{"id":12718,"date":"2026-02-17T18:46:40","date_gmt":"2026-02-17T18:46:40","guid":{"rendered":"https:\/\/csiag.de\/?p=12718"},"modified":"2026-02-17T20:56:03","modified_gmt":"2026-02-17T20:56:03","slug":"mogad-mog-antibody-associated-disease","status":"publish","type":"post","link":"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/","title":{"rendered":"MOGAD - MOG antibody-associated disease"},"content":{"rendered":"<div id=\"ez-toc-container\" class=\"ez-toc-v2_0_82_2 counter-hierarchy ez-toc-counter ez-toc-grey ez-toc-container-direction\">\n<div class=\"ez-toc-title-container\">\n<p class=\"ez-toc-title\" style=\"cursor:inherit\">Table of contents<\/p>\n<span class=\"ez-toc-title-toggle\"><\/span><\/div>\n<nav><ul class='ez-toc-list ez-toc-list-level-1' ><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-1\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Was_ist_MOGAD\" >What is MOGAD?<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-2\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Was_geht_bei_MOGAD_schief\" >What is going wrong at MOGAD?<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-3\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wo_im_Korper_passiert_das\" >Where in the body does this happen?<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-4\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wie_verlauft_die_Erkrankung\" >How does the disease progress?<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-5\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wie_haufig_ist_MOGAD\" >How common is MOGAD?<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-6\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Was_lost_MOGAD_aus\" >What triggers MOGAD?<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-7\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wie_wird_MOGAD_behandelt\" >How is MOGAD treated?<\/a><\/li><\/ul><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-8\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wissenschaftliche_Einleitung_und_Definition\" >Scientific introduction and definition<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-9\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Abgrenzung_von_MOGAD_NMOSD_und_MS\" >Differentiation between MOGAD, NMOSD and MS<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-10\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#MOG-Protein_%E2%80%93_Struktur_und_physiologische_Funktion\" >MOG protein - structure and physiological function<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-11\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Strukturdomanen\" >Structural domains<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-12\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Physiologische_Funktionen\" >Physiological functions<\/a><\/li><\/ul><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-13\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Pathogenese_und_Immunpathologie\" >Pathogenesis and immunopathology<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-14\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Trigger_und_initiale_Aktivierung\" >Trigger and initial activation<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-15\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#T-Zell-vermittelte_Pathogenese\" >T-cell mediated pathogenesis<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-16\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_1_%E2%80%93_Periphere_Aktivierung\" >Phase 1 - Peripheral activation<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-17\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_2_%E2%80%93_BHS-Penetration\" >Phase 2 - BHS penetration<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-18\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_3_%E2%80%93_Perivaskulare_Reaktivierung\" >Phase 3 - Perivascular reactivation<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-19\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#B-Zell-_und_Antikorper-vermittelte_Pathogenese\" >B-cell and antibody-mediated pathogenesis<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-20\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Molekulare_Signalwege_und_Effektormechanismen\" >Molecular signaling pathways and effector mechanisms<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-21\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalweg_1_%E2%80%93_Klassischer_Komplementweg_CDC\" >Signaling pathway 1 - classical complement pathway (CDC)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-22\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalweg_2_%E2%80%93_Fc%CE%B3-Rezeptor-Weg_FcR-vermittelt\" >Signaling pathway 2 - Fc\u03b3 receptor pathway (FcR-mediated)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-23\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalweg_3_%E2%80%93_IL-6JAK-STAT3-Weg\" >Signaling pathway 3 - IL-6\/JAK-STAT3 pathway<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-24\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalweg_4_%E2%80%93_MAPK-_und_AKT-Signalwege_B-Zellen\" >Signaling pathway 4 - MAPK and AKT signaling pathways (B cells)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-25\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalweg_5_%E2%80%93_Th17-Zytokin-Netzwerk_im_ZNS\" >Signaling pathway 5 - Th17 cytokine network in the CNS<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-26\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Signalwege_%E2%80%93_Ubersicht\" >Signal paths - overview<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-27\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Relevante_Rezeptoren_und_Zielmolekule\" >Relevant receptors and target molecules<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-28\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#MOG_selbst_als_Zielstruktur_kein_klassischer_Rezeptor\" >MOG itself as a target structure (not a classic receptor)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-29\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Fc%CE%B3-Rezeptoren_Fc%CE%B3R\" >Fc\u03b3 receptors (Fc\u03b3R)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-30\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Neonataler_Fc-Rezeptor_FcRn\" >Neonatal Fc receptor (FcRn)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-31\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#IL-6-Rezeptor_IL-6R%CE%B1_gp130\" >IL-6 receptor (IL-6R\u03b1 \/ gp130)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-32\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#T-Zell-Rezeptor_TCR_und_Kostimulationsmolekule\" >T-cell receptor (TCR) and costimulation molecules<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-33\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Komplementrezeptoren\" >Complement