Podcasts about demyelination

Renee improved CIDP, gastroparesis, anxiety, depression, migraines, eczema, and perimenopausal symptoms. Instagram: @eatingmeattowalk YouTube: @eatingmeattowalk  Timestamps: 00:00 Trailer 01:14 Introduction 05:34 Overcoming setbacks with IVIG treatment 09:53 Healing with carnivore diet 13:36 Medication weaning and lifestyle changes 15:12 Drug company influence and desperation 18:22 Normal EMG results discussion 21:38 Diet regret: harmed husband's health 26:09 Choosing health over heart risk 29:11 Reevaluating veganism and health 30:16 Veganism and misdiagnosed grip issues 34:16 Oncology: a revolving door experience 36:50 Struggles with suicide and anxiety 40:41 Vaccination experience and COVID challenges 44:54 Demyelination and nerve recovery process 48:31 Carnivore diet for chronic illness 51:57 Diagnostics beyond MRIs 52:51 Where to find Renee Join Revero now to regain your health: https://revero.com/YT Revero.com is an online medical clinic for treating chronic diseases with this root-cause approach of nutrition therapy. You can get access to medical providers, personalized nutrition therapy, biomarker tracking, lab testing, ongoing clinical care, and daily coaching. You will also learn everything you need with educational videos, hundreds of recipes, and articles to make this easy for you. Join the Revero team (medical providers, etc): https://revero.com/jobs ‪#Revero #ReveroHealth #shawnbaker  #Carnivorediet #MeatHeals #AnimalBased #ZeroCarb #DietCoach  #FatAdapted #Carnivore #sugarfree Disclaimer: The content on this channel is not medical advice. Please consult your healthcare provider.

The spinal cord serves as the main communication highway between the brain and body. Did you know that 80% of people with multiple sclerosis have spinal cord lesions on MRI? These lesions can disrupt specific neural pathways, leading to common MS symptoms like numbness, weakness, impaired coordination, balance issues, bladder problems, constipation, and sexual dysfunction. For instance, damage to the corticospinal tract on one side of the spinal cord can weaken an arm or leg. A remarkable autopsy study revealed that nearly 90% of people with MS still had active inflammation in the spinal cord. This finding brings new hope for potential treatments, even for older and progressive MS patients. Advances in imaging technology, including more powerful MRI scanners (3 Tesla and higher), are enhancing our ability to see inside the spinal cord, which is as thin as a pinky finger. Improved spinal cord imaging is driving the development of new therapies in clinical trials and helping identify those at risk for worsening disability, ultimately guiding better treatment decisions. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Gabriele De Luca MD DPhil, Professor of Clinical Neurology and Experimental Neuropathology, University of Oxford, United Kingdom Bruce Cree MD PhD, Professor of Neurology at University of California, San Francisco School of Medicine

Roger Seheult, MD of MedCram discusses, the pathophysiology of hypovolemic hyponatremia, and the pitfalls of replenishing sodium too quickly. See all Dr. Seheult's videos at: https://www.medcram.com/ (This video was recorded on May 30th, 2024) Roger Seheult, MD is the co-founder and lead professor at https://www.medcram.com He is Board Certified in Internal Medicine, Pulmonary Disease, Critical Care, and Sleep Medicine and an Associate Professor at the University of California, Riverside School of Medicine. MEDCRAM WORKS WITH MEDICAL PROGRAMS AND HOSPITALS: MedCram offers group discounts for students and medical programs, hospitals, and other institutions. Contact us at customers@medcram.com if you are interested. MEDIA CONTACT: Media Contact: customers@medcram.com Media contact info: https://www.medcram.com/pages/media-contact Video Produced by Kyle Allred FOLLOW US ON SOCIAL MEDIA: https://www.facebook.com/MedCram https://twitter.com/MedCramVideos https://www.instagram.com/medcram DISCLAIMER: MedCram medical videos are for medical education and exam preparation, and NOT intended to replace recommendations from your doctor. #hyponatremia #sodium #ods

Alexis Martinez first appeared on TOSP in Episode 71. She shared what it was like for her to manage her own MS and care for her mother who has early onset Alzheimers. This time we discussed her new job and how taking on something new has impacted her daily life and self-worth. Now that I've gotten to meet Alexis in person, it no longer felt like an interview. It was more like catching up with my friend.    Instagram: @itsallinmyhead Instagram: @thrivingoversurvivingpodcast https://thrivingoversurvivingpodcast.com  

Alexis Martinez first appeared on TOSP in Episode 71. She shared what it was like for her to manage her own MS and care for her mother who has early onset Alzheimers. This time we discussed her new job and how taking on something new has impacted her daily life and self-worth. Now that I've gotten to meet Alexis in person, it no longer felt like an interview. It was more like catching up with my friend.    Instagram: @itsallinmyhead Instagram: @thrivingoversurvivingpodcast https://thrivingoversurvivingpodcast.com  

Yes, children can get multiple sclerosis. Children ages 12 and up are more typically affected and rarely before age 8. Awareness is essential for prompt diagnosis and treatment of pediatric-onset MS (POMS). Accurate diagnosis of multiple sclerosis in children requires screening for other conditions like MOG antibody-associated disease (MOGAD). Risk factors associated with higher rates of developing MS in kids include Epstein-Barr virus infection, genetic susceptibility, pesticide exposure, smoking (and secondhand smoke), low vitamin D, obesity and diet high in saturated fats. Multiple sclerosis in kids can be very active with frequent relapses and concerning MRI activity kids. Rapid use of highly effective treatment is important to preserve brain health including cognition. Completed and ongoing global pediatric trials are redefining care. Oral fingolimod, for example, reduced relapses by 82% compared to interferon beta-1a injections weekly. Thanks to treatment advancements, teens living with MS have a brighter future ahead of them. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews Brenda Banwell MD, Chief of the Division of Neurology at the Children's Hospital of Philadelphia (CHOP) and Emmanuelle Waubant MD, PhD, Professor of Neurology , University of California San Francisco and Director of the UCSF Regional Pediatric Multiple Sclerosis Center.

