Podcasts about aqp4

The December 2024 replay wraps up the year with five previously posted episodes on autoimmune neurology. The episode begins with Drs. Michael R. Wilson and John Pluvinage discussing transcobalamin antibodies. The episode leads into an interview with Dr. Andrew McKeon, who talks about paraneoplastic CAMKV autoimmune encephalitis. In the third episode, Dr. Maarten Titulaer discusses long-term outcomes and rehab in NMDAR encephalitis. The episode continues with Prof. Zsolt Illes discussing the mortality of patients with AQP4 antibody–seropositive neuromyelitis optica spectrum disorder compared with that in the general population. In the final episode, Drs. Marius Ringelstein and Ilya Ayzenberg discuss the effectiveness and safety of Eculizumab in routine clinical care. Podcast Links: Transcobalamin receptor Antibodies in Autoimmune Vitamin B12 Central Deficiency  Paraneoplastic CAMKV Autoimmune Encephalitis Long-Term Outcomes and Rehabilitation in Anti-NMDAR Encephalitis Mortality in a Danish NMO Cohort Eculizumab Use in Neuromyelitis Optica Spectrum Disorders Article Links: Transcobalamin Receptor Antibodies in Autoimmune Vitamin B12 Central Deficiency  Paraneoplastic Calmodulin Kinase-Like Vesicle-Associated Protein (CAMKV) Autoimmune Encephalitis  Long-Term Cognitive, Functional, and Patient-Reported Outcomes in Patients With Anti-NMDAR Encephalitis  Mortality of the Danish Nationwide AQP4 Antibody-Seropositive Neuromyelitis Optica Spectrum Disorder Patient Cohort  Eculizumab Use in Neuromyelitis Optica Spectrum Disorders: Routine Clinical Care Data From a European Cohort Disclosures can be found at Neurology.org.

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021. Originally released: September 12, 2019 We just used clinical trial data regarding eculizumab in myasthenia gravis as an example of how to critically appraise the literature, and in this week's program...MORE data on the efficacy of eculizumab in another neurologic condition. This week on BrainWaves, the exciting results of the PREVENT trial, and the future treatment of NMO spectrum disorder!  Produced by James E Siegler. Special thanks to Dr. Olga Rosenveld Thon. Music courtesy of Unheard Music Concepts, TRG Banks, and Aitua. Sound effects by Mike Koenig and baby Sofia Joan Siegler. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. Be sure to follow us on Twitter @brainwavesaudio for the latest updates to the podcast. REFERENCESFDA News Release: FDA approved first treatment for neuromyelitis optica spectrum disorder, a rare autoimmune disease of the central nervous system. 27 June 2019. Available online at https://www.fda.gov/news-events/press.... Accessed 30 Aug 2019.Pittock SJ, Berthele A, Fujihara K, et al. Eculizumab in aquaporin-4-positive neuromyelitis optica spectrum disorder. N Engl J Med 2019;381(7):614-25. PMID 31050279Pittock SJ, Lennon VA, McKeon A, et al. Eculizumab in AQP4-IgG-positive relapsing neuromyelitis optica spectrum disorders: an open-label pilot study. Lancet Neurol 2013;12(6):554-62. PMID 23623397 We believe that the principles expressed or implied in the podcast remain valid, but certain details may be superseded by evolving knowledge since the episode's original release date.

Dr. Justin Abbatemarco and Prof. Zsolt Illes discuss the mortality of patients with AQP4 antibody–seropositive neuromyelitis optica spectrum disorder compared with that in the general population. Show reference: https://www.neurology.org/doi/10.1212/WNL.0000000000209147 

Dr. Justin Abbatemarco talks with Prof. Zsolt Illes about the mortality of patients with AQP4 antibody–seropositive neuromyelitis optica spectrum disorder compared with that in the general population. Read the related article in Neurology.  This podcast is sponsored by argenx. Visit www.vyvgarthcp.com for more information. Disclosures can be found at Neurology.org.   

Visit nascentmc.com/podcast for full show notes Winrevair for PAH: Sotatercept-csrk (Winrevair) is FDA-approved for treating adults with pulmonary arterial hypertension (PAH), enhancing exercise capacity, improving WHO functional class, and reducing clinical worsening events. It's the first FDA-approved activin signaling inhibitor for PAH, addressing the imbalance in vascular cell proliferation underlying the condition. The approval is based on the Phase 3 STELLAR trial, demonstrating significant improvements in walk distance and reduced risk of clinical worsening events [1]. Vafseo for CKD: Vadadustat (Vafseo) is approved for managing anemia due to chronic kidney disease (CKD) in adult dialysis patients. As an oral HIF-PH inhibitor, it stimulates endogenous erythropoietin production, offering a novel approach to anemia management. Approval is supported by efficacy and safety data from the INNO2VATE program and post-marketing safety data from Japan [2]. Ultomiris for NMOSD: Ravulizumab-cwvz (Ultomiris) is FDA-approved for treating neuromyelitis optica spectrum disorder (NMOSD) in patients with anti-AQP4 antibodies. It's a terminal complement C5 inhibitor administered once every two months, demonstrating efficacy in preventing relapses. Approval is based on the Phase 3 CHAMPION-NMOSD study, showing significant reductions in relapse risk compared to placebo [3]. Evolut FX+ for TAVR: The Evolut™ FX+ transcatheter aortic valve replacement (TAVR) system is FDA-approved for treating symptomatic severe aortic stenosis. It features enhancements for improved catheter maneuverability without compromising effectiveness. The approval expands treatment options for patients across all risk categories [4]. Vemlidy for Pediatric HBV: Tenofovir alafenamide (Vemlidy) is FDA-approved for treating chronic hepatitis B virus (HBV) infection in pediatric patients aged 6 years and older with compensated liver disease. It's a preferred or first-line treatment option, addressing a significant medical need. Approval is based on the Phase 2 clinical trial 1092, demonstrating efficacy and safety in this patient population [5]. Pemgarda for COVID: Pemgarda, a monoclonal antibody, is FDA-approved for preventive use in immunocompromised individuals aged 12 and older against COVID-19. It prevents virus attachment and has shown promising results in reducing symptomatic COVID-19 cases. Approval is based on emergency use authorization and preliminary data from the CANOPY Phase 3 clinical trial [6].