receptors<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-34\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Histopathologie_und_ZNS-Lasionsmuster\" >Histopathology and CNS lesion pattern<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-35\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Klinische_Manifestationen_und_Phanotypen\" >Clinical manifestations and phenotypes<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-36\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Diagnostik\" >Diagnostics<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-37\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Therapeutische_Strategien\" >Therapeutic strategies<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-38\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Akuttherapie_Schubbehandlung\" >Acute therapy (relapse treatment)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-39\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Prophylaktische_Langzeittherapie\" >Prophylactic long-term therapy<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-40\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Klinische_Studien_%E2%80%93_2024%E2%80%932026\" >Clinical studies - 2024-2026<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-41\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Neue_und_zukunftige_Therapiekonzepte\" >New and future therapy concepts<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-42\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#BTK-Inhibitoren_Bruton-Tyrosin-Kinase\" >BTK inhibitors (Bruton's tyrosine kinase)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-43\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Toleranzinduktion_MOG-Tolerisierung\" >Tolerance induction (MOG tolerization)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-44\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Komplementinhibitoren\" >Complement inhibitors<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-45\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Anti-Neonatal-Fc-Rezeptor-Strategien\" >Anti-neonatal Fc receptor strategies<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-46\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Autologe_hamatopoetische_Stammzelltransplantation_aHSCT\" >Autologous hematopoietic stem cell transplantation (aHSCT)<\/a><\/li><\/ul><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-47\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Biomarker_und_Verlaufsmonitoring\" >Biomarkers and follow-up monitoring<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-48\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Prognose_und_Besonderheiten\" >Forecast and special features<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-1'><a class=\"ez-toc-link ez-toc-heading-49\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Zusammenfassung_und_Ausblick\" >Summary and outlook<\/a><ul class='ez-toc-list-level-2' ><li class='ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-50\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Atherischer_Ole_%E2%80%93_Wirkstoffe_nach_Signalwegen_geordnet\" >Essential oils - active ingredients arranged according to signaling pathways<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-51\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Weihrauch_Boswellia_serrata_%E2%80%93_AKBA_und_Incensolacetat\" >Frankincense (Boswellia serrata) - AKBA and incensol acetate<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-52\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Therapeutisch_relevante_AKBA-Zieldosen\" >Therapeutically relevant AKBA target doses<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-53\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Umrechnung_auf_375_mg_AKBA_jeKapsel\" >Conversion to 37.5 mg AKBA per capsule<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-54\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wichtige_Einnahmehinweise\" >Important instructions for use<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-55\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Schwarzer_Pfeffer_oral\" >Black pepper (oral)<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-56\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Schwarzer_Pfeffer_Inhalation\" >Black pepper (inhalation)<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-57\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Copaiba-Ol_oral_%E2%80%93_NUR_doTERRA\" >Copaiba oil (oral) - doTERRA ONLY<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-58\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#MOGAD-spezifische_Dosierungstabelle_doTERRA_Copaiba_525_BCP\" >MOGAD-specific dosage table (doTERRA Copaiba 52.5 % BCP)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-59\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#MOGAD-Phasen-adaptierte_Dosierung\" >MOGAD phase-adapted dosing<\/a><ul class='ez-toc-list-level-4' ><li class='ez-toc-heading-level-4'><a class=\"ez-toc-link ez-toc-heading-60\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_1_Akuter_Schub_erste_2%E2%80%934_Wochen\" >Phase 1: Acute flare-up (first 2-4 weeks)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-4'><a class=\"ez-toc-link ez-toc-heading-61\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_2_Schubremission_Erhaltung_langfristig\" >Phase 2: relapse remission \/ maintenance (long-term)<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-4'><a class=\"ez-toc-link ez-toc-heading-62\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Phase_3_Monophasischer_Verlauf_Titer_fallend\" >Phase 3: Monophasic course (titer decreasing)<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-63\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Quellen\" >Sources<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-64\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Copaiba-Ol_Inhalation\" >Copaiba oil (inhalation)<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-65\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Zieldosen_und_benotigte_Tropfenzahl\" >Target doses and required number of drops<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-66\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Synergistische_MOGAD-Strategie_Multi-Target\" >Synergistic MOGAD strategy (multi-target)<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-67\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wichtige_MOGAD-spezifische_Hinweise\" >Important MOGAD-specific information<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-68\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#%CE%B1-Asaron_Kalmus-Ol_Acorus_calamus_%E2%80%93_direkt_oligodendrozytenprotektiv\" >\u03b1-Asarone (calamus oil, Acorus calamus) - directly oligodendrocyte-protective<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-69\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Geraniumol_Pelargonium_graveolens_%E2%80%93_Neuroinflammation_und_NO\" >Geranium