Today we have a special guest, Dr. Joel Topf, board-certified nephrologist and medical educator extraordinaire. Our listeners will likely recognize Dr. Topf from his prolific tweeting @Kidney_boy, as well as his numerous appearances on the Curbsiders podcast. He is a co-founder of the NephJC on Twitter, and host and founder of the NephJC podcast Freely Filtered. He is also host of the podcast Channel Your Enthusiasm, a deep dive monthly recap of the nephrology textbook Clinical Physiology of Acid Base and Electrolyte Disorders by Dr. Burton Rose (who, incidentally, is the creator of the original UpToDate). Dr. Topf wrote his own book on fluids, electrolytes and acid-base homeostasis.  He's the co-editor for the fourth edition of Nephrology Secrets and the first edition of The Handbook of Critical Care Nephrology. Dr. Topf joined us to talk about a new paper he co-authored on osmotic demyelination syndrome and hyponatremia. I'm also joined by Dr. Mita Hoppenfeld, hospitalist at the University of Utah, to talk about a new DOAC vs warfarin trial in On-X aortic valves, whether it's better to avoid hypertension or hypotension around time of surgery, and the diagnostic accuracy of CT abdomen scans without contrast. Check it out! Osmotic Demyelination and HyponatremiaApixaban vs Warfarin for On-X Aortic ValvePerioperative Blood Pressure Strategies Diagnostic Accuracy of CT Abdomen Without ContrastMusic from Uppbeat (free for Creators!):https://uppbeat.io/t/soundroll/dopeLicense code: NP8HLP5WKGKXFW2R

Danielle Baker was an active RN (Certified Hospice and Palliative Care) for 20 years and loved her job. Within 2.5 weeks after her last shot, she became completely disabled, suffering from severe neurological issues, demyelination of the spine, and getting the diagnosis of transverse myelitis, which her doctor confirmed was due to the Pfizer jab. Since then, Danielle has been unable to work as she has difficulty completing simple tasks such as walking and self-care. However, she has a beautiful light around her as she continues to fight to find joy and happiness. Here's her testimony to the FDA VRBPAC in January: https://rumble.com/v278u5a-heart-wrenching-testimony-danielle-baker-presentation-at-the-fda-vrbpac-mee.html This is her GiveSendGo: https://www.givesendgo.com/G9KZJPlease visit React 19's website for more information on how to help these incredible people.Please text REACT to 50155 to donate via text

Episode 9! In this episode we step a little out of our comfort zone to talk about a couple of analyses which caught our interest recently: 1) "Comparative Effectiveness of Fludrocortisone and Hydrocortisone vs Hydrocortisone Alone Among Patients With Septic Shock" published  by Bosch et al March 2023 in JAMA Internal Medicine2) "Osmotic Demyelination Syndrome in Patients Hospitalized with Hyponatremia" published by MacMillan et al March 2023 in NEJM EvidenceFludrocortisone: https://pubmed.ncbi.nlm.nih.gov/36972033/COIITSS: https://pubmed.ncbi.nlm.nih.gov/20103758/ODM: https://evidence.nejm.org/doi/full/10.1056/EVIDoa2200215ODM Editorial: https://evidence.nejm.org/doi/full/10.1056/EVIDe2300014If you enjoy the podcast please share on social media or by word of mouth! Thank you!Be sure to follow us on the social @icucast for the associated figures, comments, and other content not available in the audio format! Email us at icuedandtoddcast@gmail.com with any questions or suggestions! Thank you Mike Gannon for the intro and exit music!

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.12.536631v1?rss=1 Authors: Taherzadeh, M., Zhang, E., Londono, I., Song, S.-K., Wang, S., Cooper, J. D., Kennedy, T. E., Morales, C. R., Chen, Z., Lodygensky, G. A., Pshezhetsky, A. V. Abstract: Neurodegeneration and chronic progressive neuroinflammation are well-documented in neurological lysosomal storage diseases, including Sanfilippo disease or mucopolysaccharidosis III (MPS III). Since chronic neuroinflammation has been linked to white matter tract pathology and defects in axonal transmission, we analysed axonal myelination and white matter density in the mouse model of MPS IIIC and human post-mortem brain samples from MPS IIIA, C, and D patients. Analyses of corpus callosum (CC) and spinal cord tissues by immunohistochemistry revealed substantially reduced levels of myelin-associated proteins including Myelin Basic Protein, Myelin Associated Glycoprotein, and Myelin Oligodendrocyte Glycoprotein. Furthermore, ultrastructural analyses revealed disruption of myelin sheath organization and reduced myelin thickness in the brains of MPS IIIC mice and human MPS IIIC patients compared to healthy controls. Oligodendrocytes (OLs) in the CC of MPS IIIC mice were scarce, while examination of the remaining cells revealed numerous enlarged lysosomes containing heparan sulfate, GM3 ganglioside or "zebra bodies" consistent with accumulation of lipids and myelin fragments. In addition, OLs contained swollen mitochondria with largely dissolved cristae, resembling those previously identified in the dysfunctional neurons of MPS IIIC mice. When brains of 7-month-old MPS IIIC mice were analysed by ex-vivo Diffusion Basis Spectrum Imaging to assess microarchitectural changes in the corpus callosum, we found compelling signs of demyelination (26% increase in radial diffusivity) and tissue loss (76% increase in hindered diffusivity). Our findings demonstrate an import role for white matter injury in the pathophysiology of MPS III. Moreover, this study reveals specific parameters and brain regions for MRI analysis, a crucial non-invasive method to evaluate disease progression and therapeutic response in neurological lysosomal storage diseases. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Did you know that over 7000 people in the UK are diagnosed with multiple sclerosis (MS) every year? And recent estimates suggest there are 2.8 million sufferers worldwide, yet it remains unclear what the cause of MS is, and there is no effective cure currently. In today's episode, you will learn more about the functional medicine approach in managing symptoms of MS. Highlights from today's episode include:The leading causes of MS. Viruses as a cause of MS and molecular mimicry.Demyelination and the blood-brain barrier.Diet for MS. Vital nutrients for MS.Functional testing for multiple sclerosis. You can also read my article, 'Is EBV the leading cause of MS'.You can learn more about the MS study with epsilon toxin here. And if you would like to win a free organic acid test, please be sure to follow the instructions at the end of the podcast and send your snapshot to victoria@theautoimmunitynutritionist.comTune in today and be sure to share any of your thoughts about the show on my Instagram page: @theautoimmunitynutritionistYou can also download a free copy of The Autoimmunity Recovery Plan here.Book your free discovery call with me here.And if you would like to join my community of strong-willed people thriving with autoimmune disease, join The Autoimmunity Community. Thanks for listening! You can join The Autoimmunity Community on Facebook or find me on Instagram @theautoimmunitynutritionist Thanks for listening! You can join The Autoimmunity Community on Facebook or find me on Instagram @theautoimmunitynutritionist.

