Podcasts about remyelination

Sex hormones, such as estrogens and testosterone, affect each individual's journey living with multiple sclerosis. While both genders face equal MS risk before puberty and after menopause, women experience up to three times higher risk during their reproductive years. Pregnancy generally brings less relapses, potentially attributed to high estriol levels. However, navigating treatment decisions well while trying to conceive and after delivery requires finesse and expertise. Equip yourself with the latest women's health info regarding MS, covering topics from birth control and fertility treatments to menopause and osteoporosis. Testosterone has important anti-inflammatory and neuroprotective benefits in multiple sclerosis.  Nevertheless, men are at higher risk for disability progression then women. Declining testosterone levels over time (called andropause) and Y chromosome genes may tilt the scales towards disability. Listen to current testosterone research including potential remyelination benefits. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Maria Houtchens MD, founding director of the Women's Health Program at the Brigham MS Center and Associate Professor of Harvard Medical School in Boston, USA Jorge Correale MD, Head of Neuroimmunology and Demyelinating Diseases at the Dr. Raúl Carrea Institute of Neurological Research in Buenos Aires, Argentina  

I have a special guest with me on today's podcast episode, Dr. Terry Wahls. She's been on our podcast before, but this time, Dr. Wahls is explaining a study that she has going on right now. On today's episode, Dr. Wahls talks to us about the study, what to expect, and how to participate. She also shares some of her best tips for starting a new diet and how long you should stay consistent for before trying something new. Dr. Terry Wahls is an Institute for Functional Medicine Certified Practitioner and a clinical professor of medicine at the University of Iowa where she conducts clinical trials in the setting of Multiple Sclerosis. In 2018 she was awarded the Institute for Functional Medicine's Linus Pauling Award for her contributions in research, clinical care and patient advocacy. She is the author of The Wahls Protocol: A Radical New Way to Treat All Chronic Autoimmune Conditions Using Paleo Principles, and the cookbook, The Wahls Protocol Cooking for Life. Pick up a one-page handout for the Wahls™ Diet at https://terrywahls.com/diet/ Wahls Research https://terrywahls.com/research/ Wahls Research Lab - to learn about current clinical research studies that Dr. Wahls is conducting https://wahls.lab.uiowa.edu/ Connect with Dr. Wahls: https://www.facebook.com/TerryWahls/ https://www.instagram.com/drterrywahls/ https://twitter.com/terrywahls https://youtube.com/c/terrywahlsmd Additional Resources: https://www.doctorgretchenhawley.com/insider Reach out to Me: hello@doctorgretchenhawley.com Website: www.MSingLink.com Social: ★ Facebook: https://www.facebook.com/groups/mswellness ★ Instagram: https://www.instagram.com/doctor.gretchen ★ YouTube: https://www.youtube.com/c/doctorgretchenhawley?sub_confirmation=1 → Game Changers Course: https://www.doctorgretchenhawley.com/GameChangersCourse → Total Core Program: https://www.doctorgretchenhawley.com/TotalCoreProgram → The MSing Link: https://www.doctorgretchenhawley.com/TheMSingLink