oil (Pelargonium graveolens) - neuroinflammation and NO<\/a><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-70\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Teebaum-Ol_Melaleuca_alternifolia_%E2%80%93_Mikroglia-Modulation\" >Tea tree oil (Melaleuca alternifolia) - microglia modulation<\/a><ul class='ez-toc-list-level-3' ><li class='ez-toc-heading-level-3'><a class=\"ez-toc-link ez-toc-heading-71\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Wirkstoffubersicht_nach_MOGAD-Signalwegen\" >Overview of active substances according to MOGAD signaling pathways<\/a><\/li><\/ul><\/li><li class='ez-toc-page-1 ez-toc-heading-level-2'><a class=\"ez-toc-link ez-toc-heading-72\" href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/#Quellen_und_weiterfuhrende_Literatur\" >Sources and further reading<\/a><\/li><\/ul><\/li><\/ul><\/nav><\/div>\n<span class=\"span-reading-time rt-reading-time\" style=\"display: block;\"><span class=\"rt-label rt-prefix\">Reading time<\/span> <span class=\"rt-time\"> 17<\/span> <span class=\"rt-label rt-postfix\">minutes<\/span><\/span>\n<p><em>Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease<\/em><\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Was_ist_MOGAD\"><\/span>What is MOGAD?<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>Everyone knows electrical cables: They are provided with insulation that separates the individual conductors in the cable bundle from each other so that the signals in them do not interfere with each other and get from A to B unaltered.<br>The spinal cord contains a whole strand of many such cable bundles. They conduct the nerve signals from the brain to the various organs, muscles, tissues, etc. in the body. While the insulation of the cable is made of plastics, textiles or special materials, the insulating layer <strong>Myelin layer<\/strong>.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Was_geht_bei_MOGAD_schief\"><\/span>What is going wrong at MOGAD?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>In the case of MOGAD, the body's own immune system makes a serious mistake: it mistakenly produces <strong>Antibodies against a specific protein on the outside of this insulating layer<\/strong>, the so-called. <strong>MOG<\/strong>-protein. Antibodies are actually the body's guardians that recognize, mark and destroy pathogens such as viruses and bacteria. In MOGAD, however, they are mistakenly directed against the body's own healthy tissue, the insulation of its own nerve fibers.<\/p>\n\n\n\n<p>Compared to a cable, it's like scratching, grinding or corroding the insulation, causing it to become perforated and the electrical signals no longer reach their destination cleanly or even at all.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wo_im_Korper_passiert_das\"><\/span>Where in the body does this happen?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>MOGAD relates exclusively to the <strong>Central nervous system<\/strong>, i.e. the brain, spinal cord and optic nerves. Depending on which area is affected, different symptoms arise:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Optic nerve<\/strong> - Sudden loss of vision, blurred vision, eye pain (often only in one eye, sometimes in both eyes at the same time - this is more common in MOGAD than in other similar diseases)<\/li>\n\n\n\n<li><strong>Spinal cord<\/strong> - Symptoms of paralysis, numbness, problems urinating<\/li>\n\n\n\n<li><strong>Brain :<\/strong> Confusion, epileptic seizures, coordination disorders<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wie_verlauft_die_Erkrankung\"><\/span>How does the disease progress?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>MOGAD typically proceeds in <strong>Pushes<\/strong>. There are phases in which the inflammation is active and symptoms occur, intermittently with quieter phases in between.<br>After an attack, many patients recover surprisingly well, better than in MS, for example. This is because the nerve fibers themselves are often less likely to be permanently damaged than the insulating layer, which can partially regenerate.<\/p>\n\n\n\n<p>Around half of those affected only experience a single flare-up in their lifetime. The other half have recurrent episodes, which can lead to permanent impairment if left untreated.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wie_haufig_ist_MOGAD\"><\/span>How common is MOGAD?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>MOGAD is rare, only estimated <strong>1-2 out of 100,000 people<\/strong> fall ill. Unlike many other autoimmune diseases of the nervous system, it affects women and men in roughly equal numbers. Children can also develop the disease, which often manifests itself as extensive inflammation of the brain with confusion and fever.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Was_lost_MOGAD_aus\"><\/span>What triggers MOGAD?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>The first episode is often followed by <strong>infection<\/strong> ahead. The body fights against a pathogen and mistakenly confuses the body's own structures with the enemy. The immune system learns to attack the wrong target, so to speak, and never stops. The exact cause is not yet fully understood. <\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wie_wird_MOGAD_behandelt\"><\/span>How is MOGAD treated?<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>There is currently no specifically approved medication for MOGAD. One <strong>acute attack<\/strong> is treated with high doses of <strong>Cortisone infusions<\/strong>, which quickly reduce the inflammation. If this is not sufficient <strong>Blood washing<\/strong> (<em>Plasmapheresis<\/em>) the harmful antibody can be removed directly from the blood.<\/p>\n\n\n\n<p>To the <strong>Prevention of further relapses<\/strong> Various drugs are used to calm the immune system, for example with substances that reduce antibody-producing cells. Several new, more targeted drugs are currently being tested in clinical trials and could be approved in the next few years.<\/p>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wissenschaftliche_Einleitung_und_Definition\"><\/span>Scientific introduction and definition<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>The <strong>MOG antibody-associated disease (MOGAD)<\/strong> English: <em>Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease<\/em> is a rare, inflammatory autoimmune disease of the central nervous system (CNS) that has been recognized as an independent entity with its own diagnostic criteria since 2018. It was previously considered a variant of multiple sclerosis (MS) or neuromyelitis optica spectrum disorder (NMOSD).