranate Health' in Apple Podcasts, Spotify,Castbox or any podcasting app.

Es gibt ein neues Medikament gegen Alzheimer. Die Neurologin Elisabeth Stögmann über das Wirkprinzip, die Risiken und die Erfolgsaussichten von neuen Therapien. Ein Podcast vom Pragmaticus.Das Thema:Lecanemab heißt der neue Wirkstoff, der erstmals gegen die Ursachen der Alzheimer-Erkrankung zu Felde zieht: die Amyloid-beta-Plaques, die sich im Gehirn von Alzheimer-Kranken anlagern und die Denkfähigkeit zerstören. Anfang September hat der erste Patient in Österreich diese Substanz erhalten. „Es ist ein Meilenstein“, ist Neurologin Elisabeth Stögmann, Präsidentin der Alzheimer-Gesellschaft Österreich, überzeugt.In diesem Podcast beschreibt sie, wie dieses neue Medikament wirkt, für wen es in Frage kommt und mit welcher Wirksamkeit gerechnet werden kann. Und sie gibt auch Auskunft darüber, welche anderen Substanzen noch in der Pipeline gegen Alzheimer sind. Ein Gespräch über Status Quo, Perspektive und Prävention einer Erkrankung, von der 150.000 Menschen in Österreich betroffen sind.Unser Gast in dieser Folge: Elisabeth Stögmann ist Neurologin, ihr Spezialgebiet ist Alzheimer. Sie leitet die Gedächtnisambulanz am Wiener AKH und erforscht die Genetik, Entstehung und biomolekularen Eigenschaften der Erkrankung. Dazu ist sie an vielen internationalen Forschungsprojekten beteiligt, darunter die große EU-Horizont 2020-Studie und klinische Studien zu Medikamenten. Sie hat bei über 100 begutachteten (peer reviewed) Publikationen mitgewirkt. Stögmann ist derzeit auch Präsidentin der Österreichischen Alzheimer-Gesellschaft, Referentin auf internationalen Konferenzen und arbeitet mit Institutionen in ganz Europa zusammen.Dies ist ein Podcast von Der Pragmaticus. Sie finden uns auch auf Instagram, Facebook, LinkedIn und X (Twitter).  

Contributor: Aaron Lessen, MD Educational Pearls: The cause of Alzheimer's disease is multifactorial, but the most widely suspected mechanism is the amyloid cascade hypothesis: Beta-amyloid proteins accumulate in the central nervous system, forming plaques that impair neuronal function. In recent years, advances have led to the development of targeted therapies with monoclonal antibodies. These drugs: Work by degrading amyloid plaques Slow the rate of cognitive decline and disease progression Have major side effects, most notably the development of amyloid-related imaging abnormalities (ARIA) ARIA may present as edema, effusion, or microhemorrhages, which are only detectable on MRI Symptoms can include headache, vertigo, or focal neurologic deficits that mimic stroke For patients presenting to the emergency department with stroke-like symptoms, it is important to consider whether they have a history of Alzheimer's disease and whether they are taking these medications. This guides decisions about imaging and treatment: The work-up may require MRI, which can delay thrombolytic or endovascular therapy in patients with true strokeConversely, treating a patient with ARIA using thrombolytics increases the risk of bleeding and other complications References Ebell MH, Barry HC, Baduni K, Grasso G. Clinically Important Benefits and Harms of Monoclonal Antibodies Targeting Amyloid for the Treatment of Alzheimer Disease: A Systematic Review and Meta-Analysis. Ann Fam Med. 2024 Jan-Feb;22(1):50-62. doi: 10.1370/afm.3050. PMID: 38253509; PMCID: PMC11233076. Ma C, Hong F, Yang S. Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules. 2022 Feb 11;27(4):1210. doi: 10.3390/molecules27041210. PMID: 35209007; PMCID: PMC8876037. Perneczky R, Dom G, Chan A, Falkai P, Bassetti C. Anti-amyloid antibody treatments for Alzheimer's disease. Eur J Neurol. 2024 Feb;31(2):e16049. doi: 10.1111/ene.16049. Epub 2023 Sep 11. PMID: 37697714; PMCID: PMC11235913. Summarized by Ashley Lyons, OMS3 | Edited by Ashley Lyons and Jorge Chalit, OMS4 Donate: https://emergencymedicalminute.org/donate/