Step into the powerful realm of MRI imaging, providing us with an unparalleled view of multiple sclerosis. Discover how acute inflammation becomes vivid with contrast, and how various MRI sequences unveil the past battles fought within your brain and spinal cord. We'll explore advances in techniques, revealing brain shrinkage, gray matter disease and myelin repair. Understand the impact of MS on brain processing efficiency during rest and specific tasks through functional MRI imaging. Crucial questions regarding where and how often to get MRI scans are addressed. Latest guidance on avoiding contrast for routine MRI monitoring in MS shared. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Christina Azevedo MD, Assistant Professor of Clinical Neurology at the University of Southern California Robert Zivandinov MD, PhD, Director of the Buffalo Neuroimaging Analysis Center & Professor of Neurology at Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo, State University of New York.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.26.550644v1?rss=1 Authors: Ancau, M., Kumar, G. T., Butenschoen, V. M., Gempt, J., Yakushev, I., Nekolla, S., Muehlau, M., Scheunemann-Kutzenberger, C., Heininger, S., Loewe, B., Loewe, E., Baer, S., Fischer, J., Reiser, J., Ayachit, S. S., Liesche-Starnecker, F., Schlegel, J., Matiasek, K., Schifferer, M., Kirschke, J. S., Misgeld, T., Lueth, T., Hemmer, B. Abstract: Background Despite advances in therapy, inflammatory demyelinating diseases of the central nervous system, such as multiple sclerosis, remain important causes of morbidity among young adults. Translation of remyelinating paradigms from current murine models is encumbered by the small size and low white matter content of the brains, limiting the spatial resolution of diagnostic imaging. Large animal models might be more suited for this purpose but pose significant technological, ethical and logistical challenges. Methods We induced reversible and targeted cerebral demyelinating lesions by controlled injection of lysophosphatidylcholine in the minipig brain. One strength of the approach is the serial induction, allowing parallel imaging of successive stages of de-/remyelination. Findings We demonstrate controlled, clinically unapparent, reversible and multimodally trackable brain white matter demyelination in a large animal model. Lesions were amenable to follow-up using the same clinical imaging modalities (3T magnetic resonance imaging, 11C-PIB positron emission tomography) and standard histopathology protocols as for human diagnostics, as well as electron microscopy to compare against biopsy data from two patients with cerebral demyelination. Interpretation By employing human diagnostic tools and validating the model against data from related human diseases, our platform overcomes one important translational barrier of current animal brain demyelination models while having the potential for developing diagnostic procedures and imaging biomarkers. Remyelination and axon preservation dynamics diverge from classical rodent models. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.24.550351v1?rss=1 Authors: Mohotti, N. D. S., Kobayashi, H., Williams, J. M., Binjawadagi, R., Evertsen, M. P., Christ, E. G., Hartley, M. D. Abstract: During demyelination, lipid-rich myelin debris is released in the central nervous system (CNS) and must be phagocytosed and processed before new myelin can form. Although myelin comprises over 70% lipids, relatively little is known about how the CNS lipidome changes during demyelination and remyelination. In this study, we obtained a longitudinal lipidomic profile of the brain, spinal cord, and serum using a genetic mouse model of demyelination, known as Plp1-iCKO-Myrf mice. This model has distinct phases of demyelination and remyelination over the course of 24 weeks, in which loss of motor function peaks during demyelination. Using principal component analysis (PCA) and volcano plots, we have demonstrated that the brain and spinal cord have different remyelination capabilities and that this is reflected in different lipidomic profiles over time. We observed that plasmalogens (ether-linked phosphatidylserine and ether-linked phosphatidylcholine) were elevated specifically during the early stages of active demyelination. In addition, we identified lipids in the brain that were altered when mice were treated with a remyelinating drug, which may be CNS biomarkers of remyelination. The results of this study provide new insights into how the lipidome changes in response to demyelination, which will enable future studies to elucidate mechanisms of lipid regulation during demyelination and remyelination. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.11.548469v1?rss=1 Authors: Beyer, B. A., Sul, A., Gillen Miller, J. T., Neumann, B., Plaisted, W. C., Kondo, T., Franklin, R. J. M., Lairson, L. L. Abstract: Remyelination-promoting agents have significant potential utility as therapies for the treatment of demyelinating diseases, including multiple sclerosis. Clemastine and bexarotene have recently been evaluated in Phase II clinical trials to evaluate their potential in this context, with evidence for drug-induced remyelination being observed in both trials. Efficacy levels for both agents as monotherapies, as well as dose-limiting toxicities, highlight the need for more effective approaches. Additionally, questions about the relevance of M1R as the target of clemastine, and also around a mechanism involving accumulation of 8,9-unsaturated sterols, remain. Here, we have identified potent alternatives to clemastine (i.e., doxepin and orphenadrine), which are predicted to have superior tolerability and efficacy profiles and provide mechanistic insight related to M1R, and have completed pairwise drug combination screens using diverse classes of OPC differentiation-inducing agents. Vitamin D receptor agonists were found to enhance M1R antagonist-induced OL differentiation. Select compounds implicated in 8,9-unsaturated sterol accumulation synergistically enhanced the activity of bexarotene in OPCs, which resulted in insights that implicate a critical role for liver-X-receptor in the mechanisms of both sterol-dependent and bexarotene-induced remyelination. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Last week, the International Progressive MS Alliance convened its fourth Scientific Congress in Vienna, Austria, bringing together nearly 200 international scientists and MS leaders, including people affected by progressive MS, to report and review the progress being made in developing new, effective treatments for progressive MS. In Part 1 of our coverage, we're taking you inside this Scientific Congress, where you'll hear from some of the top MS researchers in the world who participated in this game-changing event. We have a lot to talk about! Are you ready for RealTalk MS??! This Week: The International Progressive MS Alliance Scientific Congress  :22 Dr. Robert Fox shares an overview of the Alliance and a preview of this Scientific Congress  3:17 Vanessa Fanning explains the role of the Alliance People Affected by MS Engagement Coordination Team  16:49 Professor Tanja Kuhlmann discusses the critical importance of identifying the mechanisms that drive MS progression  26:01 Remyelination is a natural process. Professor Robin Franklin explains why it stops working for people with MS  35:24 Professor Olga Ciccarelli tells us where we are in understanding remyelination and shares some of her cutting-edge research  41:48 Share this episode  53:01 Please remember to take our listener survey!  53:21 SHARE THIS EPISODE OF REALTALK MS Just copy this link & paste it into your text or email: https://realtalkms.com/303 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 The International Progressive MS Alliance https://progressivemsalliance.org RealTalk MS Episode 279: A New Framework for Researching, Diagnosing, and Treating MS with Professor Tanja Kuhlmann https://realtalkms.com/279 RealTalk MS Episode 280: How the Proposed Framework for Diagnosing and Treating MS Will Affect You with Dr. Tim Coetzee  https://realtalkms.com/280 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 280 Guests: Dr. Robert Fox, Vanessa Fanning, Prof. Tanja Kuhlmann, Prof. Robin Franklin, and Prof. Olga Ciccarelli Tags: MS, MultipleSclerosis, MSResearch, MSSociety, RealTalkMS Privacy Policy

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.03.19.533192v1?rss=1 Authors: Sajjad, M., Zahoor, I., Rashid, F., Rattan, R., Giri, s. Abstract: The metabolic need of the premature oligodendrocytes (Pre-OLs) and mature oligodendrocytes (OLs) are distinct. The metabolic control of oligodendrocyte maturation is not fully understood. Here we show that the terminal maturation and higher mitochondrial respiration in the oligodendrocyte is an integrated process controlled through pyruvate dehydrogenase (Pdh). Combined bioenergetics and metabolic studies show that mature oligodendrocytes show elevated TCA cycle activity than the premature oligodendrocytes. Our signaling studies show that the increased TCA cycle activity is mediated by the activation of Pdh due to inhibition of pyruvate dehydrogenases isoform-1 (Pdhk1) that phosphorylates and inhibits Pdh. Accordingly, when Pdhk1 is directly expressed in the premature oligodendrocytes, they fail to mature. While Pdh converts pyruvate into the acetyl-CoA by its oxidative decarboxylation, our study shows that Pdh also activates a unique molecular switch required for oligodendrocyte maturation by acetylating the bHLH family transcription factor Olig1. Pdh inhibition via Pdhk1 blocks the Olig1-acetylation and hence, oligodendrocyte maturation. Using the cuprizone model of demyelination, we show that Pdh is deactivated during the demyelination phase, which is reversed in the remyelination phase upon cuprizone withdrawal. In addition, Pdh activity status correlates with the Olig1-acetylation status. Hence, the Pdh metabolic node activation allows a robust mitochondrial respiration and activation of a molecular program necessary for the terminal maturation of oligodendrocytes. Our findings open a new dialogue in the developmental biology that links cellular development and metabolism. These findings have far-reaching implications for the development of therapies for a variety of demyelinating disorders including multiple sclerosis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

