Podcasts about Microglia

Broadcast from KSQD, Santa Cruz on 6-11-2026: Dr. Dawn discusses fascia — the gelatinous network of sugary proteins, salts, and collagen bundles that has been known to acupuncturists and osteopaths for millennia but ignored in conventional medical training. New confocal laser endomicroscopy technology has finally visualized this "interstitium" as a fluid-filled space draining to lymph nodes, present throughout the GI tract, urinary bladder, dermis, and peribronchial tissues. The structure may play roles in cancer metastasis, edema, fibrosis, and mechanical tissue function. An emailer asks about elevated organic arsenic levels (from sardines) and ultra-filtered dairy. Dr. Dawn explains that arsenobetaine—the protein-bonded form found in fish, is harmless and passes through the body, while inorganic and methylated arsenic accumulate in bone and collagen-rich tissues. In a second question about the safety of ultrafiltered dairy, she notes ultra-filtered products may carry more microplastics from extensive plastic filters and tubing exposure, with aged cheese being particularly concentrated since water removal increases plastic density. An emailer asks about breast MRI contrast options. Dr. Dawn explains that breast MRI requires gadolinium contrast because tumors leak through their poorly-formed blood vessels, creating necessary visual contrast. She strongly recommends macrocyclic gadolinium (a stable birdcage structure) over the linear form, which slips into bones, skin, the brain's caudate nucleus, liver, and spleen for at least eight years and rarely, can cause nephrogenic systemic fibrosis. There is some suggestion it may trigger brain inflammation. She suggests listing linear gadolinium as a drug sensitivity in medical charts. Researchers harvested exosomes from semen. The exosomes evolved to help sperm penetrate egg barriers, making them ideal delivery vehicles for drugs too toxic for traditional administration. These bubble-like vesicles can penetrate the eye to distribute a manganese dioxide nanozyme compound (CMG) across ocular barriers to treat retinoblastoma, a childhood eye cancer typically requiring eyeball removal. Researchers used extracellular vesicles (effectively artificial exosomes) delivered via nasal spray to reverse brain aging in mice. The vesicles carried messenger RNA targeting the NLRP2 inflammasome, restoring mitochondrial activity in neurons and improving memory and recognition in treated animals. The nasal delivery route bypasses the blood-brain barrier, opening possibilities for treating cognitive deterioration without injections or surgical implants. An emailer reports his wife two inches shorter at a new Kaiser facility in another state. Dr. Dawn first considers measurement inconsistency (shoes on or off), then suggests evaluating for compression fractures, disc disease, and parathyroid tumors. She recommends a bone scan, C-terminal telopeptide testing to assess active bone breakdown, and intact PTH to rule out parathyroid pathology if osteoporosis is identified by DEXA scan. Dr. Dawn explores a new brain model addressing how 86 billion neurons store more memory than classical models predict. Astrocytes, previously known mainly for creating myelin sheaths, form tripartite synapses with neurons connecting to thousands of synapses simultaneously, communicating via calcium signaling and gliotransmitters. This could provide the higher-order coupling needed for our dense associative memory that pairwise synaptic connections cannot explain. Disrupting astrocyte-neuron connections in the hippocampus impairs both memory storage and retrieval, supporting this theoretical model. A Nature Neuroscience study found abdominal muscle contractions compress blood vessels connected to the brain and spine via the vertebral venous plexus, physically rocking the brain within the skull. This mechanical swishing may explain how exercise helps clear brain toxins and prevent neurodegenerative disorders, potentially leading to inflatable abdominal devices that could aid brain cleansing during sleep. Montelukast, the common asthma and allergy drug, has been found to block a protein hijacked by triple-negative breast cancer that converts immune cells into "sleeper agents" that clear paths for tumor invasion rather than attacking cancer. Dr. Dawn notes AI is increasingly identifying these drug repurposing opportunities by analyzing molecular shapes and receptor compatibility.