<\/p>\n\n\n\n<p>The core element of the disease is the pathological production of autoantibodies (IgG) against the <strong>Myelin oligodendrocyte glycoprotein (MOG)<\/strong>, a transmembrane protein on the outermost layer of the myelin sheath of oligodendrocytes in the CNS. These antibodies damage myelin sheaths and lead to a characteristic perivenular demyelination.<\/p>\n\n\n\n<p>The main clinical manifestations of MOGAD are optic neuritis, transverse myelitis and acute disseminated encephalomyelitis (ADEM). The disease is usually relapsing and affects the optic nerve, spinal cord and, more rarely, the brain. The median age of onset is between 30 and 35 years; in contrast to NMOSD, women and men are affected almost equally often.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Abgrenzung_von_MOGAD_NMOSD_und_MS\"><\/span>Differentiation between MOGAD, NMOSD and MS<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><td><strong>Feature<\/strong><\/td><td><strong>MOGAD<\/strong><\/td><td><strong>AQP4+ NMOSD<\/strong><\/td><td><strong>multiple sclerosis<\/strong><\/td><\/tr><\/thead><tbody><tr><td>Target antigen<\/td><td>MOG (oligodendrocytes)<\/td><td>Aquaporin-4 (astrocytes)<\/td><td>No specific autoantibody<\/td><\/tr><tr><td>Antibody isotype<\/td><td>IgG1 (prew.)<\/td><td>IgG1 (prew.)<\/td><td>Oligoclonal IgG (CSF)<\/td><\/tr><tr><td>Primary cell damage<\/td><td>Oligodendrocytes\/myelin<\/td><td>Astrocytes (primary)<\/td><td>Oligodendrocytes<\/td><\/tr><tr><td>Histology<\/td><td>Perivenular demyelination, CD4+<\/td><td>Astrocyte lesions, granulocytes<\/td><td>Periaxial plaques<\/td><\/tr><tr><td>Gender (F:M)<\/td><td>~1:1<\/td><td>~9:1<\/td><td>~3:1<\/td><\/tr><tr><td>Complement activation<\/td><td>Moderate (less MAC)<\/td><td>Strong (MAC formation)<\/td><td>Low<\/td><\/tr><tr><td>OKB in cerebrospinal fluid<\/td><td>Rare (&lt;10%)<\/td><td>Occasionally<\/td><td>Frequent (&gt;90%)<\/td><\/tr><tr><td>Course<\/td><td>Relapsing; often well recovered<\/td><td>Thrust-shaped; accumulates disability<\/td><td>Often progedient<\/td><\/tr><tr><td>Approved therapies<\/td><td>None (as of 2026)<\/td><td>Eculizumab, ublituximab, satralizumab<\/td><td>Many DMTs<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"MOG-Protein_%E2%80%93_Struktur_und_physiologische_Funktion\"><\/span>MOG protein - structure and physiological function<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>MOG (myelin oligodendrocyte glycoprotein) is a <strong>Type I transmembrane protein<\/strong> with a total length of 218 amino acids, which is expressed exclusively in the CNS. It is a member of the immunoglobulin superfamily and, with a proportion of around 0.01-0.05 % of the total myelin protein, represents a quantitatively small but immunologically highly relevant component of the myelin sheath.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Strukturdomanen\"><\/span>Structural domains<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Extracellular Ig-V-like domain (AS 1-120): Single exposed domain, highly immunogenic; contains the critical CC\u2018 loop region (Pro42, His103, Ser104) as the major epitope binding site for MOG-IgG<\/li>\n\n\n\n<li>Single-pass transmembrane helix: Anchors the protein in the myelin membrane<\/li>\n\n\n\n<li>Short cytoplasmic C-terminal domain: possibly interacts with the cytoskeleton<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Physiologische_Funktionen\"><\/span>Physiological functions<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Adhesion molecule: Mediates structural integrity of the myelin sheath, possibly by compacting the myelin lamellae<\/li>\n\n\n\n<li>Interaction with C1q of the complement system (physiological)<\/li>\n\n\n\n<li>Interaction with nerve growth factor (NGF)<\/li>\n\n\n\n<li>Receptor for rubella virus (clinically relevant for post-infectious ADEM)<\/li>\n\n\n\n<li>Stabilization of microtubules in oligodendrocytes<\/li>\n\n\n\n<li>Expression: Late in oligodendrocyte differentiation; only after initial myelination<\/li>\n<\/ul>\n\n\n\n<p>MOG-IgG autoantibodies primarily recognize <strong>Conformational epitopes<\/strong> of the extracellular domain. As MOG is exposed on the outermost surface of the myelin sheath, it is directly accessible to circulating antibodies and immune complexes - a decisive difference to intracellular antigens.<\/p>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Pathogenese_und_Immunpathologie\"><\/span>Pathogenesis and immunopathology<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>MOGAD pathogenesis is a multistep process involving peripheral immune activation, migration across the blood-brain barrier (BBB) and CNS-local effector mechanisms. Neither T cells nor B cells alone are sufficiently pathogenic; it is the synergistic interaction of both arms of the adaptive immune system that causes the disease.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Trigger_und_initiale_Aktivierung\"><\/span>Trigger and initial activation<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>The main initial triggers are <strong>Infections<\/strong> discussed: An infectious prodrome has been documented in 37-70 % of MOGAD patients (more frequent than in NMOSD with 15-35 %). The mechanisms include:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Molecular mimicry - pathogen epitopes are structurally similar to the CC\u2018 loop region of the MOG, e.g. SARS-CoV-2 sequences or rubella viruses<\/li>\n\n\n\n<li>Bystander activation - non-specific inflammatory reaction activates dormant autoreactive lymphocytes<\/li>\n\n\n\n<li>Polyclonal B-cell activation by microbial superantigens<\/li>\n<\/ul>\n\n\n\n<p>Genetic predisposition plays a role, but specific risk haplotypes have not been conclusively identified. In contrast to MS, no consistent HLA associations have been described.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"T-Zell-vermittelte_Pathogenese\"><\/span>T-cell mediated pathogenesis<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>MOG-specific CD4+ T cells are essential for MOGAD pathogenesis. In animal models (EAE), antibodies alone are not pathogenic and require encephalitogenic T cells as co-effectors. The CD4+ pathway comprises several phases:<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_1_%E2%80%93_Periphere_Aktivierung\"><\/span>Phase 1 - Peripheral activation<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>MOG peptides are produced by antigen-presenting cells (APC) via <strong>MHC-II molecules<\/strong> to na\u00efve CD4+ T cells. Noteworthy: <em>MOG peptides can bind directly to peripheral MHC II molecules<\/em>, without further processing. This could explain the involvement of the peripheral nervous system.<\/p>\n\n\n\n<p>Effector cell subsets that can induce EAE independently of each other are <strong>Th1, Th17 and Th9<\/strong>. Th17 cells are particularly relevant for MOGAD, as Th17 cytokines (IL-17, IL-21) are markedly elevated in shearing episodes.