My guest today is Dr. Terry Wahls, a clinical professor of medicine at the University of Iowa where she conducts clinical trials testing the effect of therapeutic diet and lifestyle to treat MS and related symptoms. Through her custom protocol, Dr. Wahls overcame her own diagnosis of secondary progressive multiple sclerosis, which had confined her to a tilt recline wheelchair for four years.Now, she bikes to work, plays with the dog, and generally thrives as a health and wellness messenger of critical importance to our world. In this deeply moving and informational conversation, Dr. Wahls shares stark first-person memories from the painful early stages of her healing journey, details the nutrient-dense diet that changed everything, and looks into the future of MS treatment – spotlighting the important role that nutrition has to play in it all.If you have MS, or know someone who does, I definitely recommend her book, The Wahls Protocol: How I Beat Progressive MS Using Paleo Principles & Functional Medicine, where she details her story at length.We also cover…00:03:12 — Early Symptoms & MS DiagnosisInto the experience – Dr. Wahls details her diagnosisPrioritizing mitochondria health with supplements Developing a custom Paleo-inspired dietGoing from a tilt recline wheelchair to completing an 18.5m bike ride Realizing that recovery was possible00:11:34 — Exploring Different Treatments for MS Background on MS discovery in the 1800sMS in the brain – rapid decline usually seen between 45 and 50Supporting your body through MS with nutrient-dense foodsInspired by Loren Cordain's workBreaking 20 years as a vegetarian 00:16:52 — Healing Through Nutrition Which nutrients Dr. Wahls chased in her custom dietBenefits of a meditation practice Switching to organic ingredients Why she relied so heavily on leafy greens and liverHow her diet evolved throughout her healing journey Leveraging healthy fasting strategies Eating every other day – what, why, and how?00:31:18 — Forging a New Path & Sharing Her MessageRunning the research to make her protocol official in 2010Being threatened with loss of her medical license Working up to 26 scientific peer reviewed MS-related publicationsEfficacy of Diet on Fatigue and Quality of Life in Multiple SclerosisLifestyle changes vs. medication Treatment recommendations based on # of brain lesions Remyelination online coursesJoin Dr. Wahl's research study on quality of life Resources:Website: terrywahls.comCourses: Remyelination WorkshopsResearch: Dr. Wahl's MS research studyInstagram:

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.25.525562v1?rss=1 Authors: de la Fuente, A. G., Dittmer, M., Heesbeen, E., de la Vega-Gallardo, N., White, J. A., Young, A., Mayne, K., Falconer, J., McMurran, C. E., Innayatulah, M., Tiwari, V., Penalva, R., Ingram, R. J., Dombrowski, Y., Fitzgerald, D. C. Abstract: Myelin regeneration (remyelination) is essential to prevent neurodegeneration in demyelinating diseases such as Multiple Sclerosis but its efficiency declines with age. Regulatory T cells (Treg) recently emerged as critical players in tissue regeneration, including remyelination. However, the effect of ageing on Treg-mediated regenerative processes is poorly understood. Here, we show that expansion of aged Treg does not rescue age-associated remyelination impairment due to an intrinsically diminished capacity of aged Treg to promote oligodendrocyte differentiation and myelination. This decline in regenerative Treg functions can be rescued by a young environment. We identified Melanoma Cell Adhesion Molecule 1 (MCAM1) and Integrin alpha 2 (ITGA2) as novel candidates of Treg-mediated oligodendrocyte differentiation that decrease with age. Our findings demonstrate that ageing limits the neuroregenerative capacity of Treg, likely limiting their remyelinating therapeutic potential in aged patients and describe two novel mechanisms implicated in Treg-driven remyelination that may be targetable to overcome this limitation. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

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

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.01.04.522734v1?rss=1 Authors: Marziali, L. N., Hwang, Y., Palmisano, M., Cuenda, A., Sim, F., Volsko, C., Dutta, R., Trapp, B., Wrabetz, L., Feltri, M. Abstract: Multiple Sclerosis is a chronic inflammatory disease in which disability results from the disruption of myelin and axons. During the initial stages of the disease, injured myelin is replaced by mature myelinating oligodendrocytes that differentiate from oligodendrocyte precursor cells. However, myelin repair fails in secondary and chronic progressive stages of the disease and with aging, as the environment becomes progressively more hostile. This may be attributable to inhibitory molecules in the multiple sclerosis environment including activation of the p38MAPK family of kinases. We explored oligodendrocyte precursor cell differentiation and myelin repair using animals with conditional ablation of p38MAPKg from oligodendrocyte precursors. We found that p38{gamma}MAPK ablation accelerated oligodendrocyte precursor cell differentiation and myelination. This resulted in an increase in both the total number of oligodendrocytes and the migration of progenitors ex vivo and faster remyelination in the cuprizone model of demyelination/remyelination. Consistent with its role as an inhibitor of myelination, p38{gamma}MAPK was significantly downregulated as oligodendrocyte precursor cells matured into oligodendrocytes. Notably, p38{gamma}MAPK was enriched in samples of leukocortical multiple sclerosis lesions from patients, which represent areas of failed remyelination. Our data suggest that p38{gamma} could be targeted to improve myelin repair in multiple sclerosis. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.08.519463v1?rss=1 Authors: Vangansewinkel, T., Lemmens, S., Tiane, A., Geurts, N., Dooley, D., Vanmierlo, T., Pejler, G., Hendrix, S. Abstract: Traumatic spinal cord injury (SCI) most often leads to permanent paralysis due to the inability of axons to regenerate in the adult mammalian central nervous system (CNS). In the past, we have shown that mast cells (MCs) improve the functional outcome after SCI by suppressing scar tissue formation at the lesion site via mouse mast cell protease 6 (mMCP6). In this study, we investigated whether recombinant mMCP6 can be used therapeutically to improve the functional outcome after SCI. Therefore, we applied mMCP6 locally via an intrathecal catheter in the subacute phase after a spinal cord hemisection injury in mice. Our findings showed that hind limb motor function was significantly improved in mice that received recombinant mMCP6 compared to the vehicle-treated group. In contrast to our previous findings in mMCP6 knockout mice, the lesion size and expression levels of the scar components fibronectin, laminin, and axon growth-inhibitory chondroitin sulfate proteoglycans were not affected by the treatment with recombinant mMCP6. Surprisingly, no difference in infiltration of CD4+ T cells and reactivity of Iba-1+ microglia/macrophages at the lesion site was observed between the mMCP6 treated mice and control mice. Additionally, local protein levels of the pro- and anti inflammatory mediators IL-1{beta}, IL-2, IL-4, IL-6, IL 10, TNF-, IFN{gamma}, and MCP-1 were comparable between the two treatment groups, indicating that locally applied mMCP6 did not affect inflammatory processes after injury. However, the increase in locomotor performance in mMCP6-treated mice was accompanied by reduced demyelination and astrogliosis in the perilesional area after SCI. Consistently, we found that TNF-a/IL-1B-astrocyte activation was decreased, and that oligodendrocyte precursor cell (OPC) differentiation was increased after recombinant mMCP6 treatment in vitro. Mechanistically, this suggests effects of mMCP6 on reducing astrogliosis and improving (re)myelination in the spinal cord after injury. In conclusion, these data show for the first time that recombinant mMCP6 is therapeutically active in enhancing recovery after SCI. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Episode 493 Comic Book talk about The Batman & Scooby-Doo Mysteries #1, Blade Vampire Nation #1, Bill & Ted presents Death one shot, Do a Powerbomb #5 & 6, I Hate Fairyland #1, Harley Quinn: the Animated Series - the Real Sidekicks of New Gotham Special #1, the Jurassic League #6, Maskerade #2 & 3, Mr Easta #1. Multiple Sclerosis Health Talk about Remyelination Potential, Exergaming, at home Exercises and other stuff with health and MS. Send comments, questions and tips to kevintheduckpool@gmail.com please help us out by rating and reviewing us and telling a friend. Also check out audio and video versions of Crimson Cowl Comic Club & Under the Cowl podcasts. A fun variety of great people talk comic books, entertainment or whatever and you can see or hear me on many episodes of those podcasts as well with many more great episodes to come out in the future. #ms, #multiplesclerosis, #comicbooks, #comicbookreviews --- Send in a voice message: https://anchor.fm/kevin-kleinhans/message Support this podcast: https://anchor.fm/kevin-kleinhans/support