Send us Fan MailFructose survival hypothesis: how fructose metabolism in the liver triggers ATP depletion, uric acid production, oxidative stress, lipogenesis & leptin resistance.TOPICS DISCUSSED:Glucose vs Fructose Metabolism: Fructose is rapidly metabolized in the liver by fructokinase without feedback, causing ATP depletion and uric acid production, unlike glucose metabolism.Liver Effects: Fructose induces uric acid production, NADPH oxidase activation, mitochondrial oxidative stress, and de novo lipogenesis even under caloric restriction.Fructose Survival Hypothesis: Fructose signaling promotes fat storage, leptin resistance, foraging behavior, and metabolic syndrome as adaptations for hibernation or starvation, including metabolic water production.Brain Impacts: Endogenous fructose production from glucose (polyol pathway) triggered by high glucose, salt, or stress leads to insulin resistance, mitochondrial damage, and neuroinflammation in Alzheimer's-vulnerable regions.Evolutionary Context: Human uricase mutation ~12 million years ago enhanced fructose effects for fat storage during seasonal starvation but increases vulnerability today.Modern Triggers: Added sugars, high fructose corn syrup, salt-sugar combinations, and omega-6 fats synergize with fructose to amplify inflammation, appetite, and disease risk.Alzheimer's Link: Fructose-driven brain changes mirror Alzheimer's pathology, with high brain fructose in patients and potential for fructokinase inhibitors as therapy.ABOUT THE GUEST: Richard Johnson MD, is a professor of medicine who has conducted clinical practice and NIH-funded research on sugar metabolism since the late 1990s. His work focuses on the role of fructose in metabolic syndrome, obesity, and related diseases.RELATED CONTENT:Article | Dietary Fructose & Metabolic Health: An Evolutionary PerspectiveM&M 249: Fructose, Microglia, Anxiety & Brain Development | Justin Perry | 249Support the showHealth Products by M&M Partners:AquaTru: Water filtration devices that remove microplastics, metals, bacteria, and more from your drinking water. Through link, $100 off AquaTru Carafe, Classic & Under Sink Units; $300 off Freestanding models.OmegaQuant: At-home blood testing to see fatty acid profiles, including omega-3 fatty acids. Use link to see options and support M&M.SiPhox Health: Comprehensive, cost-effective bloodwork from the comfort of home. Use code TRIKOMES for 20% off.KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime)SporesMD: Premium mushrooms products (gourmet mushrooms, nootropics, research). Use code 'nickjikomes' for 20% off.For all the ways you can support my efforts

In this episode, Lucas Aoun interviews Ramona von Leden about the science and application of photobiomodulation with the Neuronic helmet. They explore how specific wavelengths of light can penetrate the skull, support brain health, and potentially impact neuroinflammation, microglia activity, and cognitive function. Ramona is a neuroscientist and scientific strategist with deep experience at the intersection of neuroscience, rehabilitation, and emerging health technologies. She earned her BS in Psychology from Brown University, her PhD in Neuroscience from the Uniformed Services University (where her research focused on the modulation of inflammation following Neurotrauma, including publications on the impact of photobiomodulation on microglial activation), and she completed a postdoctoral fellowship in the Neurology Department at the University of Texas at Austin Dell Medical School.GET NEURONIC HERE (Use code LUCAS10 for 10% off): https://checkout.neuronic.online/LUCAS10Chapters00:00 Introduction to Neuronic and Ramona's Journey02:35 Understanding the Neuronic Helmet05:32 Wavelengths and Their Impact on Brain Health09:27 Circadian Rhythms and Light Therapy13:23 Exciting Research in Photobiomodulation18:40 Microglia and Inflammation19:56 Blood Flow and Cognitive Function23:52 Protocols for Effective Use28:35 Measuring Effectiveness of Neuronic31:34 Optimizing Daily Routines with Light Therapy32:37 Integrating Light Therapy into Sleep Protocols33:42 Creating a Comprehensive Sleep Sanctuary37:24 Harnessing Energy for Optimal Health39:22 Exploring Different Wavelengths of Light42:43 Personal Experiences with Light Therapy48:34 Measuring Effectiveness of Light Therapy52:15 Final Thoughts on Light and HealthDisclaimer:The information provided in this podcast episode is for entertainment purposes and is NOT MEDICAL ADVICE. If you have any questions about your health, contact a medical professional. This content is strictly the opinions of Lucas Aoun and is for informational and entertainment purposes only. It is not intended to provide medical advice or to take the place of medical advice or treatment from a personal physician. All viewers of this content are advised to consult with their doctors or qualified health professionals regarding specific health questions. Neither Lucas Aoun nor the publisher of this content takes responsibility for possible health consequences of any person or persons reading or following the information in this content. All consumers of this content especially taking prescription or over-the-counter medications should consult their physician before beginning any nutritional, supplement or lifestyle program. Hosted on Acast. See acast.com/privacy for more information.

In a “surprise” role, the cells regulate the neurons that produce gonadotropin-releasing hormone.

Broadcast from KSQD, Santa Cruz on 4-30-2026:>/p> Dr. Dawn opens with a bike safety public service message, noting a 34% increase in bicycle use in Santa Cruz alongside rising e-bike accidents. She urges drivers to stay vigilant and calls for education and enforcement of helmet laws, particularly for riders under 18. A University of Michigan researcher discovered that standard nitrile, latex, and vinyl gloves shed stearate particles indistinguishable from polyethylene under spectroscopy, contaminating microplastics research with approximately 2,000 false positives per square millimeter. Only clean-room gloves avoided this problem, throwing years of microplastics studies into question. Dr. Dawn explains skin's three-layer structure and the stratum corneum's ceramide-based moisture barrier. She warns against stripping natural oils with astringents and hot showers, notes that UV disrupts proteins holding skin cells together, and cites a 2019 study showing moisturing treatment reduced circulating inflammatory cytokines in older adults. Making music coordinates sound, vision, motor control, and imagination across the brain. Studies show musicians have more gray matter, better executive function, sharper memory, and even reduced pain sensitivity. A 2010 paper found musicians who began before age seven have a larger corpus callosum, and a 2024 study showed pianists had better working memory while woodwind players did best at executive function. Stanford researcher Pascal Geldsetzer analyzed populations in Australia, New Zealand, Wales, and Ontario, finding the Shingrix vaccine reduces dementia risk by up to 20%. Dr. Dawn hypothesizes that even "dormant" varicella triggers low-level inflammation affecting brain microglia, and recommends spacing Shingrix three months apart from the second dose rather than one month to avoid side effects. A Nature study of 175 people watching movies found that observing someone being touched activates the same brain regions as being touched yourself—your brain experiences sensations in corresponding body parts. This vision-touch link could enable less invasive sensory testing for autistic individuals. Princeton and Flatiron Institute researchers identified four distinct autism phenotypes: broadly affected (10%), mixed with developmental delay (19%), moderate challenges (33%), and social/behavioral (37%). A second Nature study confirmed genetically distinct forms unfold on different timelines, with post-age-six diagnoses showing different genetic profiles than early childhood cases.