BUFFALO, NY — September 16, 2025 — A new #research paper was #published in Volume 17, Issue 8 of Aging-US on August 6, 2025, titled “Age-related trends in amyloid positivity in Parkinson's disease without dementia.” In this study, led by first author Keiko Hatano and corresponding author Masashi Kameyama from the Tokyo Metropolitan Institute for Geriatrics and Gerontology in Japan, researchers found that patients with Parkinson's disease (PD) diagnosed in their 80s showed a significantly higher rate of amyloid positivity—an indicator associated with Alzheimer's disease—compared to those diagnosed at a younger age. Importantly, none of the participants had dementia. These findings suggest that older patients with PD may face a greater risk of future cognitive decline and could benefit from early screening for Alzheimer's-related brain changes. Amyloid-beta is considered a key marker of cognitive decline. While it is known that amyloid accumulation contributes to PD with dementia, its role in patients who have not developed cognitive problems remains less understood. This study aimed to explore how age influences amyloid buildup in people with PD who do not yet show signs of dementia. The researchers analyzed data from 89 individuals with PD and no signs of dementia. Participants were divided into two age-based groups: those diagnosed before age 73 (LOW group) and those diagnosed at age 73 or older (HIGH group). Using cerebrospinal fluid samples, they measured levels of amyloid-beta, a standard method for detecting early Alzheimer's-related changes. The findings revealed that 30.6% of the older group tested positive for amyloid, compared to just 10.0% in the younger group. “[…] we elucidated the prevalence of amyloid positivity in patients with PD without dementia, whose mean age at diagnosis was 80.2 years, using CSF Aβ42 levels.” Interestingly, both age groups of Parkinson's patients had a lower rate of amyloid positivity than cognitively normal individuals of the same age in the general population. This unexpected result suggests that PD may alter how amyloid accumulates in the brain, possibly shortening the phase in which amyloid builds up silently before symptoms appear. The authors suggest that amyloid buildup could accelerate the transition from healthy cognition to dementia in patients with PD. The study also observed age-related associations with other biological markers of Alzheimer's disease, such as tau protein levels. As the global population continues to age and the number of older adults diagnosed with PD grows, identifying early warning signs of cognitive decline becomes increasingly important. These findings may help inform future screening approaches and support the development of therapies aimed at delaying or preventing dementia in people with Parkinson's disease. DOI - https://doi.org/10.18632/aging.206297 Corresponding author - Masashi Kameyama - kame-tky@umin.ac.jp Abstract video - https://www.youtube.com/watch?v=AP8S9evzCJw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206297 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, amyloid positivity, Parkinson's disease without dementia, cerebrospinal fluid Aβ42 To learn more about the journal, please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Bluesky - https://bsky.app/profile/aging-us.bsky.social Pinterest - https://www.pinterest.com/AgingUS/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

What you need to know to help patients and families decide about amyloid-targeting therapies for early-stage Alzheimer's disease. Credit available for this activity expires: 9/8/26 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/1002882?ecd=bdc_podcast_libsyn_mscpedu

Using biomarker testing and APOE genotyping to determine patient eligibility for amyloid-targeting therapies. Credit available for this activity expires: 8/19/2026 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/1002844?ecd=bdc_podcast_libsyn_mscpedu

A guest post by David Schneider-Joseph The “amyloid hypothesis” says that Alzheimer's is caused by accumulation of the peptide amyloid-β. It's the leading model in academia, but a favorite target for science journalists, contrarian bloggers, and neuroscience public intellectuals, who point out problems like: Some of the research establishing amyloid's role turned out to be fraudulent. The level of amyloid in the brain doesn't correlate very well with the level of cognitive impairment across Alzheimer's patients. Several strains of mice that were genetically programmed to have extra amyloid did eventually develop cognitive impairments. But it took much higher amyloid levels than humans have, and on further investigation the impairments didn't really look like Alzheimer's. Some infectious agents, like the gingivitis bacterium and the herpesviruses, seem to play a role in at least some Alzheimer's cases. . . . and amyloid is one of the body's responses to injury or infection, so it might be a harmless byproduct of these infections or whatever else the real disease is. Anti-amyloid drugs (like Aduhelm) don't reverse the disease, and only slow progression a relatively small amount. Opponents call the amyloid hypothesis zombie science, propped up only by pharmaceutical companies hoping to sell off a few more anti-amyloid me-too drugs before it collapses. Meanwhile, mainstream scientists . . . continue to believe it without really offering any public defense. Scott was so surprised by the size of the gap between official and unofficial opinion that he asked if someone from the orthodox camp would speak out in its favor. I am David Schneider-Joseph, an engineer formerly with SpaceX and Google, now working in AI safety. Alzheimer's isn't my field, but I got very interested in it, spent six months studying the literature, and came away believing the amyloid hypothesis was basically completely solid. I thought I'd share that understanding with current skeptics. https://www.astralcodexten.com/p/in-defense-of-the-amyloid-hypothesis