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.04.510850v1?rss=1 Authors: Molina-Gonzalez, I., Holloway, R. K., Jiwaji, Z., Dando, O. R., Emelianova, K., Lloyd, A. F., Forbes, L. H., Mahmood, A., Skripuletz, T., Gudi, V., Febery, J., Johnson, J., Fowler, J., Kuhlmann, T., Williams, A., Chandran, S., Stangel, M., Howden, A. J., Hardingham, G., Miron, V. E. Abstract: Failed regeneration of myelin around neuronal axons following central nervous system damage contributes to nerve dysfunction and clinical decline in various neurological conditions, for which there is an unmet therapeutic demand. Here, we show that interaction between glial cells, astrocytes and mature myelin-forming oligodendrocytes, is a critical determinant of remyelination. Astrocytes support the survival of regenerating oligodendrocytes, via downregulation of the Nrf2 pathway associated with increased astrocytic cholesterol biosynthesis pathway activation. Remyelination fails following sustained astrocytic Nrf2 activation yet is restored by either cholesterol biosynthesis/efflux stimulation, or Nrf2 inhibition using the existing therapeutic Luteolin. We identify that astrocyte-oligodendrocyte interaction regulates remyelination, and reveal a drug strategy for central nervous system regeneration centred on targeting this interaction. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

In this conversation Alex speaks with Dr. Terry Wahls about her health journey, from being wheel chair bound with multiple sclerosis to riding her bike. They discuss:  Dr. Wahls's decline and healing journey. How her colleagues reacted at first, and how they react now to her message. The difference between research studies (drug versus dietary patterns). Dr. Wahls's research she has conducted. The difference between the Wahls protocol and a conventional medicine approach. Remyelination drugs that are in development. Dr. Terry Wahls is an Institute for Functional Medicine Certified Practitioner and a clinical professor of medicine at the University of Iowa where she conducts clinical trials in the setting of Multiple Sclerosis. In 2018 she was awarded the Institute for Functional Medicine's Linus Pauling Award for her contributions in research, clinical care and patient advocacy. She is the author of: The Wahls Protocol: A Radical New Way to Treat All Chronic Autoimmune Conditions Using Paleo Principles: https://geni.us/pv0X The cookbook, The Wahls Protocol Cooking for Life: https://geni.us/ZYaUeaR Learn more about the current study Efficacy of Diet on Quality of Life in Multiple Sclerosis at https://wahls.lab.uiowa.edu/. Pick up a one-page handout for the Wahls™ Diet at https://terrywahls.com/diet/ Social Media Links: https://www.facebook.com/TerryWahls/ https://www.instagram.com/drterrywahls/ https://twitter.com/terrywahls https://youtube.com/c/terrywahlsmd Wahls Research Papers: https://terrywahls.com/researchpapers/ Wahls Research Lab - "Efficacy of Diet on Quality of LIfe in Multiple Sclerosis. Comparison of ketogenic, modified Palaeolithic diets to a Usual diet control" Learn more about the study here: https://wahls.lab.uiowa.edu/join-study Screen to see if you are eligible for Efficacy of Diet on Quality of Life in Multiple Sclerosis Study: https://redcap.icts.uiowa.edu/redcap/surveys/?s=JX73EYRJNPF9MHRR Download research study brochure: https://wahls.lab.uiowa.edu/sites/wahls.lab.uiowa.edu/files/wysiwyg_uploads/20220707_-_edq-ms_-_recruitment_study_brochure_-_paper_copy.pdf Gifts for public: Diet Cheat Sheet Summary: www.terrywahls.com/diet Our team at Healthpath help people take charge of their gut health. Visit our website to learn more: https://healthpath.com Order a SIBO test: https://healthpath.com/products/sibo-hydrogen-breath-test-uk/ Order a gut microbiome test: https://healthpath.com/products/microbiome-gut-bacteria-test-uk/ Work with a healthpath practitioner: https://healthpath.com/practitioners/ Visit our blog: https://healthpath.com/blog/ Follow us on Instagram here: https://www.instagram.com/ourhealthpath/ Follow Alex on Instagram here: https://www.instagram.com/alexandermanos/ Sign up to our new newsletter: https://healthpath.com/newsletter/ - Episode Sponsor: Vitality Pro has been following the latest research in longevity science to produce a range of premium-quality nutritional supplements focused on improving cellular health, sleep and energy levels. Products range from berberine and curcumin through to NMN, TMG and sulforaphane. Their products are made using the purest raw ingredients, and tested by trusted third-party labs, to provide you with TRUST and confidence in their supplements. The certificates are available to view on their website. Website: https://vitality-pro.com

Multiple Sclerosis News Today's multimedia associate, Price Wooldridge, reads the news article about an approved heart med that could promote myelin repair in MS. He also reads “MS News That Caught My Eye Last Week: Intermittent Fasting, Roe v. Wade, IRLs” by Ed Tobias, from his column "The MS Wire". =================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/

Join Nicola Graham as she chats with Brett Drummond, the co-founder of MStranslate, about the promising topic of remyelination. Remyelination is the process of the myelin sheath on nerve fibres being restored after it has broken down. This is a natural process but does not happen in people with MS. Will remyelination be possible for people with MS in the future? Brett takes listeners through the latest research on remyelination and what this could mean for people living with MS.