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]

In this episode of the Health Optimization Medicine Podcast, Dr. Scott Sherr is joined by renowned neurologist and bestselling author Dr. David Perlmutter to explore one of the most important breakthroughs in brain health — the role of microglia. Often overlooked, microglial cells are the brain's immune system and play a central role in determining whether the brain thrives or degenerates over time. Dr. Perlmutter explains how these cells can shift between protective (M2) and destructive (M1) states — and how this shift underlies neurodegenerative diseases like Alzheimer's, Parkinson's, and more. Most importantly, this episode highlights how everyday lifestyle choices — from diet and exercise to metabolic health — directly influence brain function and long-term cognitive resilience. Join us as we delve into: What microglia are and why they control brain health The difference between M1 (destructive) and M2 (protective) states How metabolism shapes the brain's immune response Why conditions like Alzheimer's are rooted in immune dysfunction The connection between blood sugar, insulin, and brain degeneration This episode is for you if: You want to protect your brain and prevent cognitive decline You're interested in the science of Alzheimer's and neurodegeneration You want actionable strategies to improve brain health You're curious about the future of brain optimization and longevity You can also find this episode on… Youtube: https://youtu.be/EMrlchMOZKk Find more from Dr. David Perlmutter Website: https://www.drperlmutter.com Book: https://braindefenders.com LinkedIn: https://www.linkedin.com/in/david-perlmutter-md/ Instagram: https://www.instagram.com/davidperlmutter/ Facebook: https://www.facebook.com/DavidPerlmutterMd/ Find more from Health Optimization Medicine and Practice (HOMeHOPe): Website: https://homehope.org/ Instagram: https://www.instagram.com/homehopeorg/ Virtual Symposium 2026: https://homehope.org/homehope-virtual-symposium-2026 Use PODCAST10 to get 10% OFF your purchase of the Clinical Metabolomics Module at https://homehope.org/products/clinical-metabolomics Find more from Troscriptions Website: https://troscriptions.com/ Instagram: https://www.instagram.com/troscriptions/ Use POD10 to get 10% OFF your Troscriptions purchase at https://troscriptions.com/collections/our-products

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

Cognitive resilience depends on how the brain responds to environment, aging, and inflammation. J. Tiago Gonçalves, Ph.D., studies the hippocampus to examine how spatial memory is shaped by factors such as cognitive enrichment, exercise, social interaction, disease, and age. Gonçalves explains how adult neurogenesis and microglia help support the brain's ability to encode information, and how disruptions in these systems can affect memory. He also shows that aging and systemic inflammation can weaken spatial encoding while still revealing signs of adaptation and recovery over time. By connecting brain plasticity, immune activity, and memory formation, Gonçalves presents a broader view of how cognition changes across the lifespan and how these mechanisms may inform future strategies for addressing cognitive decline Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 40848]

For decades, Alzheimer's disease was treated as an unavoidable consequence of aging. In this episode of Research Renaissance, Dr. Jessica Rexach explains why that framing is no longer true.Drawing on 20 years at the intersection of clinical neurology, genetics, and experimental neuroscience, Dr. Rexach walks us through a profound shift in the field. Today, scientists can model human brain circuits, measure Alzheimer's pathology through blood-based biomarkers, and study why some brains remain cognitively resilient even with disease pathology present.The science, she argues, is ready. The real question is whether society will commit the resources needed to finish the job.Key TakeawaysAlzheimer's research has moved from broad hypotheses to precise, testable mechanismsBlood-based biomarkers have transformed clinical trials and early detectionBrain resilience, not just pathology, may hold the key to preventionCOVID-era investments unintentionally accelerated dementia research toolsThe biggest risk now is not scientific failure, but loss of funding and momentumGuest InformationDr. Jessica RexachAssistant Professor, UCLA2024 Toffler Scholar

Degradation-resistant proteins pass from neurons to glial cells in a process that may spread protein clumps around the brain, according to a study in mice.