Em doenças raras, a regra é a carência de recursos terapêuticos, poucas se beneficiam de medicamentos específicos ou diagnóstico assertivo. Felizmente não é o caso da neuromielite óptica – doença autoimune e inflamatória que atinge o sistema nervoso central. No início dos anos 2000 a ciência conseguiu compreender melhor a patologia, e consequentemente foi possível mais rapidamente detectá-la. O teste anti aquaporina 4 (anti-AQP4) está disponível no Rol de Procedimentos da ANS (Agência Nacional de Saúde Suplementar) desde 2018, mas ainda não chegou ao SUS, o Sistema Único de Saúde. A inovação acelera o diagnóstico da doença – o que pode mudar completamente o prognóstico do paciente – e não é considerada de alto valor econômico. O assunto é tema do terceiro episódio do podcast especial de Health Equity, em que a repórter Carolina Abelin conversou com o neurologista e professor da Universidade de Brasília, Felipe von Glehn e com o fundador da associação Crônicos do Dia a Dia e membro da Federação Brasileira das Associações de Doenças Raras, Gustavo San Martin Este podcast é um oferecimento da Horizon Therapeutics. --- Send in a voice message: https://podcasters.spotify.com/pod/show/mittechreviewbrasil/message

For this “ABCs of NMOSD” episode, Rebecca Whitney of SRNA was joined by Dr. Michael Levy. Dr. Levy gave an overview of I-CAN, a Phase 2 study of inebilizumab in children with aquaporin-4 positive neuromyelitis optica spectrum disorder or NMOSD. As one of the principal investigators for the study, he shared details about inclusion criteria and inebilizumab, brand name Uplizna™. Dr. Levy also discussed what someone can expect if they choose to participate in this trial, how participation would impact someone's current treatment, and the timeline of this trial. Additional information is available here: https://wearesrna.org/clinical-studies-and-trials/study-of-inebilizumab-in-pediatric-subjects-with-neuromyelitis-optica-spectrum-disorder/  https://clinicaltrials.gov/study/NCT05549258?term=NCT05549258&aggFilters=status:not%20rec&rank=1

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.07.21.549379v1?rss=1 Authors: Mueller, S. M., White, K. M., Fass, S. B., Chen, S., Shi, Z., Ge, X., Engelbach, J. A., Gaines, S. H., Bice, A. R., Vasek, M. J., Garbow, J. R., Culver, J. P., Martinez-Lozada, Z., Cohen-Salmon, M., Dougherty, J. D., Sapkota, D. Abstract: Aquaporin-4 (AQP4) is a water channel protein that links astrocytic endfeet to the blood-brain barrier (BBB) and regulates water and potassium homeostasis in the brain, as well as the glymphatic clearance of waste products that would otherwise potentiate neurological diseases. Recently, translational readthrough was shown to generate a C-terminally extended variant of AQP4, known as AQP4x, that preferentially localizes around the BBB through interaction with the scaffolding protein -syntrophin, and loss of AQP4x disrupts waste clearance from the brain. To investigate the function of AQP4x, we generated a novel mouse AQP4 line (AllX) to increase relative levels of the readthrough variant above the ~15% of AQP4 in the brain of wildtype (WT) mice. We validated the line and assessed characteristics that are affected by the presence of AQP4x, including AQP4 and -syntrophin localization, integrity of the BBB, and neurovascular coupling. We compared AllXHom and AllXHet mice to wildtype, and to previously characterized AQP4 NoXHet and NoXHom mice, which cannot produce AQP4x. Increased dose of AQP4x enhanced perivascular localization of -syntrophin and AQP4, while total protein expression of the two were unchanged. However, at 100% readthrough, AQP4x localization and formation of higher-order complexes was disrupted. Electron microscopy showed that overall blood vessel morphology was unchanged except for increased endothelial cell vesicles in NoXHom mice, which may correspond to a leakier BBB or altered efflux that was identified in NoX mice using MRI. These data demonstrate that AQP4x plays a small but measurable role in maintaining BBB integrity as well as recruiting structural and functional support proteins to the blood vessel. This also establishes a new set of genetic tools for quantitatively modulating AQP4x levels. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

DrBeen#50 Omega-3 and Exercise for Brain Health Continuing with our series about brain health and lifestyle choices, today we will discuss omega-3 fish oil and exercise. Omega-3 fish oil or omega-3 polyunsaturated fatty acids (n3-PUFA) have a rich presence in our brain tissue. n3-PUFA helps keep astrocyte from becoming activated. Hence, it reduces inflammation in the brain and also keeps aquaporin 4 (AQP4) channels polarized and on the foot processes of the astrocytes. The result is a better glymphatic flow, which washes away more beta amyloids and helps protect or stall the progress of dementia. DrBeen: Medical Education Onlinehttps://www.drbeen.com/ FLCCC | Front Line COVID-19 Critical Care Alliancehttps://covid19criticalcare.com/ URL list from Monday, Mar. 23 2023 The Sleeping Brain: Harnessing the Power of the Glymphatic System through Lifestyle Choices - PMChttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7698404/ Sleep well — and reduce your risk of dementia and death - Harvard Healthhttps://www.health.harvard.edu/blog/sleep-well-and-reduce-your-risk-of-dementia-and-death-2021050322508 APOE ε4, Alzheimer's disease neuropathology and sleep disturbance, in individuals with and without dementia | Alzheimer's Research & Therapy | Full Texthttps://alzres.biomedcentral.com/articles/10.1186/s13195-022-00992-y N3 Phase of Sleep.https://chat.openai.com/chat Understanding Delta Brain Waves And Sleephttps://www.sixstepstosleep.com/understanding-delta-brain-waves/ N3: Slow Wave Sleep | Sleepopolishttps://sleepopolis.com/education/n3-slow-wave-sleep/ Stage N3 of sleep. Delta waves on EEG recordings are observed.  | Download Scientific Diagramhttps://www.researchgate.net/figure/Stage-N3-of-sleep-Delta-waves-on-EEG-recordings-are-observed_fig4_280558638 A 30-second Epoch consisting of the parameters of staging sleep... | Download Scientific Diagramhttps://www.researchgate.net/figure/4-A-30-second-Epoch-consisting-of-the-parameters-of-staging-sleep-electroencephalogram_fig4_282014972 Hallmark of Stage N3 (slow-wave sleep or Stages 3 and 4 sleep: delta... | Download Scientific Diagramhttps://www.researchgate.net/figure/Hallmark-of-Stage-N3-slow-wave-sleep-or-Stages-3-and-4-sleep-delta-waves_fig1_5812861 Frontiers | Perivascular Spaces, Glymphatic System and MRhttps://www.frontiersin.org/articles/10.3389/fneur.2022.844938/full Perivascular spaces and brain waste clearance systems: relevance for neurodegenerative and cerebrovascular pathology | SpringerLinkhttps://link.springer.com/article/10.1007/s00234-021-02718-7 Frontiers | Perivascular Unit: This Must Be the Place. The Anatomical Crossroad Between the Immune, Vascular and Nervous Systemhttps://www.frontiersin.org/articles/10.3389/fnana.2020.00017/full Neuroglia Lab : Glymphatics and virchow-robin spacehttp://visnu528.blogspot.com/2014/09/glymphatics-and-virchow-robin-space.html Physiology and Clinical Relevance of Enlarged Perivascular Spaces in the Aging Brain | Neurologyhttps://n.neurology.org/content/98/3/107 Aquaporin-4 - Wikipediahttps://en.wikipedia.org/wiki/Aquaporin-4 Astrocyte - Wikipediahttps://en.wikipedia.org/wiki/Astrocyte Neurocytology-Astrocyteshttps://neuropathology-web.org/chapter1/chapter1bAstrocytes.html#:~:text=Astrocytic%20foot%20processes%20surround%20brain,maintains%20homeostasis%20in%20the%20CNS. Blood-brain barrier | RIThttps://www.rit.edu/spotlights/blood-brain-barrier The Blood-Brain Barrier | Morphology of Nervous Systemhttps://sisu.ut.ee/histology/blood-brain-barrier Elimination of substances from the brain parenchyma: efflux via perivascular pathways and via the blood–brain barrier | Fluids and Barriers of the CNS | Full Texthttps://fluidsbarrierscns.biomedcentral.com/articles/10.1186/s12987-018-0113-6 Disclaimer:As previous