CardioNerds (Drs. Rick Ferraro and Georgia Vasilakis Tsatiris) discuss ATTR cardiac amyloidosis with expert Dr. Justin Grodin. This episode is a must-listen for all who want to know how to diagnose and treat ATTR with current available therapies, as well as management of concomitant diseases through a multidisciplinary approach. We take a deep dive into the importance of genetic testing, not only for patients and families, but also for gene-specific therapies on the horizon. Dr. Grodin draws us a roadmap, guiding us through new experimental therapies that may reverse the amyloidosis disease process once and for all.  Audio editing by CardioNerds academy intern, Christiana Dangas. This episode was developed in collaboration with the American Society of Preventive Cardiology and supported by an educational grant from BridgeBio.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: You must THINK about your patient having amyloid to recognize the pattern and make the diagnosis. Start with a routine ECG and TTE, and look for a disproportionately large heart muscle with relatively low voltages on the ECG.  Before you diagnose ATTR amyloidosis, AL amyloidosis must be ruled out (or ruled in) with serum light chains, serum/urine immunofixation, and/or tissue biopsy.  Genetic testing is standard of care for all patients and families with ATTR amyloidosis, and the future is promising for gene-specific treatments. Current FDA-approved treatments for TTR amyloidosis are TTR stabilizers and TTR silencers, but TTR fibril-depleting agents are on their way.  Early diagnosis of ATTR affords patients maximal benefit from current amyloidosis therapies.   TTR amyloidosis patients require a multidisciplinary approach for success, given the high number of concomitant diseases with cardiomyopathy.  Notes: Notes: Notes drafted by Dr. Georgia Vasilakis Tsatiris.  What makes you most suspicious of a diagnosis of cardiac amyloidosis from the typical heart failure patient?  You must have a strong index of suspicion, meaning you THINK that the patient could have cardiac amyloidosis, to consider it diagnostically. Some characteristics or “red flags” to not miss:   Disproportionately thick heart muscle with a relatively low voltages on EKG   Bilateral carpal tunnel syndrome – estimated that 1 in 10 people >65 years old will have amyloidosis   Previously tolerated antihypertensive medications  Atraumatic biceps tendon rupture   Bilateral carpal tunnel syndrome  Spinal stenosis   Concomitant with other diseases: HFpEF, low-flow low-gradient aortic stenosis  How would you work up a patient for cardiac amyloidosis?   Start with a routine ECG (looking for disproportionally low voltage) and routine TTE (looking for thick heart muscle)  CBC, serum chemistries, hepatic function panel, NT proBNP, and troponin levels  NOTE: It is critical to differentiate between amyloid light chain (AL amyloidosis) and transthyretin ATTR amyloidosis, as both make up 95-99% of amyloidosis cases.   Obtain serum free light chains, serum & urine electrophoresis, and serum & urine immunofixation to rule out AL amyloidosis. (See table below)  AL Amyloidosis ATTR Amyloidosis  → Positive serum free light chains and immunofixation (Abnormal M protein) → Tissue biopsy (endomyocardial, fat pad) to confirm diagnosis → Negative serum free light chains and immunofixation (ruled out AL amyloidosis) → Cardiac scintigraphy (Technetium pyrophosphate with SPECT imaging)  What treatment options do we have to offer now for ATTR CM, and how has this compared to prior years?   Before 2019, treatment options were limited outside of cardiac tr...