For decades, Alzheimer's research has focused on clearing amyloid plaques from the brain. But new drugs that successfully remove plaques have proven clinically "underwhelming", leaving the field searching for alternative approaches.Stanford neurologist Katrin Andreasson has spent twenty years pursuing a different path—investigating how aging triggers an energy crisis in the brain's immune and support cells. Her work reveals that inflammation and metabolic dysfunction in microglia and astrocytes may be the real drivers of Alzheimer's pathology. Most remarkably, her recent research—supported by the Knight Initiative for Brain Resilience here at the Wu Tsai Neurosciences Institute—shows that targeting inflammation in the peripheral immune system—outside the brain entirely—can restore memory in mouse models of the disease. While human trials are still needed, Andreasson's findings offer fresh hope and demonstrate the critical importance of supporting curiosity-driven science, even when it challenges prevailing dogma.Learn More:Alzheimer's Association honors Katrin AndreassonResearch links age-related inflammation, microglia and Alzheimer's DiseaseQ&A: How the aging immune system impacts brain healthRethinking Alzheimer's: Could it begin outside the brain?Why new Alzheimer's drugs may not work for patientsParkinson's comes in many forms. New biomarkers may explain why.Send 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. We want to hear from your neurons! Email us at at neuronspodcast@stanford.edu Learn more about the Wu Tsai Neurosciences Institute at Stanford and follow us on Twitter, Facebook, and LinkedIn.

Overview This special episode of the [Tick Boot Camp Podcast](https://tickbootcamp.com/podcast/) was recorded live at the 2nd Annual Alzheimer's Pathobiome Initiative (AlzPI) and PCOM Symposium in collaboration with Pathobiome Perspectives. Hosted by Ali Moresco in partnership with Nikki Schultek, Executive Director of AlzPI, the conversation continues the Tick Boot Camp mission of exploring infection-associated chronic illness (IACI)—including Lyme disease and other tick-borne infections—within the global Alzheimer's and neuroimmunology research community. Tick Boot Camp co-founders Matt Sabatello and Rich Johannesen partnered with Ali and Nikki to highlight leading scientists connecting microbes, immune dysregulation, and neurodegenerative disease. This episode features Dr. Elizabeth “Betsy” Bradshaw, Assistant Professor of Neurology at Columbia University Irving Medical Center, whose research investigates how past infections leave lasting imprints on the brain's immune system and influence the development of Alzheimer's disease. Guest Elizabeth M. Bradshaw, PhD Assistant Professor of Neurology, Columbia University Irving Medical Center Principal Investigator, Bradshaw Laboratory – Neuroimmunology and Genetics of Alzheimer's Dr. Bradshaw's laboratory focuses on the immune system's role in neurodegeneration, particularly how infection and inflammation alter brain immunity and predispose individuals to conditions like Alzheimer's disease. Her work builds on large-scale genome-wide association studies (GWAS) that identified immune-related genetic variants linked to Alzheimer's susceptibility, suggesting that subtle changes in immune function—not just neuronal factors—may underlie disease onset. Her team is exploring how pathogens such as HSV-1 (Herpes Simplex Virus Type 1) interact with the brain's immune cells, known as microglia, and how these infections can “reprogram” immune responses long after the pathogen is cleared. Key Discussion Points Dr. Bradshaw explains how her research bridges genetics, immunology, and infectious disease to better understand Alzheimer's. Through GWAS data, her team found that many of the genes linked to Alzheimer's risk involve immune pathways rather than neuronal signaling. This discovery redirected the field's attention toward how immune cells respond to pathogens and environmental stressors across a lifetime. Using human-derived microglia-like cells created from blood monocytes, her team observes how infections reshape immune cell metabolism and memory. By infecting these microglia-like cells with Alzheimer's-associated pathogens like HSV-1, they study how genetic background and infection history determine immune cell behavior. The findings suggest that past infections may epigenetically and metabolically train microglia—changing how they respond to aging, stress, and amyloid buildup. Even when the infection has resolved, these “reprogrammed” immune cells can remain altered for decades, silently increasing the brain's vulnerability to neurodegeneration. Dr. Bradshaw emphasizes that understanding how infections rewire the brain's immune landscape could transform early intervention strategies. Identifying combinations of genetic risk factors and pathogen exposures may enable targeted prevention or immune-modulating treatments long before symptoms appear. “Microglia remember. Even after the pathogen is gone, they carry its imprint—responding differently decades later when the brain faces new challenges.” — Dr. Elizabeth Bradshaw Why It Matters Dr. Bradshaw's work reframes Alzheimer's disease as a neuroimmune condition shaped by infection and host genetics. Her research highlights how microbial exposures, immune history, and inflammation converge to influence cognitive decline. By integrating infection biology with genetics and immunology, her team is redefining how scientists and clinicians view the root causes of Alzheimer's and other neurodegenerative diseases. This work strengthens the growing case that the immune system's “memory” of infection may be one of the most important and overlooked factors in brain health and aging. About the Event This interview was recorded at the 2nd Annual Alzheimer's Pathobiome Initiative (AlzPI) and Philadelphia College of Osteopathic Medicine (PCOM) Symposium, held October 3, 2025, at Ohio University in Dublin, Ohio. The event brought together more than 20 leading researchers exploring how microbes, the microbiome, and immune dysregulation contribute to Alzheimer's, dementia, and infection-associated chronic illness (IACI). Tick Boot Camp partnered with Ali Moresco and Nikki Schultek to share these conversations and connect chronic Lyme, infection, and neurodegenerative research communities. Learn More Learn more about the Alzheimer's Pathobiome Initiative (AlzPI) Listen to Tick Boot Camp Podcast episodes, including Episode 406: Pathobiome – An Interview with Nikki Schultek and Episode 101: The Young Gun – An Interview with Alex (Ali) Moresco discussed in this interview.