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_2_%E2%80%93_BHS-Penetration\"><\/span>Phase 2 - BHS penetration<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>Activated CD4+ T cells express specific adhesion molecules (integrins, selectins) and chemokine receptors (in particular <strong>CCR6<\/strong>), which enable them to enter the CNS. CCR6+ Th17 cells bind to CCL20, which is constitutively expressed in the choroid plexus, and enter the subarachnoid space via it.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Matrix metalloproteinases (MMP-2, MMP-9)<br>Degradation of the basement membrane of the BBB<\/li>\n\n\n\n<li>Neutrophil NETs (Neutrophil Extracellular Traps)<br>Provide costimulatory signals for T cells in the initiation phase<\/li>\n\n\n\n<li>Thrombocytes<br>Promote CD4+ T cell proliferation and differentiation to Th1\/Th17 through cytokines and adhesion molecules<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_3_%E2%80%93_Perivaskulare_Reaktivierung\"><\/span>Phase 3 - Perivascular reactivation<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>In the perivascular space and subarachnoid space, MOG-specific T cells are reactivated by local MOG-loaded APCs (microglia, dendritic cells). This reactivation triggers the actual inflammatory cascade: Secretion of proinflammatory cytokines, recruitment of further leukocytes and oligodendrocyte damage.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"B-Zell-_und_Antikorper-vermittelte_Pathogenese\"><\/span>B-cell and antibody-mediated pathogenesis<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>MOG-specific B cells and plasma cells are the main producers of pathogenic IgG1 autoantibodies. However, the B cell role goes beyond antibody production:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>Antigen presentation - B cells can bind MOG conformational epitopes via their BCR (pro42, his103, ser104 of the CC\u2018 loop) and act as APCs for T cells<\/li>\n\n\n\n<li>Promotion of Th17 differentiation - B cells secrete IL-6, which together with TGF-\u03b2 drives Th17 differentiation<\/li>\n\n\n\n<li>MAPK and AKT signaling activation - BCR binding to MOG activates these signaling pathways intracellularly<\/li>\n\n\n\n<li>Increase in intracellular calcium - Leads to activation of stress-associated signaling cascades<\/li>\n<\/ul>\n\n\n\n<p>Most MOG-IgG antibodies are produced in the periphery (oligoclonal bands in CSF only in ~10 % of cases, in comparison: MS ~90 %). The antibodies are <strong>bivalent-binding<\/strong> to MOG, both Fab arms bind simultaneously to two neighboring MOG molecules. This leads to less efficient C1q recruitment compared to monovalent binding of AQP4-IgG in NMOSD.<\/p>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Molekulare_Signalwege_und_Effektormechanismen\"><\/span>Molecular signaling pathways and effector mechanisms<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalweg_1_%E2%80%93_Klassischer_Komplementweg_CDC\"><\/span>Signaling pathway 1 - classical complement pathway (CDC)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>When MOG-IgG1 (and MOG-IgG3) bind to oligodendrocyte MOG, the <strong>classic complementary route<\/strong> are activated. However, complement activation is weaker in MOGAD than in AQP4+ NMOSD:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>C1q binding to the Fc part of bound IgG1 antibodies \u2192 Activation of C1r and C1s<\/li>\n\n\n\n<li>Cleavage of C4 \u2192 C4a + C4b; C4b + C2 \u2192 C3 convertase (C4b2a)<\/li>\n\n\n\n<li>Cleavage of C3 \u2192 C3a (anaphylatoxin) + C3b (opsonin)<\/li>\n\n\n\n<li>C3b \u2192 C5 convertase \u2192 Cleavage of C5 \u2192 C5a (potent anaphylatoxin) + C5b<\/li>\n\n\n\n<li>C5b + C6, C7, C8, C9 \u2192 membrane attack complex (MAC, C5b-9): Direct lysis of the oligodendrocytes<\/li>\n<\/ul>\n\n\n\n<p>Important: In the CSF of MOGAD patients, C3a and C5a are significantly elevated (comparable to AQP4+ NMOSD), but the MAC complex (C5b-9) is not significantly elevated. <strong>significantly lower<\/strong> than in NMOSD. This is due to bivalent IgG binding, which is less efficient for C1q clustering, and the relatively low density of complement regulators on oligodendrocytes (less CR1, MCP, HRF than on other cell types).<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalweg_2_%E2%80%93_Fc%CE%B3-Rezeptor-Weg_FcR-vermittelt\"><\/span>Signaling pathway 2 - Fc\u03b3 receptor pathway (FcR-mediated)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>LMU research (Mader, Kawakami, Meinl, 2024 PNAS) showed that Fc\u03b3 receptor (Fc\u03b3R)-mediated mechanisms <strong>to about 50 % of myelin damage<\/strong> and are therefore on a par with complement activation:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Fc\u03b3RIII<\/strong> (<strong>CD16<\/strong>) on NK cells and macrophages<br>Binds the Fc part of MOG-bound IgG1 \u2192 ADCC (antibody-dependent cellular cytotoxicity)<\/li>\n\n\n\n<li><strong>Fc\u03b3RI\/II\/III<\/strong> on macrophages and monocytes<br>Phagocytosis of MOG-opsonized oligodendrocyte fragments (ADCP)<\/li>\n\n\n\n<li>Crucial: The second FcR pathomechanism<br>Enhancement of T cell activation, runs exclusively via Fc receptors, NOT via the complement pathway<\/li>\n\n\n\n<li><strong>Fc\u03b3R<\/strong> on dendritic cells<br>Facilitate the processing and presentation of MOG-IgG-loaded oligodendrocyte antigens to MOG-specific T cells<\/li>\n<\/ul>\n\n\n\n<p>Clinical implication: Since two independent pathogenic pathways exist, therapeutic approaches must be <strong>Both mechanisms<\/strong> in order to achieve maximum effectiveness.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalweg_3_%E2%80%93_IL-6JAK-STAT3-Weg\"><\/span>Signaling pathway 3 - IL-6\/JAK-STAT3 pathway<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>IL-6 is a central mediator of MOGAD immunopathogenesis and acts on several levels:<\/p>\n\n\n\n<p>IL-6 binds to its receptor (IL-6R\u03b1\/gp130 complex), which leads to the <strong>JAK1\/2 phosphorylation<\/strong> leads. This primarily activates <strong>STAT3<\/strong>, which serves as a transcription factor for:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Th17 differentiation<\/strong><br>IL-6 + TGF-\u03b2 \u2192 ROR\u03b3t expression \u2192 IL-17A\/F production; IL-6 + IL-23 \u2192 maintenance of the Th17 phenotype<\/li>\n\n\n\n<li><strong>Folicular T helper cells<\/strong> (<strong>Tfh<\/strong>)<br>IL-6 \u2192 STAT3 \u2192 Bcl6 expression \u2192 Germinal center B cell maturation and IgG class switch<\/li>\n\n\n\n<li><strong>B-cell maturation to plasma cells<\/strong><br>IL-6 promotes differentiation via STAT3\/Blimp-1 axis<\/li>\n\n\n\n<li><strong>Suppression of Treg function<\/strong><br>IL-6 inhibits FoxP3 expression, which shifts the Treg\/Th17 balance towards inflammation<\/li>\n<\/ul>\n\n\n\n<p>Therapeutic relevance: IL-6 blockade (e.g. tocilizumab, satralizumab) breaks this cycle. <strong><em>Satralizumab<\/em><\/strong> (anti-IL-6R) is currently being investigated in the Phase 3 METEOROID study for MOGAD.