Learn about the who, what, and when of integrating amyloid-targeting therapies into Alzheimer's disease care.   Credit available for this activity expires: 8/18/2026 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/1002805?ecd=bdc_podcast_libsyn_mscpedu

What sequences, when, and how to report findings? Learn from the experts the recommended MRI protocols and reporting structure. Credit available for this activity expires: 8/7/26 Earn Credit / Learning Objectives & Disclosures: https://www.medscape.org/viewarticle/1002784?ecd=bdc_podcast_libsyn_mscpedu

Drs. Rick Ferraro and Sneha Nandy discuss ‘Diagnosis of ATTR Cardiac Amyloidosis' with Dr. Venkatesh Murthy.  In this episode, we explore the diagnosis of ATTR cardiac amyloidosis, a condition once considered rare but now increasingly recognized due to advances in imaging and the availability of effective therapies. Dr. Venkatesh Murthy, a leader in multimodality imaging, discusses key clinical and laboratory features that should raise suspicion for the disease. We also examine the role of nuclear imaging and genetic testing in confirming the diagnosis, as well as the importance of early detection. Tune in for expert insights on navigating this challenging diagnosis and look out for our next episode on treatment approaches for cardiac amyloidosis! Audio editing for this episode was performed by CardioNerds Intern, Julia Marques Fernandes. Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Diagnosis of Transthyretin amyloid cardiomyopathy 1. Recognizing the Red Flags – ATTR cardiac amyloidosis often presents with subtle but telling signs, such as bilateral carpal tunnel syndrome, low-voltage ECG, and a history of lumbar spinal stenosis or biceps tendon rupture. If you see these features in a patient with heart failure symptoms, think amyloidosis!    2. “Vanilla Ice Cream with a Cherry on Top” – On strain echocardiography, apical sparing is a classic pattern for cardiac amyloidosis. While helpful, it's not foolproof—multimodal imaging and clinical suspicion are key!   3. Nuclear Imaging is a Game-Changer – When suspicion for cardiac amyloidosis is high à a positive PYP scan with SPECT imaging (grade 2 or 3 myocardial uptake) in the absence of monoclonal protein (ruled out by SPEP, UPEP, and free light chains) is diagnostic for ATTR amyloidosis—no biopsy needed!   4. Wild-Type vs. Hereditary? Know the Clues – Older patients (70+) are more likely to have wild-type ATTR, while younger patients (40s-60s), especially those with neuropathy and a family history of heart failure, should raise suspicion for hereditary ATTR. Genetic testing is crucial for distinguishing between the two. Note that some ATTR variants may predispose to a false negative PYP scan!  5. Missing Amyloidosis = Missed Opportunity – With multiple disease-modifying therapies now available, early diagnosis is critical. If you suspect cardiac amyloidosis, don't delay the workup—early treatment improves outcomes!   Notes - Diagnosis of Transthyretin amyloid cardiomyopathy What clinical features should raise suspicion for ATTR cardiac amyloidosis?   ATTR cardiac amyloidosis is underdiagnosed because symptoms overlap with other forms of heart failure.   Red flags include bilateral carpal tunnel syndrome (often years before cardiac symptoms), low-voltage ECG despite increased LV wall thickness, heart failure with preserved ejection fraction (HFpEF) with a restrictive pattern, and history of lumbar spinal stenosis, biceps tendon rupture, and/or peripheral neuropathy, including possible autonomic dysfunction (e.g., orthostatic hypotension).  Remember: If an older patient presents with heart failure and unexplained symptoms like neuropathy or musculoskeletal issues, think amyloidosis!   What is the differential diagnosis for a thick left ventricle (LVH) and how does ATTR amyloidosis fit into it?    Hypertension: Most common cause of LVH, typically with a history of uncontrolled high blood pressure.   Aortic stenosis: May present with concentric LVH.   Hypertrophic cardiomyopathy (HCM): Genetic disorder typically presenting with asymmetric LVH, especially in younger patients.   Infiltrative cardiomyopathy: Often due to amyloidosis, sarcoidosis,