uniQure's “game changing” data announced in September, which showed significant slowing of Huntington's disease (HD) progression in patients treated with its gene therapy candidate AMT-130, may not be enough to secure FDA approval. We also discuss Recursion's pivotal leadership transitions, as Najat Khan, PhD, chief R&D officer and chief commercial officer, is set to take over as the company's CEO effective January 1. The AI drug developer has made big bets filling the biology data gap and recently announced a "Google Map of the brain" to advance neurodegenerative disease targets. In open-source AI for drug discovery, the release of the latest Boltz model, BoltzGen, advances the platform from structural predictions to the design of "any" therapeutic modality, all available for commercial use. Join GEN editors Corinna Singleman, PhD, Alex Philippidis, Fay Lin, PhD, and Uduak Thomas for a discussion of the latest biotech and biopharma news.    Listed below are links to the GEN stories referenced in this episode of Touching Base:  uniQure Staggers as FDA Questions Data for Huntington's Gene Therapy Candidate By Alex Philippidis, GEN Edge, November 3, 2025   StockWatch: uniQure Shares Reach Five-Year High on “Game Changing” Huntington's Data Alex Philippidis, GEN Edge, September 28, 2025 Gene Therapy Significantly Slows Huntington Disease Progression GEN, September 24, 2025 Recursion, Roche Unveil Microglia Map of Neuro Disease Targets By Alex Philippidis, GEN Edge, October 29, 2025 BoltzGen Democratizes AI Therapeutic Design, Expands Druggable Universe By Fay Lin, PhD, GEN, October 27, 2025 The State of AI in Drug Discovery On Demand    Touching Base Podcast  Hosted by Corinna Singleman, PhD  Behind the Breakthroughs  Hosted by Jonathan D. Grinstein, PhD    Hosted on Acast. See acast.com/privacy for more information.

In today's episode, we're diving into some brand new, cutting-edge research that turns the spotlight on microglia—the tiny, yet mighty immune cells in your spinal cord. Dr. Jeff explores a recent review published in Frontiers in Immunology that unpacks how microglia play a pivotal role in neuroinflammation, plasticity, and recovery after spinal cord injury.Episode Notes: Evolving insights on the role of microglia in neuroinflammation, plasticity, and regeneration of the injured spinal cordLeander Tables- Save $1,000 on the Series 950 Table using the code EBC2025 — their most advanced flexion-distraction tablePatient Pilot by The Smart Chiropractor is the fastest, easiest to generate weekly patient reactivations on autopilot…without spending any money on advertising. Click here to schedule a call with our team.Our members use research to GROW their practice. Are you interested in increasing your referrals? Discover the best chiropractic marketing you aren't currently using right here!

Send us a textCellular clean up by immune cells and how early-life fructose exposure leads to neurodevelopmental problems.Episode Summary: Dr. Justin Perry talks about the body's constant cellular turnover—about 3 million cells die per second in adults (double in children and women)—handled by phagocytes like macrophages that engulf and digest debris to prevent diseases like lupus. They explore phagocytosis steps, macrophage adaptations in tissues like the brain (microglia), and how high fructose intake impairs microglial function in developing mice, leading to uncleared brain cells and anxiety-like behaviors, with implications for human neurodevelopmental disorders amid rising fructose consumption.About the guest: Justin Perry, PhD is an immunologist and clinical psychologist who leads a lab at Memorial Sloan Kettering Cancer Center focusing on how the body clears dead cells and debris to maintain homeostasis.Discussion Points:The body turns over 1-2% of its 30 trillion cells daily, mostly blood cells, but neurons in kids and endometrium in women turnover at ~2x this ratePhagocytosis involves "find me," "eat me," and digestion signals; failures can cause autoimmunity.Microglia are brain macrophages that uptake fructose via GLUT5 transporter.Early high fructose exposure (comparable to one soda daily) impairs the pruning of synapses and dead neurons.In mice, prenatal or postnatal fructose causes phagocytosis deficits in the prefrontal cortex, leading to heightened fear responses and poor fear extinction, mimicking anxiety disorders.Fructose correlates with rising neurodevelopmental issues like autism and anxiety; it's passed via breast milk, and liquid forms (e.g., sodas) overwhelm metabolic shields more than solid fruits.Macrophages may hold keys to diseases from atherosclerosis to cancer; deleting GLUT5 in microglia reverses fructose's effects, hinting at evolutionary roles in aging or low-oxygen states.Related content:M&M 215: Cancer Metabolism: Sugar, Fructose, Lipids & Fasting | Gary PattiArticle | Dietary Fructose & Metabolic Health: An Evolutionary PerspectiveReference Paper:Study | Early life high fructose impairs microglial phagocytosis and neurodevelopment*Not medical advice.Support the showAffiliates: Seed Oil Scout: Find restaurants with seed oil-free options, scan food products to see what they're hiding, with this easy-to-use mobile app. KetoCitra—Ketone body BHB + electrolytes formulated for kidney health. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Code MIND for 10% off SiPhox Health—Affordable at-home blood testing. Key health markers, visualized & explained. Code TRIKOMES for a 20% discount. For all the ways you can support my efforts