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2023.04.03.535397v1?rss=1 Authors: Duan, W. Abstract: Huntington disease (HD) is a neurodegenerative disorder that presents with progressive motor, mental, and cognitive impairment leading to early disability and mortality. The accumulation of mutant huntingtin protein aggregates in neurons is a pathological hallmark of HD. The glymphatic system, a brain-wide perivascular network, facilitates the exchange of interstitial fluid (ISF) and cerebrospinal fluid (CSF), supporting interstitial solute clearance including abnormal proteins from mammalian brains. In this study, we employed dynamic glucose-enhanced (DGE) MRI to measure D-glucose clearance from CSF as a tool to assess CSF clearance capacity to predict glymphatic function in a mouse model of HD. Our results demonstrate significantly diminished CSF clearance efficiency in premanifest zQ175 HD mice. The impairment of CSF clearance of D-glucose, measured by DGE MRI, worsened with disease progression. These DGE MRI findings in compromised glymphatic function in HD mice were further confirmed with fluorescence-based imaging of glymphatic CSF tracer influx, suggesting an impaired glymphatic function in premanifest stage of HD. Moreover, expression of the astroglial water channel aquaporin-4 (AQP4) in the perivascular compartment, a key mediator of glymphatic function, was significantly diminished in both HD mouse brain as well as postmortem human HD brain. Our data, acquired using a clinically translatable MRI approach, indicate a perturbed glymphatic network in the HD brain as early as in the premanifest stage. Further validation of these findings in clinical studies should provide insights into potential of glymphatic clearance as a HD biomarker and for glymphatic functioning as a disease-modifying therapeutic target for HD. 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/2023.03.21.533684v1?rss=1 Authors: Kushwaha, R., Li, Y., Makarava, N., Pandit, N. P., Molesworth, K., Birukov, K. G., Baskakov, I. V. Abstract: Background. Impairment of the blood-brain barrier (BBB) is considered to be a common feature among neurodegenerative diseases, including Alzheimer's, Parkinso'n s and prion diseases. In prion disease, increased BBB permeability was reported 40 years ago, yet the mechanisms behind the loss of BBB integrity have never been explored. Recently, we showed that reactive astrocytes associated with prion diseases are neurotoxic. The current work examines the potential link between astrocyte reactivity and BBB breakdown. Results. In prion-infected mice, the loss of BBB integrity and aberrant localization of aquaporin 4 (AQP4), a sign of retraction of astrocytic endfeet from blood vessels, were noticeable prior to disease onset. Gaps in cell-to-cell junctions along blood vessels, together with downregulation of Occludin, Claudin-5 and VE-cadherin, which constitute tight and adherens junctions, suggested that loss of BBB integrity is linked with degeneration of vascular endothelial cells. In contrast to cells isolated from non-infected adult mice, endothelial cells originating from prion-infected mice displayed disease-associated changes, including lower levels of Occludin, Claudin-5 and VE-cadherin expression, impaired tight and adherens junctions, and reduced trans-endothelial electrical resistance (TEER). Endothelial cells isolated from non-infected mice, when co-cultured with reactive astrocytes isolated from prion-infected animals or treated with media conditioned by the reactive astrocytes, developed the disease-associated phenotype observed in the endothelial cells from prion-infected mice. Reactive astrocytes were found to produce high levels of secreted IL-6, and treatment of endothelial monolayers originating from non-infected animals with recombinant IL-6 alone reduced their TEER. Remarkably, treatment with extracellular vesicles produced by normal astrocytes partially reversed the disease phenotype of endothelial cells isolated from prion-infected animals. Conclusions. To our knowledge, the current work is the first to illustrate early BBB breakdown in prion disease and to document that reactive astrocytes associated with prion disease are detrimental to BBB integrity. Moreover, our findings suggest that the harmful effects are linked to proinflammatory factors secreted by reactive astrocytes. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Neuromyelitis-optica-Spektrum-Erkrankungen (NMOSD) sind seltene entzündliche Autoimmunerkrankungen des zentralen Nervensystems, die meist schubförmig verlaufen. Wie grenzen sich diese Erkrankungen von der Multiplen Sklerose (MS) ab und welche Rolle spielen Aquaporin-4-Antikörper (AQP4-AK) dabei? Was passiert bei einem Schub und warum ist es so wichtig weitere Schübe zu verhindern? Antworten auf diese Fragen gibt NMOSD-Expertin Frau Professorin Trebst in der aktuellen Podcast-Folge. Gast: Prof.in Dr. med. Corinna Trebst, Stellvertretende Direktorin der Klinik für Neurologie mit Klinischer Neurophysiologie, Medizinische Hochschule Hannover; Mitglied der Neuromyelitis optica Studiengruppe (NEMOS) Moderator: Prof. Dr. med. Martin Grond, Chefarzt der Neurologie im Kreisklinikum Siegen DE/UNB-N/0030