In today's Friday 5, I am sharing five root causes of demyelination.Multiple sclerosis is one of the most common demyelinating diseases, where your immune system attacks the myelin sheath or the cells responsible for maintaining it, which results in inflammation and injury to the sheath leading to symptoms. Early signs of demyelination include loss of vision, fatigue, bladder problems and nerve pain. Then the effect on the nerves can lead to a racing heartbeat, numbness, mobility issues, dizziness and many more. In multiple sclerosis, these symptoms often arise during a 'relapse' in relapsing-remitting MS (RRMS) or progressively worsen in progressive MS. As well as inflammatory demyelination, you can also experience myelin damage from liver damage, alcoholism, electrolyte imbalances and infections. And damage to myelin may also occur when the cells are starved of oxygen, which can happen when there is a lack of blood flow to specific areas in the brain and spinal cord. Highlights from today's episode include:Vitamin deficiencies and how they contribute to demyelination.Hypoxia and lack of blood flow can lead to demyelination.The role of toxins in the development of demyelination. How an autoimmune process can develop into multiple sclerosis, including cross-reactivity and diet.Tune in today and be sure to share any of your thoughts about the show on my Instagram page: @theautoimmunitynutritionistYou can read about Epstein-Barr virus (EBV) and multiple sclerosis here.  You can also download a free copy of The Autoimmunity Recovery Plan here.Book your free discovery call with me here.And if you would like to join my community of strong-willed people thriving with autoimmune disease, join The Autoimmunity Community. Thanks for listening! You can join The Autoimmunity Community on Facebook or find me on Instagram @theautoimmunitynutritionist.

In this episode, we review the high-yield topic of Osmotic Demyelination Syndrome (ODS) from the Neurology section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.24.525450v1?rss=1 Authors: Qiu, X., Ping, S., Kyle, M., Chin, L., Zhao, L.-R. Abstract: Severe traumatic brain injury (TBI) causes long-term disability and death in young adults. White matter is vulnerable to TBI damage. Demyelination is a major pathological change of white matter injury after TBI. Demyelination which is characterized by myelin sheath disruption and oligodendrocyte cell death leads to long-term neurological function deficits. Stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) treatments have shown neuroprotective and neurorestorative effects in the subacute and chronic phases of experimental TBI. Our previous study has revealed that combined SCF and G-CSF treatment (SCF+G-CSF) enhances myelin repair in the chronic phase of TBI. However, the long-term effect and mechanism of SCF+G-CSF-enhanced myelin repair remain unclear. In this study, we uncovered persistent and progressive myelin loss in the chronic phase of severe TBI. SCF+G-CSF treatment in the chronic phase of severe TBI enhanced remyelination in the ipsilateral external capsule and striatum. The SCF+G-CSF-enhanced myelin repair is positively correlated with the proliferation of oligodendrocyte progenitor cells in the subventricular zone. These findings reveal the therapeutic potential of SCF+G-CSF in myelin repair in the chronic phase of severe TBI and shed light on the mechanism underlying SCF+G-CSF- enhanced remyelination in chronic TBI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Welcome back to our weekend Cabral HouseCall shows! This is where we answer our community's wellness, weight loss, and anti-aging questions to help people get back on track! Check out today's questions:    Eilise: Hello Dr. Cabral, My 9 year old daughter has suffered greatly most of her life from chronic stomach pains, switching between constipation and diarrhea. She has Hyper mobility in her arms and hips, has cold hands, often feels itchy without there being any visible rash. Has very bad eyesight, thin, brittle, slow growing hair and can't gain weight. She is 40th percentile in height and 2 percentile in weight. I've been on a wait list to see a geneticist for possible ehlers-Danlos syndrome. It seems very likely that she has ehlers-Danlos and possibly some accompanying issues. We eat organic and gluten free, grass fed beef, Ive tried giving her liver capsules, omega 3's, cod liver oil, digestive enzymes, and even c60 to try and help get her as much nutrients as possible but she goes through periods of time where her stomach hurts so much she can't take them. I desperately need help to figure out what I am missing to relieve her pain and help her be able to improve her digestion and absorption of food so she can heal. Do you have recommendations for how to manage the symptoms of ehlers Danlos to improve her quality of life? Thank you for all the work you've done to help people in need. Looking forward to hearing from you. Sincerely, Eilise    Anna: Hello Dr. Cabral, I´ve just read your book and I thought it was very interesting and eyeopening. My son is 20 years old, we live in Holland, and he was born pre-mature and dismature. He´s had an eatingproblem the first 3 years and a lot of ear infections. He now wears hearing aids. I also recognised myself in your comments that you felt you never got answers at the several hospitals. My son, first discovered when he was four years old, has also numerous calcifications in his muscles. He is fairly healthy, can do sports, but it does trouble him and the calfifications in his feet are often inflamed if he does too much. Up to now, they only take blood tests, urine tests and occasional photo's. They haven´t seen a simmilar case in Holland and I find it difficult they can tell me so little. Can these calsifications be auto-immune related? Do you have any idea what could cause them? Thank you for now for all I´ve learned up to this point.   Carl: I have a sluggish (low) metabolism. Every morning I wake up feeling shaky. My morning blood sugar can be anywhere between 85-115. My morning blood pressure is 150's/100's. As the day goes on, it gets better. Every time I try to go on a diet and cut out the crap (mostly carbs) I feel shaky all day and the blood pressure stays elevated all day. even though blood sugar is fine. I realize this is most likely a Cortisol issue. I do have Candida issues/through lab testing. How can I get enough good carbs to lose weight, yet keep my metabolism up, BP low and keep Cortisol normal? Thanks, Carl   Tiffany: Hello Dr. Cabral. I am a daily listener to your podcast as I try to incorporate what I can into better healthy lifestyle for me and my family. We really appreciate it. My son is 16 and we started noticing that one of his hands shakes. I was distracted by it the other day as he was talking to me so it is noticeable. He is a healthy strong guy (6ft tall). Does pole vaulting and lifts and cardio. Not anxious or really stressed. Eats fairly good. He does not eat a lot of sugar or sweets. Can you give me some ideas to look at to help him with this? I'm not sure where to start for him. It has been going on for several months but seems to be getting more noticeable. Thanks so much   Joesph: I'll try to make the long story as short as possible: my wife has well controlled diabetes, however in the past five years she has developed complete numbness in her feet, calves, and it has now spread to her hands. Additionally, she has nearly constant muscle fasciculations, with occasional painful cramping. We know it's demyelination but no one knows why it's occurring. She has had every test available and everything shows she is the picture of health (aside from diabetes). She has had tests for tropical disease, other exotic diseases, genetic testing, you name it she had the test. She's even been to the Cleveland Clinic multiple times. Recently she had a spinal tap which also showed nothing wrong; however, it did show 3 oligoclonal bands found in both the cerebral spinal fluid and the serum. Analysis of this was basically “something autoimmune”. On a side note, her spleen occassionaly swells so much you can see it pushing against her skin. We are at our wits end, and she has said that she's not doing anything else, she's been through enough. Can you help us try to find the right path to heal her?   Jade: Hi. Dr Cabral. Thank you for sharing all your knowledge with us. Truly a blessing! I am 57 years old. I have fibromyalgia, IBS, silent reflux and Gilbert's syndrome. I suffer daily with chronic fatigue, severe stomache issues (everything I eat hurts my stomache…gas, bloating, cramping, and loose stools) anxiety, whole body pain and trouble sleeping. Oh, and my cholesterol is high. I've also had EBV in the past. I'm always in fight or flight mode. I worked full time for 30 years in a very stressful workplace and I've always felt drained. I have gone though a lot of emotional trauma in the last few months. Which has made everything worse. I do eat very clean and healthy. No processed junk at all. Everything's organic. I pray and meditate daily. I walk when I'm not in a flare up and I do yoga. CBD oil seems to help but I'm not sure if that will cause more problems with the Gilbert's so I've stopped it until I know if it's ok to continue with it. What do you suggest for me? I can't afford your 1 on 1 consultations but I will do whatever else you recommend. Thank you to you and your team for all that you do!!!   Thank you for tuning into today's Cabral HouseCall and be sure to check back tomorrow where we answer more of our community's questions!    - - - Show Notes and Resources: StephenCabral.com/2486 - - - Get a FREE Copy of Dr. Cabral's Book: The Rain Barrel Effect - - - Join the Community & Get Your Questions Answered: CabralSupportGroup.com - - - Dr. Cabral's Most Popular At-Home Lab Tests: > Complete Minerals & Metals Test (Test for mineral imbalances & heavy metal toxicity) - - - > Complete Candida, Metabolic & Vitamins Test (Test for 75 biomarkers including yeast & bacterial gut overgrowth, as well as vitamin levels) - - - > Complete Stress, Mood & Metabolism Test (Discover your complete thyroid, adrenal, hormone, vitamin D & insulin levels) - - - > Complete Food Sensitivity Test (Find out your hidden food sensitivities) - - - > Complete Omega-3 & Inflammation Test (Discover your levels of inflammation related to your omega-6 to omega-3 levels) - - - Get Your Question Answered On An Upcoming HouseCall: StephenCabral.com/askcabral - - - Would You Take 30 Seconds To Rate & Review The Cabral Concept? 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Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.22.517543v1?rss=1 Authors: Gallups, N. J., Childers, G. M., Webster, J. M., Yang, Y.-T., Zane, A., Mudium, N., Manfredsson, F., Kordower, J., Harms, A. S. Abstract: Multiple system atrophy (MSA) is a rare and fatal synucleinopathy characterized by insoluble alpha-synuclein (-syn) cytoplasmic inclusions located within oligodendroglia. Neuroinflammation, demyelination, and neurodegeneration are correlated with areas of GCI pathology, however it is not known what specifically drives disease pathogenesis. Recently in a mouse model of MSA, CD4+ T cells have been shown to drive neuroinflammation and demyelination, however the mechanism by which this occurs also remains unclear. In this study we use genetic and pharmacological approaches in a novel model of MSA to show that the pro-inflammatory cytokine interferon gamma (IFN{gamma}) drives neuroinflammation and demyelination. Furthermore, using an IFN{gamma} reporter mouse, we found that infiltrating CD4+ T cells were the primary producers of IFN{gamma} in response to -syn overexpression in oligodendrocytes. Results from these studies indicate that IFN{gamma} expression in CD4 T cells drives -syn-mediated neuroinflammation and demyelination, and strategies to target IFN{gamma} expression may be a potential disease modifying therapeutic strategy for MSA. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