Why does autoimmunity often target high functioning women? Why do so many people with autoimmune diseases also feel stuck in emotional overwhelm, exhaustion, and self-doubt? In this Biology Behind It mini episode, Dr. Aimie answers a powerful question from Maya, a therapist working with clients who have autoimmune conditions, and dives deeper into how past trauma affects the body and can lead to immune problems. Dr. Aimie breaks down how hidden stress patterns, mitochondrial damage, and emotional self-beliefs can create the perfect storm for autoimmune diseases. She shares practical ways to support healing that go beyond mindset or medication. In this epsiode, you'll discover: Why autoimmune disease is a symptom of a deeper biology of trauma How nervous system dysregulation leads to oxidative stress and mitochondrial dysfunction Why common emotional patterns like perfectionism, people-pleasing, and feeling unsafe to be authentic are linked to autoimmunity Why fatigue is the most common early sign of autoimmunity (and what's happening in your cells) The role of microglia activation in brain fog, decision fatigue, and emotional shutdown Practical tools to support nervous system healing Whether you're living with an autoimmune diagnosis or supporting someone who is, this episode will help you connect the dots between stored trauma and immune dysfunction. It gives you clear steps to start calming inflammation, restoring energy, and supporting your body's healing at the root level. 

Ever wondered why some adults struggle with anxiety, depression, or feeling overwhelmed even in safe situations? The answer might trace back to something as common as being left to cry it out as a baby. In this mini episode, Dr. Aimie dives deep into the biology behind how early childhood experiences, including seemingly normal parenting practices, can program our immune cells for danger and create lasting brain inflammation, explaining the long-term effects of crying it out on mental health. Responding to a listener's question about brain inflammation in babies, Dr. Aimie reveals what's actually happening inside tiny brains when they're left to cry it out, and how this creates the anxiety and depression we see later in life. You'll discover how your body's own biology might be perpetuating nervous system dysregulation from experiences you don't even remember. In this episode, you'll learn: How stress in early childhood creates “primed” microglia in the brain Why these primed immune cells can trigger brain inflammation, anxiety, and depression later in life The difference between stress and trauma (and why babies are especially vulnerable) Why common experiences like birth trauma, NICU stays, and “crying it out” can rewire your stress response for life The link between microglia activation, brain fog, decision fatigue, and emotional overwhelm Practical steps for healing brain inflammation from childhood trauma and calming your nervous system Whether you're working on your own healing or helping others who still feel stuck after therapy, this episode will help you understand why your body can still feel anxious and overwhelmed even when you know you're safe. Plus get simple tools to help your brain's immune system begin to heal!  

What if the autoimmune condition you're dealing with today was actually programmed into your immune system decades ago during childhood? In this mini episode, Dr. Aimie answers a listener's question about the biological mechanisms connecting early attachment trauma to autoimmunity, and most importantly, what to do about it. She goes into the biology behind how childhood fear literally programs your immune system at the cellular level, creating a biological foundation for autoimmune conditions that can emerge years or decades later, often triggered by additional stressors like accidents, infections, or major life events. You'll learn more about:  Why fear causes inflammation How early fear creates overactive brain immune cells (microglia) that cause symptoms like brain fog and decision fatigue  The three key immune system pathways that determine whether your body stays in "inflammation mode" or switches to "repair mode" Practical actions you can take to rebalance your immune system Whether you're a practitioner working with autoimmune clients or someone with your own autoimmune journey, this episode reveals the hidden biological connections between early life experiences and immune dysfunction and offers hope through practical interventions that work at the cellular level. Listen to Episode 128: How Attachment Drives Anxiety, Autoimmunity and Chronic Illness to explore the six core attachment pains and their biological impacts. Don't forget to pre-order my new book, Biology of Trauma! 

TWiN reveals that proteins travel from the blood to the brain where they are taken up by microglia, revealing a new mode of communication between the brain and the periphery. Hosts: Vincent Racaniello, Tim Cheung, and Vivianne Morrison Subscribe (free): Apple Podcasts, Google Podcasts, RSS Links for this episode MicrobeTV Discord Server Circulatory proteins taken up by brain microglia (bioRxiv) Timestamps by Jolene Ramsey. Thanks! Music is by Ronald Jenkees Send your neuroscience questions and comments to twin@microbe.tv

Microglia can have protective and also potentially harmful effects in the brain. They seem to be involved in dampening the nervous system during acute seizures – but also appear to play a role in neuronal loss and cortical thinning. Dr. Cecilie Nome spoke with Dr. Amy Brewster about the many faces of microglia and the current understanding of their role in epilepsy and seizures. Sharp Waves episodes are meant for informational purposes only, and not as clinical or medical advice.Let us know how we're doing: podcast@ilae.org.The International League Against Epilepsy is the world's preeminent association of health professionals and scientists, working toward a world where no person's life is limited by epilepsy. Visit us on Facebook, Instagram, and LinkedIn.