Get rationale and tips for using SAA in a clinical setting.To read this article, visit https://equimanagement.com/research-medical/diagnostics/practical-uses-of-serum-amyloid-a-in-horses/.Mentioned in this episode:EquiManagement on Audio All the articles you have come to love in EquiManagement Magazine are now available in this podcast for free. Each article is released as its own separate episode to make them quick and easy to listen to. EquiManagement always has the latest insights on equine health, veterinary practice management, and veterinarian wellness.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE information, and to apply for credit, please visit us at PeerView.com/ZFA865. CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE credit will be available until June 18, 2026.Navigating Advances in Alzheimer's Disease: Practical Strategies for Integrating New Diagnostic Tools and Amyloid-Targeting Therapies Into Patient Care In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and BrightFocus Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE information, and to apply for credit, please visit us at PeerView.com/ZFA865. CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE credit will be available until June 18, 2026.Navigating Advances in Alzheimer's Disease: Practical Strategies for Integrating New Diagnostic Tools and Amyloid-Targeting Therapies Into Patient Care In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and BrightFocus Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE information, and to apply for credit, please visit us at PeerView.com/ZFA865. CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE credit will be available until June 18, 2026.Navigating Advances in Alzheimer's Disease: Practical Strategies for Integrating New Diagnostic Tools and Amyloid-Targeting Therapies Into Patient Care In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and BrightFocus Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE information, and to apply for credit, please visit us at PeerView.com/ZFA865. CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE credit will be available until June 18, 2026.Navigating Advances in Alzheimer's Disease: Practical Strategies for Integrating New Diagnostic Tools and Amyloid-Targeting Therapies Into Patient Care In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and BrightFocus Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE information, and to apply for credit, please visit us at PeerView.com/ZFA865. CME/MOC/NCPD/AAPA/ASWB-ACE/APA/IPCE credit will be available until June 18, 2026.Navigating Advances in Alzheimer's Disease: Practical Strategies for Integrating New Diagnostic Tools and Amyloid-Targeting Therapies Into Patient Care In support of improving patient care, this activity has been planned and implemented by PVI, PeerView Institute for Medical Education, and BrightFocus Foundation. PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This content has been developed for healthcare professionals only. Patients who seek health information should consult with their physician or relevant patient advocacy groups.For the full presentation, downloadable Practice Aids, slides, and complete CME/MOC/EBAC/NCPD/AAPA information, and to apply for credit, please visit us at PeerView.com/QPX865. CME/MOC/EBAC/NCPD/AAPA credit will be available until May 31, 2026.Implementing Amyloid-Targeting Treatment for Early AD: Strategies for Overcoming Real-World Challenges In support of improving patient care, PVI, PeerView Institute for Medical Education, is jointly accredited by the Accreditation Council for Continuing Medical Education (ACCME), the Accreditation Council for Pharmacy Education (ACPE), and the American Nurses Credentialing Center (ANCC), to provide continuing education for the healthcare team.SupportThis activity is supported by an educational grant from Lilly.Disclosure information is available at the beginning of the video presentation.

This week on the show, we're have our sights set on healthy aging. What would it mean to be able to live to 80, 90 or 100 with our cognitive abilities intact and able to maintain an independent lifestyle right to the end of our days? We're joined by Beth Mormino and Anthony Wagner who lead the Stanford Aging and Memory Study, which recruits cognitively healthy older adults to understand what makes their brains particularly resilient — and how more of us could join them in living the dream of healthy aging.Learn MoreStanford Aging and Memory Study (SAMS)Stanford Memory LabMormino LabFurther ReadingAlzheimer's 'resilience signature' predicts who will develop dementia—and how fast (Knight Initiative for Brain Resilience, 2025)Latest Alzheimer's lab tests focus on memory loss, not brain plaques (NPR, 2025)ReferencesTrelle, A. N., ... & Wagner, A. D. (2020). Hippocampal and cortical mechanisms at retrieval explain variability in episodic remembering in older adults. eLife, 9:e55335. doi: 10.7554/eLife.55335 PDF | PMID:32469308Trelle, A. N., ..., Wagner, A. D., Mormino, E. C., & Wilson, E. N. (2025). Plasma Aβ42/Aβ40 is sensitive to early cerebral amyloid accumulation and predicts risk of cognitive decline across the Alzheimer's disease spectrum. Alzheimer's & Dementia, 21:e14442. PDF | PMID:39713875Sheng, J., ..., Mormino, E., & Wagner, A. D. (submitted). Top-down attention and Alzheimer's pathology impact cortical selectivity during learning, influencing episodic memory in older adults.  PreprintEpisode CreditsThis episode was produced by Michael Osborne at 14th Street Studios, with sound design by Morgan Honaker. Our logo is by Aimee Garza. The show is hosted by Nicholas Weiler at Stanford's Wu Tsai Neurosciences Institute and supported in part by the Knight Iniative for Brain Resilience.Get in touchWe want to hear from your neurons! Email us at at neuronspodcast@stanford.edu if you'd be willing to help out with some listener rSend us a text!Thanks for listening! If you're enjoying our show, please take a moment to give us a review on your podcast app of choice and share this episode with your friends. That's how we grow as a show and bring the stories of the frontiers of neuroscience to a wider audience. Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