Dr. Gretchen Hawley shares Part 1 of everything she brought home from the CMSC annual MS conference in Orlando this year! In this episode she discusses remyelination, fatigue, spasticity and how sleep can affect individuals with MS and so much more! Additional Resources: https://www.doctorgretchenhawley.com/insider Behind the Scenes of The MSing Link online wellness program: https://www.doctorgretchenhawley.com/TheMSingLink Reach out to Me: Gretchen@DoctorGretchenHawley.com Website: www.MSingLink.com Social: ★ Facebook: https://www.facebook.com/groups/mswellness ★ Instagram: https://www.instagram.com/doctor.gretchen ★ YouTube: https://www.youtube.com/c/DoctorGretchenHawley/featured

Are you curious about more of the science behind Multiple Sclerosis? This week we are so honored to have Dr. David Baker with us to share all of his knowledge. Professor David Baker trained in immunology at The Hunterian Institute, University of London and received his Ph.D. in 1987 for studies on control of immune responses in delayed hypersensitivities of the skin. He moved to the Blizard Institute at the end of 2006 and developed a novel model of secondary progressive multiple sclerosis and has been focusing recent research on neuroprotection. An internationally recognized neuroimmunologist Professor Baker has identified novel treatment strategies for experimental neuroimmunological conditions. Dr. Baker will discuss Cannabis treatments and Stem Cell Therapy amongst many other things. In this episode he also mentions the The MS Blog, a great resource with a ton of information of different treatments and research for MS! Check it out at the following link ---> https://multiple-sclerosis-research.org/ Behind the Scenes of The MSing Link Wellness Program: https://www.doctorgretchenhawley.com/TheMSingLink Additional Resources: https://www.doctorgretchenhawley.com/insider Reach out to Me: Gretchen@DoctorGretchenHawley.com Website: www.MSingLink.com Social: ★ Facebook: https://www.facebook.com/groups/mswellness ★ Instagram: https://www.instagram.com/doctor.gretchen ★ YouTube: https://www.youtube.com/c/DoctorGretchenHawley/featured

Interested in improving MS care? Participating in a clinical trial may have personal advantages and help others in the future. Trial design discussed including whether or not a placebo (no treatment) will be used. Criteria needed to enroll in a clinical study called inclusion and exclusion criteria explained. Key elements of clinical trials outlined including multiple safety measures and informed consent. Current clinical trials in multiple sclerosis are covered including using highly effective treatment early for someone living with multiple sclerosis. Current studies in progressive MS and remyelination shared. Compounds highlighted include BTK inhibitors, masitinib, ibudilast, simvastatin and gold nanocrystals. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Jiwon Oh MD PhD is the Director of the BARLO MS Centre at St. Micheal's Hospital in Toronto. She is an Associate Professor of Neurology University of Toronto. Dr. Oh's research focuses on developing advanced imaging techniques of the spinal cord and brain for use in clinical settings. She is the principal investigator on local and collaborative, multi-center MRI studies. Dr. Oh is the lead of the Canadian National Progression Cohort, which is focused on better understanding progression in MS. She completed her undergraduate degree at the University of Toronto and medical school from Queen's University. Dr. Oh completed her residency at the University of Toronto, PhD in Public Health at John Hopkins and neuroimmunology fellowship at John Hopkins. Robert Bermel MD is a neurologist specializing in multiple sclerosis at the Mellen Center for Multiple Sclerosis at Cleveland Clinic. He received a medical degree with thesis honors from the State University of New York at Buffalo. Dr. Bermel completed his neurology residency training and served as Chief Resident at Cleveland Clinic. He was funded as a National MS Society postdoctoral fellow in clinical neuroimmunology and advanced imaging at Cleveland Clinic. Dr. Bermel cares for patients, conducts imaging research, and an investigator in multiple clinical trials at the Mellen Center. His current research interests focus on the identification of advanced imaging methods to evaluate and improve recovery from inflammatory demyelinating disease. Visit www.mslivingwell.org for more information.

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

Progressive multiple sclerosis can be a worrisome diagnosis, filled with questions about one's personal future including independence. In this podcast, Mark Webb shares his personal story of transition to secondary progressive multiple sclerosis with incredible resiliency, brilliant humor and tenacious optimism. He explains how MS has affected his career from Euro Disney to Head of Communications at Shift.ms, a global online MS community. He candidly describes the impact of the disease on his functioning including cognition, mobility and bladder and how he has adapted to these obstacles. Mark reflects on his acceptance of progressive MS and emphasizes his motivation to make a difference for himself, his family and the MS community. Dr. Gavin Giovannoni describes in the podcast primary progressive MS, secondary progressive MS and active secondary progressive MS and whether or not these are truly different conditions. He moves beyond labels and explains that people with progressive disease, even those with limited mobility, can still be at risk of relapses affecting vision and arms. Continuing, switching or stopping disease-modifying therapy in progressive multiple sclerosis patients are covered. The impact of early MS damage, aging and ongoing, smoldering inflammation on progressive disease is described. Progressive multiple sclerosis treatments in clinical trials are highlighted including masitinib, BTK inhibitors, ibudilast, simvastatin, biotin, lipoic acid and remyelination strategies. Mark Webb is Head of Communications for Shift.ms, an online community of over 38,000 people living with MS. Mark lives with secondary progressive multiple sclerosis and first developed MS symptoms back in 1992. He's a blog writer: onemanandhiscatheters.com, public speaker and rugby wheelchair player. Mark lives in the U.K. with wife and 2 sons. Gavin Giovannoni MBBCh, PhD, FCP, FRCP, FRCPath is the Chair of Neurology of the Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry at Queen Mary University of London. Professor Giovannoni completed his medical training and neurology training in South Africa. In addition, he completed a PhD in immunology from the University of London in 1998. He is particularly interested in clinical issues related to optimizing MS disease-modifying therapies including progressive disease. 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.