Sean J. Pittock, MD, Director of Mayo Clinic's Center for Multiple Sclerosis and Autoimmune Neurology and of Mayo's Neuroimmunology Laboratory discusses the latest results from Phase III CHAMPION-NMOSD trial recently presented at European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) Congress. The results showed that treatment with ravulizumab-cwvz significantly reduced relapse risk in adults with anti-aquaporin-4 (AQP4) antibody-positive (Ab+) neuromyelitis optica spectrum disorder (NMOSD).NMOSD is a rare central nervous disorder that primarily affects the spinal cord and optic nerves. Symptoms of NMOSD may include blindness in one or both eyes, weakness or paralysis of arms or legs, spasming, loss of sensation, uncontrollable vomiting and hiccups, and bladder/bowel problems due to spinal cord damage. Relapse is very common in persons with NMOSD and episodes can be severe enough to cause permanent disability.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.12.19.520991v1?rss=1 Authors: Obenaus, A., Rodriguez-Grande, B., Jeong Bin, L., Dubois, C., Fournier, M.-L., Cador, M., Caille, S., Badaut, J. Abstract: Traumatic brain injury (TBI) has the highest incidence amongst the pediatric population and its mild severity represents the most frequent cases. Moderate and severe injuries as well as repetitive mild TBI result in lasting morbidity. However, whether a single mild TBI sustained during childhood can produce long-lasting modifications within the brain is still debated. We aimed to assess the consequences of a single juvenile mild TBI (jmTBI) at 12 months post-injury in a mouse model. Non-invasive diffusion tensor imaging (DTI) revealed significant microstructural alterations in the hippocampus and the in the substantia innominata/nucleus basalis (SI/NB), structures known to be involved in spatial learning and memory. DTI changes paralled neuronal loss, increased astrocytic AQP4 and microglial activation in the hippocampus. In contrast, decreased astrocytic AQP4 expression and microglia activation were observed in SI/NB. Spatial learning and memory were impaired and correlated with alterations in DTI-derived derived fractional ansiotropy (FA) and axial diffusivity (AD). This study found that a single juvenile mild TBI leads to significant region-specific DTI microstructural alterations, distant from the site of impact, that correlated with cognitive discriminative novel object testing and spatial memory impairments at 12 months after a single concussive injury. Our findings suggest that exposure to jmTBI leads to a chronic abnormality, which confirms the need for continued monitoring of symptoms and the development of long-term treatment strategies to intervene in children with concussions. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Sean J. Pittock, MD, Director of Mayo Clinic's Center for Multiple Sclerosis and Autoimmune Neurology and of Mayo's Neuroimmunology Laboratory discusses the latest results from Phase III CHAMPION-NMOSD trial recently presented at European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) Congress. The results showed that treatment with ravulizumab-cwvz significantly reduced relapse risk in adults with anti-aquaporin-4 (AQP4) antibody-positive (Ab+) neuromyelitis optica spectrum disorder (NMOSD).NMOSD is a rare central nervous disorder that primarily affects the spinal cord and optic nerves. Symptoms of NMOSD may include blindness in one or both eyes, weakness or paralysis of arms or legs, spasming, loss of sensation, uncontrollable vomiting and hiccups, and bladder/bowel problems due to spinal cord damage. Relapse is very common in persons with NMOSD and episodes can be severe enough to cause permanent disability. As Dr. Pittock explains, the CHAMPION-NMOSD study is a global Phase III, open-label, multicenter trial evaluating the safety and efficacy of ravulizumab in adults with AQP4-Ab+ NMOSD (n-58). The data presented by Dr. Pittock at ECTRIMS showed that no relapses were observed in patients receiving ravulizumab, with a median treatment duration of 73 weeks. Further, 100% of patients receiving ravulizumab remained relapse-free at 48 weeks, compared to 63% of patients in the external placebo arm.To learn more about NMOSD and other rare neurologic disorders, visit checkrare.com/ neurology/

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.10.03.510559v1?rss=1 Authors: Okada, S., Kobayashi, M., Lee, H., Morita, M. Abstract: The brain abundantly expresses adenosine receptors, which are involved in the regulation of neural activity, blood flow, and inflammation. In a previous study using our originally developed adenosine biosensor, we reported that hippocampal astrocytes release ATP upon water influx from the water channel AQP4, which is degraded extracellularly to increase adenosine (Yamashiro et al., 2017). On the other hand, the interaction between adenosine and dopamine is widely known, and when adenosine release from astrocytes is altered by inflammation or other factors, abnormal dopamine neurotransmission and related ataxia and psychiatric disorders may develop. In the present study, we examined pathological changes in adenosine or dopamine release in depressive-like behavior that develops as a symptom of cocaine withdrawal. The results showed that A1 receptor inhibitors and AQP4 gene disruption suppressed depressive-like behavior. In the striatum, AQP4-dependent adenosine release inhibited dopamine release via A1 receptors, and cocaine inhibited dopamine release by increasing this adenosine release. In contrast, in the medial frontal cortex, AQP4-dependently released adenosine enhanced dopamine release via A1 receptors, and cocaine abolished this adenosine effect. Furthermore, adenosine action was restored in AQP4 knockout mice, suggesting that cocaine reduced A1 receptor function via AQP4-dependent adenosine. In conclusion, astrocytes modulate dopaminergic neurotransmission through AQP4-mediated adenosine release, and this disruption leads to depression-like behavior. Copy rights belong to original authors. Visit the link for more info Podcast created by PaperPlayer