CardioNerds Cardiac Amyloidosis Series Chair Dr. Rick Ferraro and Episode Lead Dr. Anna Radakrishnan discuss the biology of transthyretin amyloid cardiomyopathy (ATTR-CM ) with Dr. Daniel Judge.  Notes were drafted by Dr. Anna Radakrishnan. The audio was engineered by student Dr. Julia Marques.  This episode provides a comprehensive overview of transthyretin (ATTR) cardiac amyloidosis, a complex and rapidly evolving disease process. The discussion covers the key red flags for cardiac amyloidosis, the diagnostic pathway, and the implications of hereditary versus wild-type ATTR. Importantly, the episode delves into the current and emerging therapies for ATTR, including stabilizers, gene silencers, and promising treatments like CRISPR-Cas9 and antibody-based approaches. Dr. Judge shares his insights and excitement about the rapidly advancing field, highlighting the need for early diagnosis and the potential to improve long-term outcomes for patients with this condition.  Enjoy this Circulation Paths to Discovery article to learn more about the CardioNerds mission and journey.  US Cardiology Review is now the official journal of CardioNerds! Submit your manuscripts here.  CardioNerds Cardiac Amyloid PageCardioNerds Episode Page Pearls: - Biology of Transthyretin amyloid cardiomyopathy Maintain a high index of suspicion! Look for subtle (yet telling) signs like ventricular hypertrophy, discordant EKG findings, bilateral carpal tunnel syndrome, and spontaneous biceps tendon rupture.  Utilize the right diagnostic tests. Endomyocardial biopsy remains the gold standard, but non-invasive tools like PYP scan with SPECT imaging and genetic testing are essential for accurate diagnosis.  Differentiating hereditary from wild-type ATTR is critical, as genetic forms may have a more aggressive course and familial implications.  Early diagnosis and intervention significantly improve prognosis, making vigilance in screening and prompt treatment initiation essential.  The future is now! Cutting-edge therapies are transforming the treatment landscape, including TTR stabilizers, gene silencers, and emerging technologies like CRISPR-Cas9 and antibody-based treatments.  Notes - Biology of Transthyretin amyloid cardiomyopathy What is transthyretin amyloid (aTTR) and how is it derived?  Transthyretin (TTR) is a transport protein primarily synthesized by the liver, responsible for carrying thyroid hormones (thyroxine) and retinol (vitamin A) in the blood. It circulates as a tetramer, composed of four identical monomers, which is essential for its stability and function.  In transthyretin amyloid (ATTR) amyloidosis, the TTR protein becomes unstable, leading to its dissociation into monomers. These monomers misfold and aggregate into insoluble amyloid fibrils, which deposit extracellularly in tissues such as the heart, nerves, and gastrointestinal tract. This progressive amyloid deposition leads to organ dysfunction, including restrictive cardiomyopathy and neuropathy.  There are two main forms of ATTR amyloidosis: hereditary (variant) and wild-type (senile) ATTR.  Hereditary ATTR (ATTRv) is caused by mutations in the TTR gene. These mutations destabilize the TTR tetramer, making it more prone to dissociation. This increases misfolding and amyloid fibril formation, resulting in systemic amyloid deposition.   Wild-type ATTR (ATTRwt) occurs without genetic mutations and is primarily age-related. Over time, even normal TTR tetramers can become unstable, leading to gradual misfolding and amyloid deposition, particularly in the heart. ATTRwt is a common but often underdiagnosed cause of heart failure with preserved ejection fraction (HFpEF) in elderly individuals.  How does aTTR lead to deleterious effects in the heart and other organ systems?    Transthyretin amyloidosis leads to organ dysfunction through the deposition of misfolded TTR protein as amyloid fib...

This week, we look at the new pharmaceuticals that the FDA has approved for treating Alzheimer disease. Although they are effective at removing amyloid plaques from the brain, they don't seem to help patients function better. Is it time to turn away from an exclusive focus on amyloid to consider other factors that might affect […]