It's flu season and that makes it an excellent time to talk about vaccines. People living with MS often have questions about whether a particular vaccine is good for them or whether it might carry with it the risk of a relapse or other negative health consequence. Dr. Lisa Doggett joins me to brief us on all things related to vaccines and MS. Dr. Doggett is a family doctor as well as the Senior Medical Director at HGS AxisPoint Health. She was a 2021-2022 American Academy of Family Physicians Vaccine Science Fellow, and Dr. Doggett has lived with MS since being diagnosed in 2009. I'm also sharing my major take-away from the 2022 National Conference on Caregiving Research. And, speaking of caregiving, we'll review the results of a study that measured the risk of family caregivers experiencing future illness and disability. You're going to want to hear the results of a study that measured the effects of a keto diet on people living with MS. And we'll tell you what researchers learned when they analyzed the effect of autologous hematopoietic stem cell transplantation (aHSCT) on tissue damage in the central nervous system (And we'll explain why that may be really important!). We have a lot to talk about! Are you ready for RealTalk MS??! This Week: Vaccines and MS  :22 Caregiving as a social determinant of health  1:37 Family caregivers carry a significantly higher risk of future illness and disability   5:52 The effects of a ketogenic diet on people living with MS  8:57 The impact of autologous hematopoietic stem cell therapy (aHSCT) on tissue damage in the central nervous system   11:49 Dr. Lisa Doggett discusses which vaccines are important for people living with MS, and which vaccines should be avoided  17:30 Share this episode  33:23 Download the RealTalk MS app for your iOS or Android device   33:44 SHARE THIS EPISODE OF REALTALK MS Just copy this link & paste it into your text or email: https://realtalkms.com/267 ADD YOUR VOICE TO THE CONVERSATION I've always thought about the RealTalk MS podcast as a conversation. And this is your opportunity to join the conversation by sharing your feedback, questions, and suggestions for topics that we can discuss in future podcast episodes. Please shoot me an email or call the RealTalk MS Listener Hotline and share your thoughts! Email: jon@realtalkms.com Phone: (310) 526-2283 And don't forget to join us in the RealTalk MS Facebook group! LINKS If your podcast app doesn't allow you to click on these links, you'll find them in the show notes in the RealTalk MS app or at www.RealTalkMS.com National MS Society COVID-19 Vaccine Guidance for People Living with MS https://www.nationalmssociety.org/coronavirus-covid-19-information/multiple-sclerosis-and-coronavirus/covid-19-vaccine-guidance The National Strategy to Support Family Caregivers https://acl.gov/CaregiverStrategy STUDY: Caregiving and Allostatic Load Predict Future Illness and Disability: A Population-Based Study https://www.sciencedirect.com/science/article/pii/S2666354621000983 STUDY: Phase II Study of Ketogenic Diets in Relapsing Multiple Sclerosis: Safety, Tolerability, and Potential Clinical Benefits https://pubmed.ncbi.nlm.nih.gov/35418509 STUDY: Biomarkers of Demyelination and Axonal Damage are Decreased After Autologous Hematopoietic Stem Cell Transplantation for Multiple Sclerosis https://www.msard-journal.com/article/S2211-0348(22)00715-5/fulltext Join the RealTalk MS Facebook Group https://facebook.com/groups/realtalkms Download the RealTalk MS App for iOS Devices https://itunes.apple.com/us/app/realtalk-ms/id1436917200 Download the RealTalk MS App for Android Deviceshttps://play.google.com/store/apps/details?id=tv.wizzard.android.realtalk Give RealTalk MS a rating and review http://www.realtalkms.com/review Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 267 Guest: Dr. Lisa Doggett Tags: MS, MultipleSclerosis, MSResearch, MSSociety, RealTalkMS Privacy Policy