Send us a textEpisode Summary: Dr. Michael Wheeler talks about neuroimmune interactions, exploring how the immune system and brain communicate, particularly through the blood-brain barrier and meninges; how chronic stress and inflammation can alter brain circuits, contributing to mood disorders like depression; how drugs like psilocybin and MDMA may reduce inflammation by modulating immune cells in the meninges, offering potential therapeutic benefits.About the guest: Michael Wheeler, PhD is an Assistant Professor of Neurology at Harvard Medical School. His lab studies how immune responses influence behavior, mood disorders, and addiction.Key Conversation Points:The blood-brain barrier (BBB) is not as impermeable as once thought, allowing immune signals like cytokines to influence brain function even in healthy states.Chronic stress can weaken the BBB, increasing inflammation and affecting mood-regulating circuits, potentially contributing to depression.Microglia, the brain's resident immune cells, help maintain neural circuits by pruning synapses and regulating metabolism.Psychedelics like psilocybin and MDMA can reduce inflammation by prompting immune cells (monocytes) to leave the meninges, potentially via vascular effects.These psychedelics may act in a context-specific “window,” requiring a dysregulated tissue state to exert anti-inflammatory effects, not as broad-spectrum anti-inflammatories.Neuroinflammation may underlie some treatment-resistant depression cases, suggesting immunotherapy could complement traditional psychiatric treatments.The brain encodes peripheral immune signals, like gut inflammation, in specific circuits, which can “remember” and recreate inflammatory responses.Aging may naturally increase blood-brain barrier leakiness, heightening the brain's susceptibility to peripheral inflammation.Future research aims to explore how psychedelics influence plasticity and their potential in treating inflammation-related diseases beyond psychiatry.Related episode:M&M 2: Psilocybin, LSD, Ketamine, Inflammation & Novel Support the showAll episodes, show notes, transcripts, and more at the M&M Substack Affiliates: KetoCitra—Ketone body BHB + potassium, calcium & magnesium, formulated with kidney health in mind. Use code MIND20 for 20% off any subscription (cancel anytime) Lumen device to optimize your metabolism for weight loss or athletic performance. Use code MIND for 10% off Readwise: Organize and share what you read. 60 days FREE through link Athletic Greens: Comprehensive & convenient daily nutrition. Free 1-year supply of vitamin D with purchase. MASA Chips—delicious tortilla chips made from organic corn and grass-fed beef tallow. No seed oils or artificial ingredients. Use code MIND for 20% off For all the ways you can support my efforts

Cancer cachexia isn't just weight loss—it's a hijacking of motivation

There is a cell in the brain called the microglia which has been traditionally overlooked as a target for therapies. New research supported by ASF and @FraxAresearch suggests that altering the function of microglia in the brain may help support the development of healthy and functional connections in the brain that may be impaired in … Continue reading "Microglia as a target for new interventions"

This year's AD/PD Conference was held in Vienna, Austria from the 1st to 5th April. In this second of a two-part special we bring you highlights from the last three days of the conference. The AD/PD Conference focuses on basic science and translational and clinical research bringing New insights on disease mechanisms and etiologies, the latest findings from clinical trials, innovative outlooks on therapy and prevention and advances in diagnostic markers. In this special on-location recording our guest host Dr Isabel Castanho, Instructor the Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School talks with: Dr Emma Garland, Research Associate at The University of Sheffield. An early career researcher with a focus on Alzheimer's, and an interest in protein pathogenesis, iPSC culture and inflammation in neurodegenerative disease. Susan Rohde, PhD Student at UMC Amsterdam. Susan is a Neurobiologist interested in (healthy) brain aging and related diseases, and currently work on the Dutch 100 Plus Study. Dr Martyna Matuszyk, Research Communications Officer at the Alzheimer's Society. Supporting the charity to communicate dementia research with the public, having previously completed a PhD and Postdoc working on Alzheimer's and MND. -- Here are just a few highlights from the discussion:

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

Martin Kampmann, Ph.D., explores how CRISPR screening and induced pluripotent stem cell (iPSC) technology can uncover new insights into neurological diseases such as Alzheimer's. His lab uses CRISPR to identify genes that influence protein aggregation and cellular vulnerability, focusing on neurons, astrocytes, and microglia derived from human stem cells. Kampmann highlights the roles of mitochondria, autophagy, and other cellular pathways in disease progression, emphasizing the importance of understanding both protective and damaging processes. He also discusses the potential contributions of glial cells—especially microglia and astrocytes—to neurodegeneration, sparking ideas for therapeutic targets. Series: "Stem Cell Channel" [Health and Medicine] [Science] [Show ID: 39461]