Today, remyelination holds real promise as a strategy for restoring lost function and slowing or even stopping MS progression.  This week, we're taking a deep dive into the current state of remyelination research.  Joining me are Dr. Jeffrey Cohen, the Hazel Prior Hostetler Professor of Neurology at the Cleveland Clinic and the director of the Cleveland Clinic’s Mellen Center for Multiple Sclerosis Treatment and Research, and Dr. Ian Duncan, a neuroscientist, and Professor of Neurology at the University of Wisconsin-Madison and the recipient of the 2020 Dystel Prize for MS Research.   We're also talking about the publication of the Atlas of MS, the most extensive global MS prevalence study to date. And we're even including a copy of the published study as bonus content in the RealTalk MS app!   We're sharing an excellent explanation of comorbidities in MS by Dr. Ruth Ann Marrie. And we're sharing some news about Dr. Marrie, as well.   The European MS Platform's annual conference begins Thursday. This year, the theme is Understanding Progressive MS. We'll tell you how and where to register for this free virtual event. And we'll remind you where you can register for next week's virtual 2020 MS-CONNECT conference, hosted by the MS Society of Canada.   We have a lot to talk about! Are you ready for RealTalk MS??! Veterans with MS are eligible to join the PVA  :22 The largest MS prevalence study to date has been published. And it's yours in the RealTalk MS app!  3:26 Dr. Ruth Ann Marie on comorbidities in MS   4:29 European MS Platform Annual Conference: Understanding Progressive MS begins Thursday   5:56 MS Society of Canada 2020 MS-CONNECT Conference begins next Monday  6:56 Dr. Jeffrey Cohen talks about remyelination  9:13 Dr. Ian Duncan talks about the science behind remyelination  21:48 Share this episode  31:31 Donate to the National MS Society COVID-19 Response Fund  31:52 SHARE THIS EPISODE OF REALTALK MS Just copy this link & paste it into your text or email: https://realtalkms.com/168 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.comPhone: (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 Give RealTalk MS a Rating and Review National MS Society's Ask An MS Expert Video Replay What You Need to Know About Coronavirus (COVID-19) Paralyzed Veterans Of America VIDEO: Dr. Ruth Ann Marrie on comorbidities in MS Register for the European MS Platform Annual Conference: Understanding Progressive Multiple Sclerosis Register for the MS Society of Canada's 2020 MS-CONNECT Conference National MS Society COVID-19 Response Fund Join the RealTalk MS Facebook Group Download the RealTalk MS App for iOS Download the RealTalk MS App for Android Give RealTalk MS a Rating and Review Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 168 Guests: Dr. Jeffrey Cohen, Dr. Ian Duncan Tags: MS, MultipleSclerosis, MSResearch, MSSociety, MSActivist, EMSPVirtual2020, MSConnect, RealTalkMS Privacy Policy

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.10.22.350181v1?rss=1 Authors: Benitez-Fernandez, R., Melero-Jerez, C., Gil, C., de la Rosa, E. J., Martinez, A., de Castro, F. Abstract: The need for remyelinating drugs is essential for healing important diseases such as multiple sclerosis (MS). One of the reasons for the lack of this class of therapies is the impossibility to follow remyelination in vivo, which is of utmost importance to perform good clinical trials. Here, we show how the optical coherence tomography (OCT), a cheap and non-invasive technique commonly used in ophthalmology, may be used to follow remyelination in vivo in MS patients. Our pioneer study validates the study of myelin/remyelination in the optic nerve using OCT and reflects what is occurring in non accessible CNS structures, like the spinal cord. For this study we used the oral bioavailable small molecule VP3.15, confirming its therapeutical potential as neuroprotective, antinflammatory and remyelinating drug for MS. Altogether, our present results confirm the usefulness of OCT to monitor the effectivity of remyelinating therapies in vivo and underscore the relevance of VP3.15 as potential disease modifying drug for MS therapy. Copy rights belong to original authors. Visit the link for more info

Multiple Sclerosis News Today's columnist, Jenn Powell, discusses how a mechanism controlling remyelination may have MS therapy implications. Plus, Multiple Sclerosis News Today's columnist, Jessie Ace, reads from her DISabled to Enabled column entitled One Way To Be More Successful with MS. ===================================== Treatment for Relapsing MS Progression | MAYZENT® (siponimod) Read about MAYZENT, a once daily pill that can significantly slow down disability progression in people with relapsing MS. See full prescribing & safety info. http://ChangesInRMS.com ===================================== Are you interested in learning more about multiple sclerosis? If so, please visit: https://multiplesclerosisnewstoday.com/ ===================================== To join in on conversations regarding multiple sclerosis, please visit: https://multiplesclerosisnewstoday.com/forums/

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/2020.05.26.111856v1?rss=1 Authors: Carlstrom, K. E., Zhu, K., Ewing, E., Krabbendam, I., Harris, R. A., Mendanha Falcao, A., Jagodic, M., Castelo Branco, G., Piehl, F. Abstract: Arrest of oligodendrocyte (OL) differentiation and remyelination following myelin damage in Multiple Sclerosis (MS) are associated with disease progression but the underlying mechanism are elusive. We show that Glutathione S-transferase 4 (Gsta4) is highly expressed during adult OL differentiation and that its loss prevents differentiation into myelinating OLs. Also, Gsta4 appeared to be a novel target for Clemastine, in clinical trial for MS. Over-expression of Gsta4 reduced the expression of Fas and activity along the mitochondria-associated Casp8/Bid-axis in adult pre-OLs from the corpus callosum, together promoting enhanced pre-OL survival during differentiation. The Gsta4-mediated input on apoptosis during adult OL differentiation was further verified in the LPC and EAE model, where Casp8 were reduced in pre-OLs with high Gsta4 expression in an immune response-independent fashion. Our results place Gsta4 as a key regulator of intrinsic mechanisms beneficial for OL differentiation and remyelination, and as a possible target for future MS therapies. Copy rights belong to original authors. Visit the link for more info