Let's get ready to rumble with Cynthia Monteleone! She is a World Champion Masters Track and Field athlete and a certified holistic metabolic analytics practitioner. Cynthia comes from the beautiful island of Maui and is full of positive energy and enthusiasm, and our conversation today is interesting and inspiring, and trust me, the minute the show is over, you are going to be ready to sprint! She is a huge proponent of the overall fitness and health lifestyle benefits of sprinting, and at the very end of the show, she shares a fabulous list detailing the 10 reasons why sprinting is superior to cardio for fitness, health, and everything else. You'll hear about her background as a college athlete, the 20-year break she took to live real life and raise kids in Hawaii, and then her rapid ascension to winning the World Title for sprinting in her age group. Her time for a 400-meter sprint is 57 seconds! If you need a reference point for that time, it's an extraordinary performance: I will admit, she's faster than me! It's also faster than how she ran in college as a D1 athlete! Cynthia is turning back the clock like nobody's business, and she has this amazing and unique blend of steep scientific knowledge as well as practical application from being an all-around World Champion jock. We'll get into some science at the very end with this well-read, well-researched certified practitioner, who also started MAM: Metabolic Analytics of Maui, a company that helps clients reach their nutrition and physical fitness goals. Through analytics, consultation and education, she helps everyday folks as well as elite athletes. Enjoy hearing this lively conversation with Cynthia, and if you want to learn more about her work, click here.   TIMESTAMPS: World champion sprinter is here to talk about sprinting, supplements, and the timing of workouts as part of her training. [00:57]    After running in college, Cynthia took a hiatus to raise a family and then journeyed forward to win a world championship. [03:43] Your body does a great job cleaning up your system by storing toxins in the body fat. [06:09] While training with Charles Poliquin, she improved her running skills by 50%. [08:28] She ran the 400 in 58 flat at age 42, in the Masters meet. [13:11] When you are going for marginal improvements and you're already at the elite level trying to get faster, the training is pretty difficult. [19:02] Cynthia talks about the supplements she has found that works well, especially when traveling. The timing of your workouts is important too. [21:18] Stop icing and stop static stretching when trying to recover. [27:30] Cynthia basically is on an animal protein-based diet. Lactate is a valuable energy source. [30:12] You can tell by the bicep measurement how their testosterone is and the tricep measurement how the estrogen is.  [34:13] Especially an issue with women is the toxins that reside in the body that come from scented candles, beauty products, lotions, etc.  [39:13] Dietary optimization is still an important goal, even with elite athletes. [48:19] Ditch the AirPods! They are microwaving your brain. There is a lot of research on EMF. [54:00] What percentage of the workouts are working within your capacity so that you can recover and rebuild? [56:35] Sprinting is better than cardio for fat loss and gut health. There are 10 reasons why. One is you get better hormone balance. [01:03:34] The micro bacteria in your microbiome is dictated by what foods you eat and what type of exercise you do. [01:07:38] Sprinters are smarter than distance runners. Number 4 is sprinting makes you happier. [01:09:38] Overuse injuries are more abundant in endurance training. There is a high risk in endurance for heart remodeling. [01:10:43] Body fat percentage is number seven. If you are too thin, you have poor hormone health. [01:13:11] You can damage the DNA in the cells when participating in endurance. [01:15:18] AQP4 is a water channel which is in your brain like the lymphatic system. [01:17:06] LINKS: Brad Kearns.com Brad's Shopping page Metabolic Analytics of Hawaii Cynthia Monteleone Cynthia racing against high school girls Cynthia's Instagram What is MAM Peak Human podcasts Game Changers Fast Over 40   QUOTES: "If you're in the gym longer than an hour, you are making friends, not progress!"(Poliquin) "Sprinting is better for aging, than endurance training." (Monteleone)   Join Brad for more fun on: Instagram: @bradkearns1 Facebook: @bradkearnsjumphigh Twitter: @bradleykearns YouTube: @BradKearns TikTok: @bradkearns   We appreciate all feedback, and questions for Q&A shows, emailed to podcast@bradventures.com. If you have a moment, please share an episode you like with a quick text message, or leave a review on your podcast app. Thank you! Check out each of these companies because they are absolutely awesome or they wouldn't occupy this revered space. Seriously, Brad won't promote anything he doesn't absolutely love and use in daily life. Butcher Box: Convenient, affordable home delivery - free shipping! - of the highest quality meat, poultry, and seafood with customizable box design. Click here for special promotion.  Brad's Macadamia Masterpiece: Mind-blowing, life-changing nut butter blend Male Optimization Formula with Organs (MOFO): Optimize testosterone naturally with 100% grassfed animal organ supplement BeautyCounter: Complete line of cosmetics tested to be free of typical toxins and endocrine disruptors. Try Brad's favorite vitamin-C skin serum and make the switch away from toxic mainstream skin-care products! 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Dr. Nicolas Collongues discusses pregnancy in patients with neuromyelitis optica spectrum disorder.

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.11.01.363945v1?rss=1 Authors: Sapkota, D., Dougherty, J. Abstract: An unusual stop codon readthrough event generates a conserved C-terminally elongated variant of the water channel protein Aquaporin 4 (AQP4). In the brain, AQP4 is astrocyte-specific, required for normal functioning of the glymphatic system, and involved in the clearance of the Alzheimers associated protein Amyloid beta. Further, the readthrough variant is localized exclusively perivascularly, and the perivascular pool of AQP4 is reduced in Alzheimers and several other neurological diseases. However, there are currently no means of increasing or restoring the perivascular pool AQP4. Here we identify a compound that can enhance Aqp4 stop codon readthrough. We screened 2600 compounds, mostly approved drugs and pharmacologically active natural compounds, using a luciferase reporter system. 28 candidate lead compounds were then subjected to a variety of secondary screening steps using orthogonal reporter systems and characterizing dose-response activities. Finally, we tested the top compounds abilities to generate readthrough of the endogenous Aqp4 transcript, identifying Apigenin as an enhancer of this biological phenomenon. This compound can allow modulation of readthrough in experimental systems, mechanistic studies of programmed readthrough, and suggests the potential for modulating Alzheimers disease through pharmacological enhancement of perivascular AQP4. Copy rights belong to original authors. Visit the link for more info

Dr. Geoffrey Eubank, M.D., Medical Director of the Mid Ohio MS Center at OhioHealth Neurological Physicians, discusses 2 Phase lll clinical trials of Enspryng™ (satralizumab-mwge) that demonstrated robust efficacy and safety profiles for the treatment of adults living with anti-aquaporin-4 (AQP4) antibody-positive NMOSD, a rare disabling neurological disorder often misdiagnosed as multiple sclerosis. Enspryng represents significant therapeutic progress for the NMOSD community, offering the only FDA-approved injectable treatment option that can be self-administered every four weeks by a person living with NMOSD or a caregiver following training from a healthcare provider.