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalweg_4_%E2%80%93_MAPK-_und_AKT-Signalwege_B-Zellen\"><\/span>Signaling pathway 4 - MAPK and AKT signaling pathways (B cells)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>BCR binding to MOG conformational epitopes activated in B cells:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>MAPK path<\/strong> (<strong>MEK\/ERK<\/strong>)<br>Promotion of B-cell proliferation and differentiation<\/li>\n\n\n\n<li><strong>PI3K\/AKT path<\/strong><br>Cell survival and differentiation of B cells into plasma cells<\/li>\n\n\n\n<li><strong>Calcium influx<\/strong><br>Activation of calcineurin\/NFAT axis \u2192 Cytokine production<\/li>\n\n\n\n<li><strong>NK cell activation<\/strong><br>BCR-MOG binding induces NK cell-mediated cytotoxicity<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalweg_5_%E2%80%93_Th17-Zytokin-Netzwerk_im_ZNS\"><\/span>Signaling pathway 5 - Th17 cytokine network in the CNS<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>In the CNS, Th17 cells maintain an inflammatory environment through multiple mediators:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>IL-17A and IL-17F<\/strong><br>Activate astrocytes and microglia; induce release of chemokines (CXCL-1\/5\/8) that recruit neutrophils<\/li>\n\n\n\n<li><strong>IL-21<\/strong> (auto- and paracrine)<br>Enhances Th17 differentiation; promotes B-cell differentiation and IgG class switch (especially IgG1)<\/li>\n\n\n\n<li><strong>IL-22<\/strong><br>Dysregulation of BBB integrity<\/li>\n\n\n\n<li><strong>GM-CSF<\/strong> (<strong>via IL-23<\/strong>)<br>Activates microglia and macrophages, increases local demyelination<\/li>\n\n\n\n<li><strong>CXCL13<\/strong><br>Chemotaxis of B cells in perivascular spaces \u2192 local antibody production<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Signalwege_%E2%80%93_Ubersicht\"><\/span>Signal paths - overview<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><td><strong>Signal path<\/strong><\/td><td><strong>Key molecules<\/strong><\/td><td><strong>Effect<\/strong><\/td><td><strong>Therapeutic targets<\/strong><\/td><\/tr><\/thead><tbody><tr><td>Classic complementary route<\/td><td>C1q, C3, C5, MAC (C5b-9)<\/td><td>Direct oligodendrocyte lysis<\/td><td>C5 inhibitors (eculizumab), C3 inhibitors<\/td><\/tr><tr><td>Fc\u03b3R path (ADCC\/ADCP)<\/td><td>Fc\u03b3RI\/II\/III, NK cells, macrophages<\/td><td>Cytotoxicity, phagocytosis, T-cell potentiation<\/td><td>FcRn inhibitors (IgG degradation), FcR blockade<\/td><\/tr><tr><td>IL-6\/JAK-STAT3<\/td><td>IL-6, IL-6R\u03b1, gp130, JAK1\/2, STAT3, ROR\u03b3t<\/td><td>Th17 differentiation, B-cell maturation, IgG production<\/td><td>Anti-IL-6R (tocilizumab, satralizumab)<\/td><\/tr><tr><td>PI3K\/AKT\/MAPK (B cells)<\/td><td>BTK, PI3K, AKT, ERK, NFAT<\/td><td>B-cell activation, plasma cell maturation<\/td><td>BTK inhibitors (ibrutinib, tolebrutinib)<\/td><\/tr><tr><td>Th17 cytokine network<\/td><td>IL-17, IL-21, IL-22, GM-CSF, CXCL13<\/td><td>BBB damage, leukocyte recruitment, demyelination<\/td><td>Anti-IL-17, Anti-IL-21<\/td><\/tr><tr><td>FcRn-IgG recycling<\/td><td>FcRn (neonatal Fc receptor)<\/td><td>Prolonged IgG half-life<\/td><td>Anti-FcRn (rozanolixizumab)<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Relevante_Rezeptoren_und_Zielmolekule\"><\/span>Relevant receptors and target molecules<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"MOG_selbst_als_Zielstruktur_kein_klassischer_Rezeptor\"><\/span>MOG itself as a target structure (not a classic receptor)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>In MOGAD, the MOG protein acts as an antigen, not as a signal receptor. Nevertheless, the following interactions are pathophysiologically significant:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>C1q binding<\/strong><br>MOG can physiologically bind C1q, which leads to complement activation in the case of pathological antibody coverage<\/li>\n\n\n\n<li><strong>DC-SIGN (CD209)<\/strong><br>Lectin receptor on dendritic cells; can bind MOG and contribute to antigen presentation<\/li>\n\n\n\n<li><strong>Rubella virus receptor<\/strong>_<br>MOG serves as an entry molecule for rubella viruses, which could explain post-infectious ADEM in children<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Fc%CE%B3-Rezeptoren_Fc%CE%B3R\"><\/span>Fc\u03b3 receptors (Fc\u03b3R)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>Fc\u03b3 receptors on immune cells are central effectors of IgG1-mediated damage:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Fc\u03b3RI (CD64)<\/strong><br>High affinity, on macrophages and dendritic cells; mediation of ADCP and antigen presentation<\/li>\n\n\n\n<li><strong>Fc\u03b3RIII (CD16)<\/strong><br>Low affinity, on NK cells; main mediator of ADCC against MOG-opsonized oligodendrocytes<\/li>\n\n\n\n<li><strong>Fc\u03b3RIIA\/B (CD32A\/B)<\/strong><br>Activating or inhibiting; modulation of B-cell activation and phagocytosis<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Neonataler_Fc-Rezeptor_FcRn\"><\/span>Neonatal Fc receptor (FcRn)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>FcRn (\u03b22m\/FcRn-\u03b1 complex) is responsible for the intracellular recycling of IgG antibodies. It binds IgG in acidified endosomes (pH 6.0) and prevents its lysosomal degradation, thereby extending the IgG half-life to approx. 21 days.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>In MOGAD, FcRn causes the persistent circulation of pathogenic MOG-IgG1<\/li>\n\n\n\n<li>Therapeutic blockage due to <em>Rozanolixizumab<\/em> (anti-FcRn IgG4): Forces lysosomal IgG degradation and lowers plasma IgG by ~50%<\/li>\n\n\n\n<li>FcRn expression - epithelial cells, endothelial cells, monocytes, hepatocytes<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"IL-6-Rezeptor_IL-6R%CE%B1_gp130\"><\/span>IL-6 receptor (IL-6R\u03b1 \/ gp130)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>The IL-6 receptor consists of the ligand-binding \u03b1-subunit (IL-6R\u03b1, CD126) and the signal transduction co-receptor gp130 (IL-6R\u03b2, CD130). Two signaling modes:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Classic signaling<\/strong><br>Membrane-bound IL-6R\u03b1 on T cells, B cells, monocytes \u2192 IL-6\/IL-6R\u03b1\/gp130 complex \u2192 JAK1\/2 \u2192 STAT3, STAT1, MAPK, PI3K\/AKT<\/li>\n\n\n\n<li><strong>Trans signaling<\/strong><br>Soluble IL-6R\u03b1 (sIL-6R) binds IL-6 and activates gp130 even on cells without membrane-bound IL-6R\u03b1 (e.g. endothelial cells of the BBB)<\/li>\n<\/ul>\n\n\n\n<p>Relevant downstream effects: ROR\u03b3t expression (Th17), Bcl-6 (Tfh and germinal centers), Blimp-1 (plasma cells), suppression of FoxP3 (Treg).