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.05.21.108373v1?rss=1 Authors: Foerster, S., Neumann, B., McClain, C., Di Canio, L., Chen, C., Reich, D., Simons, B. D., Franklin, R. Abstract: Oligodendrocytes that generate new myelin sheaths around demyelinated axons in the regenerative process of remyelination are generally derived from oligodendrocyte progenitor cells (OPCs). During this process, OPCs become activated, populate the area of myelin loss, and finally differentiate. Although much is known about the individual stages of remyelination, the exact sequence of events and whether a dependency of each individual stage on each other exists is unknown. Understanding the biology behind these questions is important for the development of remyelination therapies to overcome the age-related decline in remyelination efficiency observed in the chronic phase of multiple sclerosis (MS). Here we show that, following toxin-induced demyelination, all re-populating OPCs first migrate into the site of damage, undergo relatively few rounds of division and eventually differentiate. We further show that OPC proliferation is a requirement for differentiation. Together, our results reveal an unexpected link between OPC proliferation and differentiation, and opens up the possibility of novel regenerative strategies in MS focussing on stimulating OPC proliferation. Copy rights belong to original authors. Visit the link for more info

Myelin is the coating on the nerve cells (neurons) of the nervous system that allows messages to travel rapidly in our body. Myelin wrapped around the neurons also keeps neurons healthy. In multiple sclerosis, the immune system attacks myelin disrupting electrical signals and making neurons vulnerable to chronic damage. Remyelination is the strategy to recoat the nerves with new myelin. Myelin-making cells called oligodendrocytes (“oligos”) are described. The podcast reviews recent laboratory breakthroughs in screening for new treatments to turn on immature oligos to repair myelin. The exciting initial steps are presented regarding the transition from the laboratory research into clinical trials with multiple sclerosis patients. Barry Singer, MD, Director of The MS Center for Innovations in Care at Missouri Baptist Medical Center interviews: Ari J Green, MD, Chief of Division of Neuroinflammation and Glial Biology, Medical Director of Multiple Sclerosis and Neuroinflammation Center, Debbie and Andy Rachleff Distinguished Professor of Neurology, Departments of Neurology and Ophthalmology, University of California San Francisco. To learn more, www..mslivingwell.org To share your MS story, check out www.ICanWithMS.org 

Robots?? Really??? The answer is YES! World renowned robotics expert Dr. Maja Mataric joins us on the podcast, and we're talking about how socially assistive robots could be real game-changers for people living with MS and other chronic conditions, as well as their caregivers. We're also talking about the $24.4 million investment by the National MS Society that will support 64 new MS research projects. We'll tell you about the research team at Oregon Health & Science University that believes they have solved remyelination! We'll show you how you can stay cool this summer and how you can get a brand new laptop or desktop computer from the Multiple Sclerosis Foundation...for free! We're reminding you that there's still time for you to see the video replay of an outstanding progressive MS webinar, and we'll even tell you about the woman living with MS who decided to get her stem cell transplant live on Facebook! We have a lot to talk about. Are you ready for RealTalk MS??! You Can Be My Special Guest on RealTalk MS  :22 National MS Society Invests $24.4 Million in 64 New MS Research Projects  3:15 Oregon Health & Sciences University Investigators Announce Remyelination Breakthrough  6:14 Free Resources Available from the Multiple Sclerosis Foundation   10:15 Progressive MS Webinar Hosted by Multiple Sclerosis International Federation  12:15 Hematopoietic Stem Cell Transplantation on Facebook Live  14:21 Diagnosing & Treating MS Video Series Is Available Online  16:11 My Interview with Dr. Maja Mataric  17:27 ___________ 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.comPhone: (310) 526-2283 ___________ 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 Be My Guest on RealTalk MS Episode #100 MS Society Invests $24.4 Million in 64 New MS Research Projects Myelin Repair Stimulated by CNS-Selective Thyroid Hormone Action MS-FOCUS Cooling Program MS-FOCUS Computer Program VIDEO: Solving Progressive MS: Progress Achieved and Hope for the Future VIDEO: Jacksonville Nurse Gets Experimental Stem Cell Treatment Live on Facebook VIDEO: Advances in the Diagnosis and Treatment of Multiple Sclerosis Download the RealTalk MS App for iOS Download the RealTalk MS App for Android Give RealTalk MS a Rating & Review  ___________ Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 87 Hosted By: Jon Strum Guest: Dr. Maja Mataric Tags: MS, MultipleSclerosis, MSResearch, Robotics, Stemcells, Remyelination, MSFocus, MSIF, ProgressiveMS, RealTalkMS  

The logistics involved in traveling can be cumbersome, and that's twice as true if you're living with MS. Mobility issues and other special requirements can make travel challenging. But whether you're out exploring the world or just checking into a local hotel for a pampered staycation, travel can add so much to your quality of life. My guest on the podcast is Tarita Davenock. It's been 20 years since Tarita's MS diagnosis. And today, Tarita is the CEO of Travel For All, a travel agency that embraces the philosophy that travel should be inclusive, and not exclusive.       Last week, a federal judge declared the Affordable Care Act to be unconstitutional, and we're talking about what that means for people living with MS. We'll share some newly published results of a stem cell therapy clinical trial, we'll tell you about a study that demonstrates how exercise improves myelin repair in the mouse model of MS, and we'll tell you about CanProCo, a large MS research project just getting underway in Canada.    Jon and RealTalk MS were featured in last week's Causepods podcast. We'll tell you what that's all about, and how Causepods has created a way for you to support the National MS Society.   We have a lot to talk about! Are you ready for RealTalk MS?! ___________ The Affordable Care Act Was Ruled Unconstitutional -- What This Means for People Living with MS   2:11 RealTalk MS Is Featured on the CausePods Podcast  6:33 Encouraging Results From Stem Cell Therapy Study, But Questions Still Need To Be Answered  8:18 Ocrevus Approved for Treating Relapsing-Remitting MS in Scotland  10:53 Exercise Promotes Myelin Repair in Mouse Model of MS  12:07 The Canadian Proactive Cohort Study for People Living with MS Will Study 1,000 Canadians Living with MS   14:02 My Interview with Travel For All CEO, Tarita Davenock  16:37 ___________ LINKSIf 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 Download the RealTalk MS App for iOS Download the RealTalk MS App for Android National Patient Groups Denounce District Court Ruling Overturning Health Care Law Jon Strum & RealTalk MS on the Causepods Podcast GoFundMe Page Benefiting The National MS Society Prospective Phase II Clinical Trial of Autologous Hematopoietic Stem Cell Transplant for Treatment Refractory Multiple Sclerosis Multimodal Enhancement of Remyelination by Exercise with a Pivotal Role for Oligodendroglial PGC1a Travel For All Give RealTalk MS a Rating & Review ___________ Follow RealTalk MS on Twitter, @RealTalkMS_jon, and subscribe to our newsletter at our website, RealTalkMS.com. RealTalk MS Episode 69 Hosted By: Jon Strum Guest: Tarita Davenock Tags: MS, MultipleSclerosis, MS, RealTalkMS, TravelForAll, ACA, ProtectOurCare, MSActivist, HSCT, Ocrevus, CanProCo, MSSocietyCanada, Causepods