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.09.15.508082v1?rss=1 Authors: McKie, S. J., Nicholson, A. S., Smith, E., Fawke, S., Caroe, E., Williamson, J. C., Butt, B. G., Kolarov, D., Peterka, O., Holcapek, M., Lehner, P. J., Graham, S. C., Deane, J. E. Abstract: Myelin is a multi-layered membrane that tightly wraps neuronal axons enabling efficient, high-speed signal propagation. The axon and myelin sheath form tight contacts, mediated by specific plasma membrane proteins and lipids, and disruption of these contacts causes devastating demyelinating diseases. Using two cell-based models of demyelinating sphingolipidoses, we demonstrate that altered lipid metabolism changes the abundance of specific plasma membrane proteins. These altered membrane proteins have known roles in cell adhesion and signalling, with several implicated in neurological diseases. The cell surface abundance of the adhesion molecule Neurofascin, a protein critical for the maintenance of myelin-axon contacts, changes following disruption to sphingolipid metabolism. This provides a direct molecular link between altered lipid abundance and myelin stability. We show that the Neurofascin isoform NF155, but not NF186, interacts directly and specifically with the sphingolipid sulfatide via multiple binding sites and that this interaction requires the full-length extracellular domain of NF155. We demonstrate that NF155 adopts an S-shaped conformation and preferrentially binds sulfatide-containing membranes in cis, with important implications for protein arrangement in the tight axon-myelin space. Our work links glycosphingolipid imbalances to disturbance of membrane protein abundance and demonstrates how this may be driven by direct protein-lipid interactions, providing a mechanistic framework to understand the pathogenesis of galactosphingolipidoses. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

July 2022The papers behind the pod: Ferreira DA et al. (2021). Alternative to Soft Lithography for the Fabrication of Organ-on-a-Chip Elastomeric-Based Devices and Microactuators. Advanced Science 8:2003273. https://doi.org/10.1002/advs.202003273Eigel D et al. (2019). Cryogel scaffolds for regionally constrained delivery of lysophosphatidylcholine to central nervous system slice cultures: A model of focal demyelination for multiple sclerosis research. Acta Biomaterialia 97:216. https://doi.org/10.1016/j.actbio.2019.08.030It's the third Thursday of July, and you're listening to 3 Minute 3Rs, your monthly recap of efforts to replace, reduce, and refine the use of animals in research. This month, we've got a special double feature highlighting the publications commended in the International 3Rs Prize, awarded by the NC3Rs and sponsored by GSK. Follow this link for the full transcript: https://nc3rs.org.uk/3-minute-3rs-podcast-july-2022-transcript See acast.com/privacy for privacy and opt-out information.

episode 8talking about Covid-19 Demyelination in journal of neuroimmunologyDOI of  study:10.1016/j.jneuroim.2021.577765https://www.sciencedirect.com/science/article/pii/S0165572821002927thanks' Nano Alvand Co. for sponsorship MScasthttps://www.nanoalvand.com/

Dr. Pearce Korb discusses the long-term outcomes of osmotic demyelination syndrome in an updated cohort with Dr. Whitney Fitts.

In the first part of the podcast, Dr. Alberto Espay talks with Prof. Julian Gillmore about CRISPR-Cas9 in vivo gene editing for transthyretin amyloidosis. In the second segment, Dr. Pearce Korb discusses the long-term outcomes of osmotic demyelination syndrome in an updated cohort with Dr. Whitney Fitts.

Dr. Rani Banik is an integrative neuro-ophthalmologist. She focuses on both western and holistic medicine. She joins me for the first of three episodes focusing on brain and eye health. In this episode, Dr. Banik shares her insights about Optic Neuritis; causes, triggers, and how to prevent future occurrences.  More about Dr. Banik: Her practice promotes an integrative approach to vision and brain health that incorporates nutrition botanicals supplements and lifestyle modification, along with traditional western medical therapies. Instagram: @dr.ranibanik Facebook Groups: Eye on Migrain & EnVision Health Sign up for my weekly newsletter beginning in October www.thrivingoversurvivingpodcast.com Instagram: @thrivingoversurvivingpodcast

Dr. Rani Banik is an integrative neuro-ophthalmologist. She focuses on both western and holistic medicine. She joins me for the first of three episodes focusing on brain and eye health. In this episode, Dr. Banik shares her insights about Optic Neuritis; causes, triggers, and how to prevent future occurrences.  More about Dr. Banik: Her practice promotes an integrative approach to vision and brain health that incorporates nutrition botanicals supplements and lifestyle modification, along with traditional western medical therapies. Instagram: @dr.ranibanik Facebook Groups: Eye on Migrain & EnVision Health Sign up for my weekly newsletter beginning in October www.thrivingoversurvivingpodcast.com Instagram: @thrivingoversurvivingpodcast

Brain toxicity: What does it look like?Symptoms of brain toxicity:FatigueMoodinessMemory problemsDifficulty focusing (ADD/ADHD)Speech/language problems (Autism)Mood disorders (OCD, depression, etc.)Stiff, uncoordinated muscles (Demyelination. More severely: Multiple sclerosis, ALS, or other diseases)Neurodegenerative diseases (such as Dementia/Alzheimers)Do you experience any of those symptoms?Let's go over the physiology: how we intake toxins, how we absorb them, and ways that our bodies struggle to excrete them.I also share six things you can do to begin healing!Of the things I want to share, one is a freebie: MEDITATION!While meditation won't cure a condition, it is a powerful tool to use in reducing brain toxicity!Are you ready to dive into today's episode? Let's get started!Other episodes mentioned in this episode:Sleep and the gut - Ep. 42// 6 Secrets Your Sleep Can Tell You About Your GutFind a chiropractor - Ep. 36// How to Choose The Best Chiropractor with Dr. Zach Simkins and Dr. Tygue ArvidsonStomach acid test - Ep. 40// Reduce Acid Reflux with the Magic Power of ZincCST/VM - Ep. 05 // Two Treatments for IBS That You Probably Have Never Heard OfFood sensitivities - Ep. 14// #1 Lie About Food That I Hate!Next week's episode on meditation!Other links from the show:To find your own Craniosacral Therapist, Google or head to IAHP “Find a Practitioner”Schedule Your Qualifying Call with AllisonConnect with us on social media!Facebook: @betterbellytherapiesInstagram: @betterbellytherapiesWebsite: betterbellytherapies.com*This episode was first published at BetterBellyTherapies.com/podcast/43.