The Development of a Cocktail of Microglia and GFAP For Easy Diagnosis - Anisha Bhasin B.S, Sarah Holguin, MBA. B.S, Joe Vargas, M.S Microglia and GFAP are distinct neural markers, typically used separately to diagnose the degree of neurological infection and injury. Microglia, a glial cell, is used in the immune response of the central nervous system. GFAP is an astrocyte marker; astrocytes provide structural support and make up the blood-brain barrier. Using the two in conjugation with one another would prove to be an efficient diagnostic tool. A cocktail was constructed with optimal titration to observe the two markers in unison. In clinical usage, it will provide an efficient diagnosis of chronic inflammatory conditions of the central nervous system. The staining was conducted in IHC and fluorescence to compare morphology and count. Due to anatomical similarities, there tends to be morphological confusion between microglia and GFAP. However, when stained in conjunction with one another, notable differences can allow for easy distinction. This is why a cocktail run with a dual staining technique would be a superior diagnostic tool in comparison to testing the two markers independently.

In this episode, we dive into the role of microglial cells, the brain's resident immune defenders, and how their chronic activation at the cellular level contributes to neurodegeneration. We'll explore the cellular mechanisms behind microglial activation, including the involvement of P2Y12 receptors and the release of pro-inflammatory cytokines like IL-1β and TNF-α. Additionally, we'll discuss how everyday environmental toxins and stressors can trigger long-term microglial activity, potentially increasing the risk of conditions like Alzheimer's. Topics: 1. Introduction - Overview: Microglia and neurodegeneration. - Environmental toxins affecting microglia. 2. Brain and Microglial Overview - Brain has neurons and glial cells. - Microglia are the brain's immune cells. - Roles: Immune defense, synaptic pruning, neuroprotection. 3. Microglial Immune Function - Constantly monitor for infection and damage. - Activated microglia perform phagocytosis. - Clear debris and maintain brain health. 4. Cellular Mechanisms of Activation - P2Y12 receptors respond to ATP/ADP. - Microglia shift from resting to activated. - Activated microglia are highly phagocytic. 5. Role in Synaptic Pruning - Microglia help in synaptic pruning. - Remove weak synapses for efficient brain circuits. 6. Microglia in Neurodegeneration - Chronic activation leads to inflammation. - Release of cytokines like IL-1β, TNF-α, IL-6. - Contributes to Alzheimer's, Parkinson's. - MHC molecules 7. Environmental Toxins and Activation - Mycotoxins cross BBB and activate microglia - Heavy metals like lead, aluminum affect neurons - Pesticides/herbicides linked to Parkinson's risk 8. Other Factors Activating Microglia - Industrial chemicals, BPA - Artificial additives, alcohol - Chronic stress 9. Conclusion - Recap: Microglial functions and overactivation. - Lifestyle factors influence microglial health. Thank you to our episode sponsors: 1. Check out ⁠⁠⁠⁠⁠⁠⁠Daily Nouri⁠⁠⁠⁠⁠⁠⁠ and use code ⁠⁠⁠⁠⁠⁠⁠CHLOE20⁠⁠⁠⁠⁠⁠⁠ for 20% off your order. 2. Check out the TruAge ⁠Biological Age Test⁠ from ⁠TruMe Labs⁠. Thanks for tuning in! Get Chloe's Book Today! "⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠75 Gut-Healing Strategies & Biohacks⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠" Follow Chloe on Instagram ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠@synthesisofwellness⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ Follow Chloe on TikTok @chloe_c_porter Visit ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠synthesisofwellness.com⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ to purchase products, subscribe to our mailing list, and more! --- Support this podcast: https://podcasters.spotify.com/pod/show/chloe-porter6/support

Immune discusses two stories of immune cells eating other cells: microglia engulfing brain neurons to shape cortical development and behavior, and mast cells trapping neutrophils to increase their functional and metabolic fitness. Hosts: Vincent Racaniello, Cindy Leifer, and Brianne Barker Subscribe (free): Apple Podcasts, RSS, email Become a patron of Immune! Links for this episode MicrobeTV Discord Server Microglia shape cortical development and behavior (Cell) Neutrophil trapping by mast cells (Cell) Time stamps by Jolene. Thanks! Music by Steve Neal. Immune logo image by Blausen Medical Send your immunology questions and comments to immune@microbe.tv

References FASEB J .2008. 22:2541-2551 Nat Commun. 2023 Jul 7;14(1):4029. Seminars in Cell & Developmental Biology.2015. Volume 40, April : 115-126 CHIRALITY. 2023. Volume35, Issue9 September:577-585 Lake, G . 1972. "From theBeginning". Trilogy.lp ELP. Begihttps://open.spotify.com/track/1rw12PalmC8IDoygHT3fm1?si=535ae4023d064b16 Telemann, GP. 1720-1740. Various Concertos. https://open.spotify.com/album/1KYduuF73q2mCqoeEWmpw9?si=pNd2NVG1Sbu_B_z8vbQalA --- Support this podcast: https://podcasters.spotify.com/pod/show/dr-daniel-j-guerra/support