NDCN Departmental Seminar

Chronic demyelination is a pathological hallmark of multiple sclerosis (MS). Only a minority of MS lesions remyelinates completely. Enhancing remyelination is, therefore, a major aim of future MS therapies. Here we took a novel approach to identify factors that may inhibit or support endogenous remyelination in MS. We dissected remyelinated, demyelinated active, and demyelinated inactive white matter MS lesions, and compared transcript levels of myelination and inflammation-related genes using quantitative PCR on customized TaqMan Low Density Arrays. In remyelinated lesions, fibroblast growth factor (FGF) 1 was the most abundant of all analyzed myelination-regulating factors, showed a trend towards higher expression as compared to demyelinated lesions and was significantly higher than in control white matter. Two MS tissue blocks comprised lesions with adjacent de- and remyelinated areas and FGF1 expression was higher in the remyelinated rim compared to the demyelinated lesion core. In functional experiments, FGF1 accelerated developmental myelination in dissociated mixed cultures and promoted remyelination in slice cultures, whereas it decelerated differentiation of purified primary oligodendrocytes, suggesting that promotion of remyelination by FGF1 is based on an indirect mechanism. The analysis of human astrocyte responses to FGF1 by genome wide expression profiling showed that FGF1 induced the expression of the chemokine CXCL8 and leukemia inhibitory factor, two factors implicated in recruitment of oligodendrocytes and promotion of remyelination. Together, this study presents a transcript profiling of remyelinated MS lesions and identified FGF1 as a promoter of remyelination. Modulation of FGF family members might improve myelin repair in MS.

Trials of potential neuroreparative agents are becoming more important in the spectrum of multiple sclerosis research. Appropriate imaging outcomes are required that are feasible from a time and practicality point of view, as well as being sensitive and specific to myelin, while also being reproducible and clinically meaningful. Conventional MRI sequences have limited specificity for myelination. With colleagues Shahrukh Mallik, Department of Neuroinflammation, NMR Research Unit, Queen Square Multiple Sclerosis Centre, evaluated the imaging modalities which are potentially more specific to myelin content in vivo. He explains what they found. Read the full paper: http://goo.gl/chxZq7

We find out if banking our bone marrow early in life, and transplanting down the line, may help halt the aging process. Plus we ask, why are we so good at forgetting names?..... Like this podcast? Please help us by supporting the Naked Scientists

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) accompanied by demyelination and axonal loss. Only a minority of the demyelinated MS lesions gets remyelinated. In animal models, however, remyelination is the default program following immune-mediated or toxic demyelination. This thesis aims to find factors regulating remyelination in MS. The starting point was autoptic tissue from MS patients. First, different types of MS lesions were macrodissected namely, chronic inactive demyelinated lesions that had failed to remyelinate, lesions undergoing active demyelination and remyelinated lesions. Healthy white matter was used as control tissue. Gene expression profiles of these lesions were established using quantitative PCR low density arrays. Thereby the focus was on the extracellular matrix (ECM) and on factors known to regulate the biology of oligodendrocytes. ECM components can regulate oligodendrocyte differentiation and modify immune reactions in multiple ways, e.g., by sequestering or displaying growth factors and by directly interacting with immune cells and glial cells. The expression of 50 ECM components and 34 ECM degrading enzymes was measured by qPCR. COL1A1, COL3A1, COL5A1 and COL5A2 chains were strongly induced in active lesions and even more in chronic inactive lesions. These collagen polypeptide chains interact to form collagen types I, III and V, which are grouped as fibrillar collagens. Furthermore, two Small Leucine Rich Proteoglycans (SLRPs), biglycan and decorin, which can decorate fibrillar collagens, were also strongly induced. Immunostaining localized the fibrillar collagens, biglycan, and decorin around blood vessels. These ECM molecules were largely seen in the perivascular space closely associated with infiltrating immune cells forming a mesh between the endothelium and the astrocytic glia limitans. In active lesions collagen V was also seen in the heavily infiltrated brain parenchyma. Since these ECM molecules were found largely in the perivascular space close to immune cells and hardly in the surrounding parenchyma where oligodendrocyte differentiation takes place, the interaction of these ECM components with immune cells was further analysed. In vitro experiments revealed that the fibrillar collagens I and III inhibited the monocytic production of CCL2 (MCP-1), an inflammatory chemokine thought to be involved in the recruitment of immune cells to the inflamed brain. This suggests that the induced fibrillar collagens may contribute to the limitation of MS lesions expansion by inhibition of the CCL2 production by monocytes. The second set of analysed genes comprised 32 factors regulating survival, proliferation and/or differentiation of oligodendrocytes and 18 receptors of these genes. The key factors for oligodendrocyte differentiation (IGF1, IGF2 and CNTF) and oligodendrocyte proliferation (FGF2 and PDGFAA) were still present in demyelinated lesions, although their expression ratio was altered. The most striking result was the up-regulation of FGF9 in a subset of chronically demyelinated lesions, but in none of the remyelinated shadow plaques. The potential functional role of this observation was investigated by treating myelinating rat central nervous system cultures with exogenous FGF9. In this experimental setting, FGF9 inhibited the ability of mature oligodendrocytes to myelinate and ensheath axons. All these data suggests that the induction of FGF9 in some chronic MS lesions is one of the inhibitory mechanisms accounting for the failure of remyelination. Together, this thesis has two main findings: A) Fibrillar collagens, biglycan and decorin form a perivascular fibrosis and the fibrillar collagens I and III inhibit production of CCL2 by monocytes. Inhibition of CCL2 production by fibrillar collagens might contribute to lesion confinement. B) Expression profiles of remyelinated MS lesions were established for the first time and thereby, up-regulation of FGF9 in demyelinated, but not in remyelinated lesions was revealed. The inhibition of myelination in vitro by FGF9 suggests that this is one potential mechanism to explain why demyelinated lesions expressing higher FGF9 level fail to remyelinate.