Brain toxicity: What does it look like?Symptoms of brain toxicity:FatigueMoodinessMemory problemsDifficulty focusing (ADD/ADHD)Speech/language problems (Autism)Mood disorders (OCD, depression, etc.)Stiff, uncoordinated muscles (Demyelination. More severely: Multiple sclerosis, ALS, or other diseases)Neurodegenerative diseases (such as Dementia/Alzheimers)Do you experience any of those symptoms?Let's go over the physiology: how we intake toxins, how we absorb them, and ways that our bodies struggle to excrete them.I also share six things you can do to begin healing!Of the things I want to share, one is a freebie: MEDITATION!While meditation won't cure a condition, it is a powerful tool to use in reducing brain toxicity!Are you ready to dive into today's episode? Let's get started!Other episodes mentioned in this episode:Sleep and the gut - Ep. 42// 6 Secrets Your Sleep Can Tell You About Your GutFind a chiropractor - Ep. 36// How to Choose The Best Chiropractor with Dr. Zach Simkins and Dr. Tygue ArvidsonStomach acid test - Ep. 40// Reduce Acid Reflux with the Magic Power of ZincCST/VM - Ep. 05 // Two Treatments for IBS That You Probably Have Never Heard OfFood sensitivities - Ep. 14// #1 Lie About Food That I Hate!Next week's episode on meditation!Other links from the show:To find your own Craniosacral Therapist, Google or head to IAHP “Find a Practitioner”Schedule Your Qualifying Call with AllisonConnect with us on social media!Facebook: @betterbellytherapiesInstagram: @betterbellytherapiesWebsite: betterbellytherapies.com*This episode was first published at BetterBellyTherapies.com/podcast/43.

Cutting-edge research is revolutionizing how multiple sclerosis is diagnosed and monitored. The central vein sign on MRI may soon be a key way of confirming if someone has multiple sclerosis versus other conditions such as migraine, vasculitis, neurosarcoidosis and blockage of small blood vessels (from age, smoking and hypertension). Early clues on MRI imaging are shared in people with evidence of MS prior to developing symptoms (called radiologically isolated syndrome or RIS). New imaging techniques in development visualize changes in progressive multiple sclerosis like slowly-expanding lesions and inflammatory cells called microglia. Dr. Daniel Reich from the NIH covers additional topics from routine MRI monitoring of the brain and spinal cord to remyelination imaging. With incredible medical advances, some people that were considered to have multiple sclerosis are now diagnosed with neuromyelitis optica (NMO) and MOG Antibody Disease (MOGAD). Dr. Sean Pittock from Mayo Clinic shares how NMO and MOGAD are different from multiple sclerosis and reviews the alternate approaches to treatment including the 3 FDA-approved treatments for NMO, Soliris (eculizumab), Uplinza (inebilizumab) and Enspyrng (satralizumab). Latest research in screening spinal fluid and blood for clues of multiple sclerosis discussed to improve diagnosis and monitoring of the disease. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Daniel Reich MD PhD is the Chief of the Translational Neuroradiology Section of the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health (NIH). He obtained his undergraduate degree in math and physics at Yale, PhD in neuroscience at The Rockefeller University and MD degree at Cornell. Dr. Reich completed residencies in both neurology and diagnostic radiology and a neuroradiology fellowship at John Hopkins Hospital. Sean Pittock MD is a Professor of Neurology at Mayo Clinic. His is the Director of Mayo Clinic's Center for Multiple Sclerosis and Autoimmune Neurology and Director of Mayo's Neuroimmunology Research Laboratory. He earned his medical degree from University College Dublin, post-doctoral degree at the Royal College of Surgeons in Ireland followed by residency and fellowship at Mayo Clinic in Rochester, Minnesota. Visit www.mslivingwell.org for more information. Share your MS story on https://ICanWithMS.org

Multiple sclerosis (MS) is a debilitating autoimmune disease in which immune cells infiltrate the central nervous system and attack the myelin sheath surrounding axons.  Dr. Simons explains that myelin is necessary for signal conduction by nerve cells and for the metabolic support of axons. Demyelination results in axonal loss and formation of lesions in the brain. A small percentage of MS lesions are capable of remyelination following steps similar to axonal myelination during normal development.  Since lesion remyelination correlates with reduced neurodegeneration, Simons and his colleagues strive to understand why remyelination occurs in only a small number of MS patients and to identify drugs that may promote it.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.16.384354v1?rss=1 Authors: Geng, J., Liu, G., Wu, Y., Kong, F., Ma, S., Fu, L. Abstract: Multiple sclerosis (MS) is a complex, progressive neuroinflammatory disease associated with autoimmunity. Currently, effective therapeutic strategy was poorly found in MS. Experimental autoimmune encephalomyelitis (EAE) is widely used to study the pathogenesis of MS. Previous studies have shown that bone marrow mesenchymal stem Cells (BMSCs) transplantation could treat EAE animal models, but the mechanism was divergent. Here, we systematically evaluated whether BMSCs can differentiate into neurons, astrocytes and oligodendrocytes to alleviate the symptoms of EAE mice. We used Immunofluorescence staining to detect MAP-2 neurons marker, GFAP astrocytes marker, and MBP oligodendrocytes marker expression to evaluate whether BMSCs can differentiate. The effect of BMSCs transplantation on inflammatory cell invasion and demyelination in EAE mice were detected by Hematoxylin-Eosin (H&E) and Luxol Fast Blue (LFB) staining. Inflammatory factors expression was detected by ELISA and RT-qPCR. Our results showed that BMSCs could be induced to differentiate into neuron cells, astrocytes and oligodendrocyte in vivo and in vitro. In addition, BMSCs transplant improved the survival rate and weight, and reduced neurological function scores and disease incidence of EAE mice. Moreover, BMSCs transplant alleviated the inflammation and demyelination of EAE mice. Finally, we found that BMSCs transplantation down-regulated the expression levels of pro-inflammatory factors TNF-, IL-1{beta} and IFN-{gamma}, and up-regulated the expression levels of anti-inflammatory factors IL-10 and TGF-{beta}. In conclusion, this study found that BMSCs could alleviate the inflammatory response and demyelination in EAE mice, which may be achieved by the differentiation of BMSCs into neurons, astrocytes and oligodendrocytes in EAE mice. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.10.377226v1?rss=1 Authors: Hu, X., Xiao, G., He, L., Niu, X., Li, H., Xu, Q., Wei, Z., Qiu, M., Tanaka, K. F., Shen, Y., Tao, Y. Abstract: Oligodendrocytes are vulnerable to genetic and environmental insults and its injury leads to demyelinating diseases. The roles of ErbB receptors in the CNS myelin integrity are largely unknown. Here we overactivate ErbB receptors that mediate signaling of either neuregulin or EGF family growth factors and found their synergistic activation caused deleterious outcomes in white matter. Sustained ErbB activation induced by the tetracycline-dependent mouse tool Plp-tTA resulted in demyelination, axonal degeneration, oligodendrocyte precursor cell (OPC) proliferation, astrogliosis, and microgliosis in white matter. Moreover, there was hypermyelination prior to these pathological events. In contrast, sustained ErbB activation induced by another tetracycline-dependent mouse tool Sox10+/rtTA caused hypomyelination in the corpus callosum and optic nerve, which appeared to be a developmental deficit and did not associate with OPC regeneration, astrogliosis, or microgliosis. By analyzing the differentiation states of cells that were pulse-labeled with a viral reporter, we found that, during juvenile to adolescent development, Plp-tTA targeted mainly mature oligodendrocytes (MOs), while Sox10+/rtTA targeted OPCs and newly-formed oligodendrocytes. The distinct phenotypes of mice with ErbB overactivation induced by Plp-tTA and Sox10+/rtTA supported the reporter pulse-labeling results, and consolidated their non-overlapping targeting preferences in the oligodendrocyte lineage after early development. These features enabled us to demonstrate that ErbB overactivation in MOs induced necroptosis that caused pathological demyelination, whereas in OPCs induced apoptosis that caused developmental hypomyelination. These results established an upstream pathogenic role of ErbB overactivation in oligodendrocytes, providing molecular and cellular insights into the primary oligodendropathy in demyelinating diseases. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.09.17.302042v1?rss=1 Authors: Zoupi, L., Booker, S. A., Eigel, D., Werner, C., Kind, P. C., Spires-Jones, T., Newland, B., Williams, A. Abstract: In multiple sclerosis (MS), a chronic demyelinating disease of the central nervous system, neurodegeneration is detected early in the disease course and is associated with the long-term disability of patients. Neurodegeneration is linked to both inflammation and demyelination, but its exact cause remains unknown. This gap in knowledge contributes to the current lack of treatments for the neurodegenerative phase of MS. Here we ask if neurodegeneration in MS affects specific neuronal components and if it is the result of demyelination. Neuropathological examination of secondary progressive MS motor cortices revealed a selective vulnerability of inhibitory interneurons in MS. The generation of a rodent model of focal subpial cortical demyelination proved that this selective neurodegeneration is secondary to demyelination providing the first temporal evidence of demyelination-induced neurodegeneration and a new preclinical model for the study of neuroprotective treatments. Copy rights belong to original authors. Visit the link for more info