Dr. Kathleen Hawker, M.D., Group Medical Director, Neuroscience at Genentech discusses the recent FDA approval of Enspryng™ (satralizumab-mwge) and the findings from the clinical trial program for the treatment of adults living with anti-aquaporin-4 (AQP4) antibody-positive NMOSD, a rare disabling neurological disorder often misdiagnosed as multiple sclerosis. She explains the unique mechanism of action of IL-6 receptor activity (which is believed to be a clinical hallmark of NMOSD) and the novel recycling technology which allows for subcutaneous dosing every four weeks.

The Sumaira Foundation and Connor B Judge Foundation are proud to present their first episode of their new joint podcast, 'Demystifying NMO!' Follow along with Austin Hoover, who lives with multiple sclerosis (the 'cousin' of NMO), and Chelsey Judge, PhD immunologist, as they chat about the basic science of autoimmune disease and NMO. They'll cover 3 main questions: 1) What is an autoimmune disease? 2) How does autoimmunity happen? 3) How does the immune response contribute to NMO?   Glossary of Key Terms Discussed: Antigen: a particular component of a molecule/substance that the immune system recognizes Autoimmune disease: when the immune system targets some component of its own body and reacts against it Immune tolerance:When the immune system decides not to react against an antigen; ‘don’t react’ Anergy: when an immune cell becomes exhausted or functionless Serum: a component of the blood that contains proteins, including antibodies Seropositive: NMOSD patients who have the autoreactive AQP4 antibody in their serum Seronegative: NMOSD patients who do not have the anti-AQP4 antibody in their serum

We just used clinical trial data regarding eculizumab in myasthenia gravis as an example of how to critically appraise the literature, and in this week's program...MORE data on the efficacy of eculizumab in another neurological condition. This week on BrainWaves, the exciting results of the PREVENT trial and the future treatment of NMO spectrum disorder! Produced by James E. Siegler. Special thanks to Dr. Olga Rosenveld Thon. Music courtesy of Unheard Music Concepts, TRG Banks, and Aitua. Sound effects by Mike Koenig and baby Sofia Joan Siegler. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision making. Be sure to follow us on Twitter @brainwavesaudio for the latest updates to the podcast. REFERENCES  Pittock SJ, Lennon VA, McKeon A, Mandrekar J, Weinshenker BG, Lucchinetti CF, O'Toole O and Wingerchuk DM. Eculizumab in AQP4-IgG-positive relapsing neuromyelitis optica spectrum disorders: an open-label pilot study. The Lancet Neurology. 2013;12:554-62. Pittock SJ, Berthele A, Fujihara K, Kim HJ, Levy M, Palace J, Nakashima I, Terzi M, Totolyan N, Viswanathan S, Wang KC, Pace A, Fujita KP, Armstrong R and Wingerchuk DM. Eculizumab in Aquaporin-4-Positive Neuromyelitis Optica Spectrum Disorder. The New England journal of medicine. 2019;381:614-625. FDA News Release: FDA approved first treatment for neuromyelitis optica spectrum disorder, a rare autoimmune disease of the central nervous system. 27 June 2019. Available online at https://www.fda.gov/news-events/press-announcements/fda-approves-first-treatment-neuromyelitis-optica-spectrum-disorder-rare-autoimmune-disease-central. Accessed 30 Aug 2019.

Myelin Oligodendrocyte Glycoprotein (MOG) is one of the few proteins known to be localized on the outermost sheath of central nervous system (CNS) myelin. Due to this localization, MOG is accessible to antibodies. Anti-MOG antibodies are demyelinating and enhance clinical symptoms in a number of animal models of CNS inflammation. Autoantibodies recognizing conformationally intact MOG are found in different inflammatory diseases of the CNS, but their antigenic epitopes had not been mapped. In this work, 9 variants of MOG with an intracellular enhanced green fluorescent protein (EGFP) tag were expressed on the cell surface of human HeLa cells and used to analyze sera from 111 patients (104 children, 7 adults), who had antibodies recognizing cell-bound human MOG. These patients had different diseases, namely acute disseminated encephalomyelitis (ADEM), one episode of transverse myelitis or optic neuritis, multiple sclerosis (MS), anti-aquaporin-4 (AQP4)–negative neuromyelitis optica (NMO), and chronic relapsing inflammatory optic neuritis (CRION). The expression levels of the mutants were comparable and cells with a defined expression level (fluorescence intensity in the EGFP channel of 102-103) were gated. Each MOG-mutant was recognized by at least one MOG-specific mAb. This allowed the comparison of binding to the different mutants. In order to assess the reproducibility of the system, binding of the 111 sera to the mutants was analyzed up to three times in independent experiments, yielding a very good reproducibility of the binding percentage with an absolute SD of 7.8% in the case of low recognition of a mutant and a relative SD of 20% in the case of high recognition of a mutant. The applied variants of MOG gave insight into epitope recognition of 98 patients. All epitopes identified in this work were located at loops connecting the ß-strands of MOG. The immunodominant epitope of human anti-MOG antibodies was at the membrane-proximal CC’-loop containing aa42, which is not present in rodent MOG. This loop was recognized by about half of all patients. Overall, seven epitope patterns were distinguished, including the one mainly recognized by mouse mAbs at the FG-loop around aa104. Evidence from mouse models of CNS inflammation shows that anti-MOG antibodies recognizing different epitopes can be demyelinating and thus pathogenic. This suggests that not only those antibodies recognizing the same epitope of MOG as the pathogenic mAbs (i.e. the FG-loop), but also the ones recognizing the CC'-loop are pathogenic in humans, as both epitopes allow for the recognition of cell-bound MOG. In half of the patients, the anti-MOG response was directed to a single epitope. To analyze the effect of glycosylation on the recognition of MOG by human autoantibodies, a “non-glycosylation mutant” N31D was made. Digestion with PNGaseF and Western blot analysis confirmed that N31 was the only used N-glycosylation site of the MOG constructs in HeLa cells. Glycosylation of MOG was not needed for antibody binding, but 8% of the patients recognized deglycosylated MOG at least two-fold better. The epitope specificity was not linked to certain disease entities. The individual epitope recognition patterns stayed constant in 11 analyzed patients over an observation period of up to 5 years without evidence for intramolecular epitope spreading. Some patients with acute syndromes had anti-MOG IgG at disease onset, but rapidly lost their anti-MOG IgG reactivity. These patients were able to generate a long-lasting IgG response to measles and rubella virus vaccine indicating that the loss of anti-MOG reactivity was not reflective of a lack of capacity for longstanding IgG responses. Human anti-MOG antibodies are mainly of the IgG1 isotype, which can activate complement and antibody dependent cellular cytotoxicity. Upon binding to MOG in the CNS, human anti-MOG antibodies are hence expected to cause demyelination. Transfer experiments with purified human anti-MOG antibodies have not been performed yet. The fact that the majority of human anti-MOG antibodies did not recognize rodent MOG has implications for animal studies. Using the described assay will help to identify patient samples appropriate for these transfer experiments and finally lead to the formal proof of the pathogenicity of human anti-MOG antibodies. This work also gives important information for future detection of potential mimotopes and the development of anti-MOG antibody detection assays and might pave the way to antigen-specific depletion.