<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"T-Zell-Rezeptor_TCR_und_Kostimulationsmolekule\"><\/span>T-cell receptor (TCR) and costimulation molecules<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>TCR\/MHC-II-MOG peptide complex<\/strong><br>Central activation axis for MOG-specific CD4+ T cells<\/li>\n\n\n\n<li><strong>CD28\/B7<\/strong><br>Costimulation during T-cell activation<\/li>\n\n\n\n<li><strong>CCR6\/CCL20 axis<\/strong><br>CCR6 on Th17 cells binds CCL20 at the choroid plexus \u2192 CNS entry<\/li>\n\n\n\n<li><strong>CXCR3\/CXCL10<\/strong><br>Chemotaxis of Th1 cells in areas of inflammation<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Komplementrezeptoren\"><\/span>Complement receptors<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>C1qR<\/strong><br>Mediates C1q binding to immune complexes on oligodendrocyte membranes<\/li>\n\n\n\n<li><strong>C3aR <\/strong>and<strong> C5aR1 (CD88)<\/strong><br>Anaphylatoxin receptors on microglia\/macrophages \u2192 Proinflammatory activation<\/li>\n\n\n\n<li><strong>Complement regulators on oligodendrocytes<\/strong><br>CR1 (CD35), MCP (CD46), HRF (CD59) are lowly expressed on oligodendrocytes, which makes them more susceptible to complement damage than astrocytes, for example<\/li>\n<\/ul>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Histopathologie_und_ZNS-Lasionsmuster\"><\/span>Histopathology and CNS lesion pattern<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>MOGAD lesions are histopathologically fundamentally different from MS and NMOSD:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Perivenous demyelination<\/strong><br>Lesions form concentrically around small veins (perivenous pattern), not periaxially as in MS. The typical \u201acentral vein sign\u2018 of MS is absent on MRI<\/li>\n\n\n\n<li><strong>CD4+ T-cell infiltrate<\/strong><br>Dominant inflammatory cell pattern are CD4+ T cells and macrophages, fewer neutrophils and hardly any eosinophil granulocytes (unlike AQP4+ NMOSD)<\/li>\n\n\n\n<li><strong>Oligodendrocyte damage<\/strong> (primary)<br>In contrast to NMOSD, where astrocytes are primarily damaged, MOGAD focuses on oligodendrocyte degeneration<\/li>\n\n\n\n<li><strong>C9neo deposition<\/strong><br>Detection of MAC (terminal complement complex) in lesions, albeit weaker than in NMOSD<\/li>\n\n\n\n<li><strong>Relative axon conservation<\/strong><br>In acute attacks, axonal damage is often less severe than in MS, which explains the often good clinical recovery<\/li>\n\n\n\n<li><strong>Cortical lesions<\/strong><br>Leptomeningeal inflammation and cortical demyelination (common in the ADEM variant)<\/li>\n<\/ul>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Klinische_Manifestationen_und_Phanotypen\"><\/span>Clinical manifestations and phenotypes<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>MOGAD is clinically heterogeneous. Important phenotypes:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><td><strong>Phenotype<\/strong><\/td><td><strong>Frequency<\/strong><\/td><td><strong>Clinical features<\/strong><\/td><td><strong>MRI special features<\/strong><\/td><\/tr><\/thead><tbody><tr><td>Optic neuritis (ON)<\/td><td>Most common (approx. 50%)<\/td><td>Often bilateral, loss of vision, retrobulbar, painful eye movements. eye movements<\/td><td>Long optic nerve involvement, perinervous contrast medium accumulation<\/td><\/tr><tr><td>Transverse myelitis<\/td><td>Approx. 30%<\/td><td>Longitudinal myelitis (LETM), sensory\/motor, bladder disorders<\/td><td>Longitudinal T2 lesions, H2 syndrome (\u201alenticular\u2018)<\/td><\/tr><tr><td>ADEM<\/td><td>Most common manifestation in children<\/td><td>Encephalopathy, polyfocal neurolog. deficits<\/td><td>Bilateral, large-volume T2 lesions, also basal ganglia<\/td><\/tr><tr><td>Brain stem encephalitis<\/td><td>Approx. 15%<\/td><td>Diplopia, ataxia, area postrema syndrome (hiccup, vomiting)<\/td><td>Brain stem \/ cerebellar T2 lesions<\/td><\/tr><tr><td>Cortical encephalitis<\/td><td>Rarer<\/td><td>Epileptic seizures, confusion<\/td><td>Cortical FLAIR signal changes<\/td><\/tr><tr><td>CRION<\/td><td>Rarer<\/td><td>Chronic recurrent inflam. Optic neuropathy<\/td><td>Persistent optic nerve involvement<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Diagnostik\"><\/span>Diagnostics<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>Diagnostic criteria (Banwell et al, <em>Lancet Neurology<\/em> 2023) are required: <\/p>\n\n\n\n<p>(1) Detection of MOG-IgG in serum or cerebrospinal fluid using a cell-based assay (CBA)<br>(2) appropriate clinical phenotype<br>(3) Exclusion of alternative diagnoses.<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Cell-based immunofluorescence test (CBA)<\/strong><br>with naturally folded, membrane-bound MOG (HEK293 cells transfected with human MOG); detects conformation-dependent epitopes<\/li>\n\n\n\n<li><strong>ELISA and line\/strip blots<\/strong><br>Unreliable for MOGAD, as linear epitopes are recognized<\/li>\n\n\n\n<li><strong>IgG subclasses<\/strong><br>Primarily IgG1; occasionally IgG2, IgG3, IgG4. Exclusive IgG3 positivity is a diagnostic pitfall (Jarius 2024)<\/li>\n\n\n\n<li><strong>Titre kinetics<\/strong><br>Persistently high titers correlate with relapse risk; often decreasing in monophasic course<\/li>\n\n\n\n<li><strong>Liquor<\/strong><br>Pleocytosis possible; oligoclonal bands rare (&lt;10 %), intrathecal IgG synthesis rare<\/li>\n\n\n\n<li><strong>Biomarkers<\/strong><br>sNfL (serum neurofilament light chain) as a disease activity marker; sGFAP (glial fibrillary acidic protein) as a marker of astrocytic involvement<\/li>\n<\/ul>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Therapeutische_Strategien\"><\/span>Therapeutic strategies<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Akuttherapie_Schubbehandlung\"><\/span>Acute therapy (relapse treatment)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>Standard treatment of a MOGAD relapse:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>High-dose <em>Methylprednisolone<\/em> (HDMP)<\/strong><br>1000 mg i.v. daily for 5 days - first line<\/li>\n\n\n\n<li><em><strong>Plasmapheresis \/ immunoadsorption<\/strong><\/em><br>In case of insufficient HDMP response; removes MOG-IgG from plasma; 5-7 cycles (retrospective data show efficacy in approx. 50-70% of cases)<\/li>\n\n\n\n<li><strong><em>Intravenous immunoglobulins<\/em> (IVIG)<\/strong><br>2 g\/kg over 5 days; in the absence of a response to HDMP and as an option after plasmapheresis; possibly effective via FcRn saturation and Fc\u03b3R competition<\/li>\n\n\n\n<li><strong>Taper off corticosteroids<\/strong><br>Particularly important in MOGAD (frequent steroid dependence) - rapid reduction can trigger rebound episodes<\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Prophylaktische_Langzeittherapie\"><\/span>Prophylactic long-term therapy<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>(off-label, no approved preparation - status 2026)<\/p>\n\n\n\n<p>The indication for long-term therapy is individual - not all patients need it. Factors: Relapse rate, severity of relapses, persistent MOG-IgG titres, phenotypic risk factors.