Dr. Fabio Nascimento discusses an article from the Neurology Resident and Fellow section entitled, "Neurology: Extrapontine Osmotic Demyelination in Hypernatremia". Show references: https://n.neurology.org/content/94/16/e1780

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.22.216598v1?rss=1 Authors: Mozafari, S., Deboux, C., Laterza, C., Ehrlich, M., Kuhlmann, T., Martino, G., Baron-Van Evercooren, A. Abstract: Oligodendrocytes are extensively coupled to astrocytes, a phenomenon ensuring glial homeostasis and maintenance of CNS myelin. Molecular disruption of this communication occurs in demyelinating diseases such as multiple sclerosis. Less is known about the vulnerability and reconstruction of the panglial network during adult demyelination-remyelination. Here, we took advantage of LPC-induced demyelination to investigate the expression dynamics of the oligodendrocyte specific connexin 47 (Cx47) and whether this dynamic could be modulated by grafted iPSC-neural progeny. Our data show that deconstruction of the panglial network following demyelination is larger in size than demyelination. Loss of Cx47 expression is timely rescued during remyelination and accelerated by the grafted neural precursors. Moreover, mouse and human iPS-derived oligodendrocytes express Cx47, which co-labels with astrocyte Cx43, indicating their integration into the panglial network. These data suggest that full lesion repair following transplantation occurs by panglial reconstruction in addition to remyelination. Targeting panglial elements by cell therapy or pharmacological compounds may help accelerating or stabilizing re/myelination in myelin disorders. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.06.18.158782v1?rss=1 Authors: Brousse, B., Magalon, K., Daian, F., Durbec, P., Cayre, M. Abstract: In response to corpus callosum (CC) demyelination, subventricular zone-derived neural progenitors (SVZdNP) are mobilized and generate new myelinating oligodendrocytes. Here, we examine the putative immunomodulatory properties of endogenous SVZdNP during demyelination in the cuprizone model. We observed that SVZdNP density is higher in the lateral and rostral CC regions that show weaker demyelination and is inversely correlated with activated microglia density and pro-inflammatory cytokines levels. Single-cell RNA-sequencing further revealed CC areas with high SVZdNP mobilization are enriched in a microglial cell subpopulation with immunomodulatory signature. We identified ligand/receptor couple MFGE8 (milk fat globule-epidermal growth factor-8)/integrin {beta}3 as a ligand/receptor couple implicated in SVZdNP/microglia dialog. MFGE8 is highly enriched in immature SVZdNP mobilized to the demyelinated CC and promotes myelin debris phagocytosis in vitro. Altogether these results demonstrate that beyond their cell replacement capacity endogenous progenitors display immunomodulatory properties highlighting a new role for endogenous SVZdNP in myelin regeneration. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.22.110551v1?rss=1 Authors: Neely, S. A., Williamson, J. M., Klingseisen, A., Zoupi, L., Early, J. J., Williams, A., Lyons, D. A. Abstract: Regeneration of myelin (remyelination) in the central nervous system (CNS) has long been thought to be principally mediated by newly generated oligodendrocytes, a premise underpinning therapeutic strategies for demyelinating diseases, including multiple sclerosis (MS). Recent studies have indicated that oligodendrocytes that survive demyelination can also contribute to remyelination, including in MS, but it is unclear how remyelination by surviving oligodendrocytes compares to that of newly generated oligodendrocytes. Here we studied oligodendrocytes in MS, and also imaged remyelination in vivo by surviving and new oligodendrocytes using zebrafish. We define a previously unappreciated pathology in MS, myelination of neuronal cell bodies, which is recapitulated during remyelination by surviving oligodendrocytes in zebrafish. Live imaging also revealed that surviving oligodendrocytes make very few new sheaths, but can support sheath growth along axons. In comparison, newly made oligodendrocytes make abundant new sheaths, properly targeted to axons, and exhibit a much greater capacity for regeneration. Copy rights belong to original authors. Visit the link for more info

Dr. Sylvia Tenembaum discusses whether plasma exchange was safe and effective for children in her study this week in Neurology.

In the first part of the podcast, Dr. David Lapides talks with Dr. Thomas Kilduff about his Science report article reporting that REM sleep–active MCH neurons are involved in forgetting hippocampus-dependent memories, which you can read here: https://science.sciencemag.org/content/365/6459/1308. In the second segment, Dr. Stacey Clardy talks with Dr. Sylvia Tenembaum about her paper on prognostic indicators of improvement with therapeutic plasma exchange in pediatric demyelination.