Das Schädel-Hirntrauma (SHT) ist bei Kindern und jungen Erwachsen bis zum 45. Lebensjahr mit einer Inzidenz von 332 Verletzten pro 100.000 Einwohner in Deutschland die häufigste Krankheits- und Todesursache. Neben dem persönlichen Leiden und der hohen Rate an posttraumatischer Pflegebedürftigkeit, sollte auch die sozioökonomische Tragweite mit, allein in Deutschland, gesamtgesellschaftlichen Kosten von 2,8 Milliarden Euro pro Jahr berücksichtigt werden. Zwei wesentliche Verletzungsmuster des SHT werden unterschieden: die fokale Kontusion sowie der diffuse Axonschaden. Beide Mechanismen führen zum posttraumatischen Hirnödem und intrakraniellem Druckanstieg, Hauptprädiktoren für ein schlechtes Ergebnis der Patienten. Die daraus resultierende zerebrale Minderperfusion und Hirnischämie münden in einen Circulus vitiosus mit Progredienz des Hirnödems. Ca. 50% des Hirnödems entsteht sekundär und wäre daher einer Behandlung prinzipiell zugänglich. Trotz intensiver Forschung fehlt weiterhin eine kausale und anti-ödematöse Therapie. Vasopressin und V1a-Rezeptoren scheinen eine wesentliche Rolle in der Pathophysiologie von Hirnschädigungen zu spielen, da einerseits die Höhe des Vasopressin-Serumspiegels positiv mit der Schwere von verschiedenen Hirnläsionen korreliert und andererseits eine pharmakologische Hemmung des V1a-Rezeptors das Hirnödem und den sekundären Hirnschaden nach experimentellem Schädel-Hirntrauma mindert. Während die systemische Regulation der Wasserhomöostase in der Niere über den antidiuretischen Effekt von Vasopressin sehr gut bekannt ist, vermittelt über V2-Rezeptoren und Aquaporin 2 (AQP2), ist sowohl die zentrale Funktion von Vasopressin als auch die Regulation zerebraler AQP noch unzureichend verstanden. Ziel der vorliegenden Arbeit war es daher 1. den Einfluss von Vasopressin V1a-Rezeptoren auf den sekundären Hirnschaden nach experimentellem SHT an einem hochspezifischen V1a-Rezeptor knock-out Mausmodell zu untersuchen, 2. die Bedeutung der zerebralen AQP 1, 4 & 9 für den Hirnwassertransport und die post-traumatische Hirnödem Entstehung zu erforschen sowie 3. die Frage zu klären, ob die gezeigten anti-ödematösen Effekte des V1a-Rezeptors über zerebrale AQP nach Controlled Cortical Impact (CCI) im Mausmodell vermittelt werden. An tief anästhesierten Wildtyp und V1a-Rezeptor knock-out Mäusen wurde nach mikrochirurgischer Präparation ein standardisiertes und mittelschweres CCI ausgelöst. Die Hirnentnahme erfolgte je nach Zielparameter jeweils von unbehandelten Mäusen sowie 15 Minuten, 1, 3, 6, 12, 24 h oder 7 Tage nach Trauma. Für die Validierung des knock-out Modells wurden die physiologischen Parameter intrakranieller Druck, mittlerer arterieller Druck und die zerebrale Durchblutung vor und über 30 Minuten nach CCI bestimmt. Für die Untersuchung der neuroprotektiven Effekte des V1a Rezeptors waren die Zielparameter: Hirnwassergehalt, sekundäres Nekrosevolumen, die neurologische Funktion, Gewichtsänderung sowie die Mortalität. Die Entwicklung von maushirnspezifischen Primern war wesentliche Voraussetzung für die Quantifizierung von AQP1, 4 & 9 mRNA durch quantitative Real-Time PCR. Immunhistochemisch wurden mit der Fluorchrom-Methode und dem Infrarot Scan AQP1 & 4 lokalisiert und quantifiziert. Wesentliche Ergebnisse waren der Nachweis der neuroprotektiven Effekte durch die Deletion des V1a-Rezeptors, wodurch das posttraumatische Hirnödem und der sekundäre Hirnschaden 24 h nach Trauma um knapp 30% reduziert wurde, der posttraumatische Gewichtsverlust über 7 Tage verringert sowie die neurologische Funktion über 7 Tage nach experimentellem SHT signifikant verbessert war. Die murinen AQP1, 4 & 9 Primer waren spezifisch und für die quantitative RT-PCR geeignet. Auf Transkriptionsebene wurde AQP1 V1a-Rezeptor-abhängig 24 h nach CCI hochreguliert. AQP4 mRNA wurde konstitutiv exprimiert. AQP9 unterlag auf Transkriptionsebene keiner posttraumatischen Regulation. Auf Proteinebene wurde AQP1 nicht nur auf dem Ependym des Plexus choroideus, sondern erstmals auf kortikalen Neuronen im Maushirn detektiert. AQP4 war ubiquitär auf kortikalen und subkortikalen Astrozyten lokalisiert. Posttraumatisch wurde AQP1 kontralateral und AQP4 periläsional V1a-Rezeptor-abhängig sowohl kurz- als auch langfristig reguliert. Zusammenfassend ist zu sagen, dass Vasopressin an der Entstehung des sekundären Hirnschadens über V1a Rezeptoren nach experimentellem SHT im Mausmodell beteiligt ist. Die gezeigten anti-ödematösen Effekte werden im V1a-Rezeptor knock-out Mausmodell über Aquaporine vermittelt. Die kurz- und langfristige V1a-Rezeptor-abhängige AQP1 & 4 Regulation im Hirnparenchym korreliert dabei mit der Bildung des posttraumatischen Hirnödems. Somit sind der V1a-Rezeptor sowie AQP1 & 4 ein möglicher pharmakologischer Angriffspunkt für die Prävention und Reduktion des posttraumatischen, sekundären Hirnödems.