Psalm 2, Psalm 32, Psalm 62, Psalm 92, Psalm 122.Today’s Daily Reading read from the Living BibleUnless otherwise noted, all Scripture quotations are taken from THE LIVING BIBLE copyright© 1971. Used by permission of Tyndale House Publishers, Inc., Carol Stream, Illinois 60188. All rights reserved.

Bruce Trapp and Daniel Ontaneda discuss their retrospective study investigating cortical neuronal loss and cerebral white-matter demyelination in mulitple sclerosis.

We've abused the term, 'idiopathic.' Not all clinical conditions have to have an unclear cause. More and more, we are finding out the answers. This week, using transverse myelitis as an example, Dr. Clyde Markowitz shares his experience in working up unknown etiologies of spinal cord inflammation. Produced by James E. Siegler. Music by Quantum Jazz, Rui, and Steve Combs. Voiceover by Erika Mejia. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision making. REFERENCES Zalewski NL, Flanagan EP and Keegan BM. Evaluation of idiopathic transverse myelitis revealing specific myelopathy diagnoses. Neurology. 2018;90:e96-e102. Bevan CJ and Cree BA. Fulminant Demyelinating Diseases of the Central Nervous System. Semin Neurol. 2015;35:656-66. Greenberg BM and Frohman EM. Immune-mediated myelopathies. Continuum (Minneap Minn). 2015;21:121-31. Kimbrough DJ, Mealy MA, Simpson A and Levy M. Predictors of recurrence following an initial episode of transverse myelitis. Neurol Neuroimmunol Neuroinflamm. 2014;1:e4. Cobo Calvo A, Mane Martinez MA, Alentorn-Palau A, Bruna Escuer J, Romero Pinel L and Martinez-Yelamos S. Idiopathic acute transverse myelitis: outcome and conversion to multiple sclerosis in a large series. BMC Neurol. 2013;13:135. Jacob A and Weinshenker BG. An approach to the diagnosis of acute transverse myelitis. Semin Neurol. 2008;28:105-20.

Alan Thompson and Steven Goodrick discuss a new three-part Series on progressive MS. 

Multiple Sclerosis is most probably an autoimmune inflammatory disease of the central nervous system. Demyelination of neurons and axonal loss occur in temporal and spatial resolution in multiple areas of the brain and spinal cord. This impairment manifests in neurological symptoms. The course of disease varies between individuals and the causing mechanisms still remain elusive. Environmental factors as well as genetic predispositions are widely discussed. Recent studies stressed the prominent role of CD8+ T lymphocytes in the autoimmune pathomechanism. They notably exceed the amount of CD4+ T cells in acute lesions yet target cells and activating antigens remain elusive. A genetic linkage between the human leukocyte antigen gene locus and disease susceptibility was observed. Carrying the HLA A*0301 allele or the HLA A*0201 allele correlates with a risk factor or protective effect for Multiple Sclerosis susceptibility, respectively. Thus during this thesis two main questions were followed: 1. Which CD8+ T lymphocytes participate in the autoimmune attack on central nervous system tissue and what are their receptors for antigen recognition? 2. How does the expression of HLA-A2 molecules lead to a decreased disease susceptibility? In the first part, the T cell receptor molecules of potentially disease-related single CD8+ T cells from frozen patient tissue samples were characterized. T lymphocytes were considered disease-related when they either belonged to a clonally expanded T cell population or expressed an activation marker on their cell surface. In a clone-specific approach, the T cell receptor beta chains of pre-analyzed, clonally expanded T cell populations were investigated. Further an unbiased approach independent of pre-analyses was established. In the second part, antigen recognition of the probably disease-related T cell receptor 2D1 was investigated. This receptor was isolated from a Multiple Sclerosis patient and was known to be activated by a myelin-derived peptide presented on HLA-A3 molecules. In an animal model double-transgenic mice expressing HLA-A3 and the 2D1 T cell receptor developed a Multiple Sclerosis-like disease after immunization with the known peptide. Surprisingly not a single triple-transgenic mouse expressing HLA-A3, the T cell receptor 2D1 and HLA-A2 showed symptoms after immunization. In these mice 2D1 T lymphocytes were shown to be depleted in the thymus. To characterize HLA-A2-bound peptides which mediate this protective effect a novel technology for unbiased identification of antigenic peptides recognized by human leukocyte antigen class I-restricted T lymphocytes was employed. 28 peptides presented on HLA-A2 molecules were found to be recognized by the T cell receptor 2D1. Those peptides displayed very closely related sequences. Eight possible parent proteins existing in mouse, therefrom even four equally expressed in humans were identified. Finally those putative parent proteins were further characterized and first investigations of antigen processing in different antigen presenting cell lines were performed.

Interferon-β therapy is only effective in treating a mouse model of multiple sclerosis when the disease is dependent upon the NLRP3 inflammasome.

Brenda Banwell discusses the potential of MRI screening after a first demyelinating event as a future predictor of MS in children.

Background: CADASIL is responsible for diffuse hyperintensities in the white matter on FLAIR images. These lesions are often associated with focal lesions in the basal ganglia such as lacunar infarctions. The prevalence and significance of diffuse or confluent thalamic hyperintensities (CTH) remain unknown. Methods: The frequency of hyperintensities on FLAIR images in the thalamus was assessed in 147 CADASIL patients, and signal abnormalities on both FLAIR and T(1)-weighted images were categorized as focal/punctuate or diffuse/confluent by the same reader. The areas of increased diffusion were also analyzed on apparent diffusion coefficient maps. The association of CTH with vascular risk factors, the main clinical manifestations of the disease and MRI markers (brain parenchymal fraction, volume of white matter hyperintensities, volume of lacunar infarcts and number of microbleeds) was analyzed with generalized linear regression models. Results: CTH were detected in 12% of the CADASIL subjects in association with hypointensities on T(1)-weighted images. CTH corresponded to areas of increased diffusion apparent diffusion coefficient maps. CTH were found significantly associated with age and independently related to the volume of white matter hyperintensities but not to that of lacunar infarctions or to cerebral atrophy after adjustment for age and sex. No significant association was found between CTH and global cognitive performances. Conclusion: CTH are observed on FLAIR images in a sizeable proportion of CADASIL patients. They are mainly related to the extent of white matter hyperintensities and do not correlate with cognitive decline. Demyelination and/or loss of glial cells appear to be the most plausible cause of these confluent signal changes in the thalamus. Copyright (C) 2010 S. Karger AG, Basel

Guest: Richard Ransohoff, MD Host: Leslie P. Lundt, MD Cortical demyelination now appears to be an important pathologic substrate for functional deficits in MS and PML yet the pathology differs from that in the white matter. What is our current understanding? Dr. Richard Ransohoff, the Director of the Neuroinflammation Research Center at the Lerner Research Institue of the Cleveland Clinic joins host Dr. Leslie Lundt to discuss his work in this exciting branch of neurology.