Neuromyelitis optica (NMO) predominantly affects women, some in childbearing age, and requires early therapeutic intervention to prevent disabling relapses. We report an anti-AQP4 antibody-seropositive patient who became pregnant seven months after low-dose (100 mg) rituximab application. Pregnancy showed no complications, and low-dose rituximab restarted two days after delivery resulted in neurological stability for 24 months. Remarkably, her otherwise healthy newborn presented with anti-AQP4 antibody and reduced B lymphocyte counts in umbilical cord blood, which normalized three months later. Confirming and extending previous reports, our case suggests that low-dose rituximab might be compatible with pregnancy and prevent rebound NMO disease activity postpartum.

Die equine rezidivierende Uveitis (ERU) stellt weltweit die häufigste Ursache für eine erworbene Blindheit bei Pferden dar. Diese spontan auftretende, autoimmun-mediierte Augenentzündung tritt in der Pferdepopulation mit einer Prävalenz von 10% auf. Die ERU ist zudem das einzige spontane Tiermodell für die autoimmune Uveitis, dessen Erforschung einen wertvollen Beitrag für die humane Uveitisforschung leistet. Ablaufende Pathogenese-assoziierte Vorgänge in der Retina, dem Zielorgan der ERU, sind bisher noch weitgehend ungeklärt, tragen jedoch zu einer fortwährenden Schädigung der retinalen Gewebearchitektur, sowie der physiologischen Funktion der Retina bei. Die Müllerzellen, die retinalen Gliazellen, sind durch ihre besonderen strukturellen und funktionellen Glia-Neuron-Interaktionen von entscheidender Bedeutung für die Aufrechterhaltung der retinalen Struktur, sowie der Physiologie. Gliose bezeichnet eine bekannte Reaktion der Müllerzellen auf nahezu alle beschriebenen pathologischen Bedingungen und hat einen fundamentalen Einfluss auf den Verlauf einer Netzhauterkrankung. Die neuroprotektive Wirksamkeit steht dabei den für die Retina schädlichen Auswirkungen der Gliose gegenüber. Das Ziel dieser Studie war die Verifizierung und nähere Charakterisierung der bei der ERU auftretenden Gliose, um die Bedeutung der Müllerzelle bei der autoimmunen Uveitis zu bemessen und somit ein besseres Verständnis der Pathogenese-assoziierten Vorgänge im Zielorgan dieser Erkrankung zu ermöglichen. Dies wurde durch die Untersuchung der Expression von Müllerzell-spezifischen Membranproteinen, welche maßgeblich an der Regulation der retinalen Ionen- und Wasserhomöostase beteiligt sind, in gesunden im Vergleich zu uveitischen Retinae erzielt. Die Regulation der retinalen Kalium- und Wasserhomöostase ist eine der wichtigsten Müllerzellfunktionen und wird durch die einwärtsgleichrichtenden Kaliumkanäle Kir2.1 und Kir4.1, sowie dem Wasserkanal Aquaporin 4 (AQP4) bewerkstelligt. Gesunde Pferderetinae zeigten im Gegensatz zu anderen Spezies ein gleichmäßiges Verteilungsmuster von Kir4.1 entlang der Müllerzelle, dessen Expression bei der ERU signifikant vermindert war. Hingegen war die Expression von Kir2.1 in uveitischen Retinae signifikant erhöht, welche auch ein verändertes Expressionsmuster für Kir2.1 von Müllerzellfortsätzen hin zu den Zellkörpern der inneren Körnerschicht aufwiesen. Diese Befunde deuten auf eine gestörte Kaliumpermeabilität der Müllerzellmembran hin, die eine Beeinträchtigung der retinalen Kaliumhomöostase, sowie weiterer Funktionen der Müllerzelle zur Folge haben könnte. AQP4 war signifikant erhöht exprimiert und zeigte eine massive Re-Lokalisation in uveitischen Retinae im Vergleich zu Kontrollen. Während gesunde Retinae eine AQP4 Expression vor allem in Stammfortsätzen der Müllerzelle aufwiesen, wurde ein kreisförmiges Expressionsmuster in der äußeren Körnerschicht von uveitischen Retinae detektiert. Dies könnte möglicherweise in Verbindung mit der Entstehung eines retinalen Ödems stehen, einer der Hauptursachen für den Verlust der Sehfähigkeit bei Uveitis. In der vorliegenden Studie wurde zudem das Verteilungsmuster eins weiteren Mitglieds der Aquaporin-Familie (AQP5) charakterisiert und erstmalig dessen Expression in der Müllerzelle beschrieben. Außerdem wurde eine signifikant verminderte Expression bei der autoimmun-mediierten Uveitis gefunden und damit erstmals eine Beteiligung dieses Membranproteins bei einer retinalen Erkrankung dokumentiert. Die in dieser Studie gewonnenen Ergebnisse deuten daraufhin, dass die Müllerzelle von entscheidender Bedeutung für die Pathogenese der ERU ist, da die auftretende Gliose schädliche Auswirkungen auf die physiologische Funktion der Retina zu haben scheint. Weitere funktionelle Untersuchungen der Müllerzelle sind zukünftig notwendig, um ein besseres Verständnis der Physiologie der Müllerzelle und ihrer Beeinträchtigung bei der ERU zu erlangen. Durch die Etablierung der ersten equinen Müllerzelllinie eqMC-7 wurde mit dieser Studie die Grundvoraussetzung für dieses Vorhaben geschaffen.

Vortrag in der Ringvorlesung des TR 3 - Mesiale Temporallappen-Epilepsie.