<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><td><strong>Substance<\/strong><\/td><td><strong>Mechanism of action<\/strong><\/td><td><strong>Data situation<\/strong><\/td><td><strong>Level of evidence<\/strong><\/td><\/tr><\/thead><tbody><tr><td>Azathioprine<\/td><td>Purine synthesis blockade (TPMT-dependent); inhibits T and B cell proliferation<\/td><td>Retrospective studies; national RCT ongoing (France, TOMATO study)<\/td><td>IIb-III (off-label)<\/td><\/tr><tr><td>Mycophenolate mofetil (MMF)<\/td><td>Inosine monophosphate dehydrogenase inhibitor; inhibits lymphocyte proliferation<\/td><td>Case series; possibly effective, lower relapse prevention than rituximab<\/td><td>III (off-label)<\/td><\/tr><tr><td>Rituximab<\/td><td>Anti-CD20 \u2192 B-cell depletion; inhibits MOG-IgG production<\/td><td>Largest retrospective cohort; effective, not for everyone; increased risk of infection<\/td><td>IIb (off-label)<\/td><\/tr><tr><td>Tocilizumab<\/td><td>Anti-IL-6R\u03b1 (iv); blocks IL-6 signaling pathway (JAK\/STAT3); inhibits Th17\/plasma cells<\/td><td>Positive retrospective data; RCT results for NMOSD positive (TANGO)<\/td><td>IIb (off-label)<\/td><\/tr><tr><td>IVIG (iv\/subcutaneous)<\/td><td>Fc receptor saturation; MOG-IgG neutralization; FcRn saturation<\/td><td>Retrospective data positive; option in case of desire to have children, pregnancy, infection<\/td><td>IIb (off-label)<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Klinische_Studien_%E2%80%93_2024%E2%80%932026\"><\/span>Clinical studies - 2024-2026<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>For the first time, several randomized, placebo-controlled phase 3 studies are underway for MOGAD, which are expected to provide class I evidence:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><td><strong>study<\/strong><\/td><td><strong>Substance<\/strong><\/td><td><strong>Mechanism<\/strong><\/td><td><strong>Target group<\/strong><\/td><td><strong>status<\/strong><\/td><\/tr><\/thead><tbody><tr><td>cosMOG<\/td><td>Rozanolixizumab (UCB7665)<\/td><td>Anti-FcRn IgG4-mAb: blocks IgG recycling \u2192 accelerates IgG degradation, lowers MOG IgG titre ~50 %<\/td><td>Adults (\u226518 years), relapsing, \u22651 relapse\/12 months<\/td><td>Phase 3, international; first ever MOGAD Phase 3 study<\/td><\/tr><tr><td>METEOROID<\/td><td>Satralizumab (anti-IL-6R sc.)<\/td><td>Anti-IL-6R (subcutaneous); inhibits JAK\/STAT3 \u2192 Th17 differentiation, B-cell maturation, IgG production<\/td><td>Adults + adolescents (\u226512 yrs); relapsing, preceded by \u22651 relapse<\/td><td>Phase 3, international, ongoing<\/td><\/tr><tr><td>TOMATO<\/td><td>Azathioprine<\/td><td>Purine synthesis inhibition; broadly immunosuppressive<\/td><td>French multicenter study; adults with MOGAD<\/td><td>National RCT, phase 3<\/td><\/tr><tr><td>MOGwAI<\/td><td>Not specified (Observational)<\/td><td>Biomarker study: validation of MOG-IgG titer, sNfL, sGFAP, sCD83 as progression markers<\/td><td>International cohort study<\/td><td>Ongoing<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Neue_und_zukunftige_Therapiekonzepte\"><\/span>New and future therapy concepts<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>Based on the molecular findings of recent years, the following approaches for MOGAD are discussed:<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"BTK-Inhibitoren_Bruton-Tyrosin-Kinase\"><\/span>BTK inhibitors (Bruton's tyrosine kinase)<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>BTK is a central kinase in the B-cell receptor signaling cascade (PI3K\/AKT\/MAPK). <strong><em>Tolebrutinib<\/em><\/strong> and other BTK inhibitors are in MS and NMOSD research; clinical trials are pending for MOGAD. Oral application would be an advantage. Inhibition of both B-cell activation and myeloid cells (microglia-BTK).<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Toleranzinduktion_MOG-Tolerisierung\"><\/span>Tolerance induction (MOG tolerization)<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>Antigen-specific tolerance induction (e.g. via MOG peptides or nanoparticle-based approaches) is a promising concept. The <strong><em>Guthy-Jackson Charitable Foundation<\/em><\/strong> promotes research into curative approaches. Advantage: No global immunosuppression, <strong>Selective elimination of MOG autoreactivity<\/strong>.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Komplementinhibitoren\"><\/span>Complement inhibitors<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>Since complement activation (C3a, C5a, MAC) is detectable in MOGAD lesions, it would be <strong><em>Eculizumab<\/em> (Anti-C5)<\/strong> or a C3 inhibitor is theoretically effective. However, as the MAC complex (C5b-9) is formed to a much lesser extent in MOGAD than in NMOSD (where <em>Eculizumab<\/em> is approved), the clinical relevance is uncertain.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Anti-Neonatal-Fc-Rezeptor-Strategien\"><\/span>Anti-neonatal Fc receptor strategies<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>Besides <em>Rozanolixizumab<\/em> will also <strong><em>Efgartigimod<\/em><\/strong> (an IgG-Fc fragment that competitively blocks FcRn) for other IgG-mediated diseases. Since the pathomechanism of FcRn blockade directly lowers MOG IgG levels, this is a particularly target-oriented approach.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Autologe_hamatopoetische_Stammzelltransplantation_aHSCT\"><\/span>Autologous hematopoietic stem cell transplantation (aHSCT)<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>For severe, refractory courses, aHSCT is a potentially curative concept: deep immunoablation and reconstitution of the immune system could eliminate the autoreactive T and B cell clones. Data for MOGAD very limited; use only in specialized centers.<\/p>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Biomarker_und_Verlaufsmonitoring\"><\/span>Biomarkers and follow-up monitoring<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>Biomarker-based therapy decisions are the goal of current research:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>MOG-IgG titer (serum)<\/strong><br>Persistence correlates with relapse risk; in monophasic course often spontaneous drop in titer; therapy decision co-determinant<\/li>\n\n\n\n<li><strong>Serum Neurofilament Light (sNfL)<\/strong><br>Marker for axonal damage; elevated during relapse; normalization as therapy response marker<\/li>\n\n\n\n<li><strong>Serum GFAP (sGFAP)<\/strong><br>Astrocytic activation; lower in MOGAD than in NMOSD; can provide complementary information<\/li>\n\n\n\n<li><strong>sCD83<\/strong><br>New candidate biomarker (under validation); possibly marker for dendritic cell activation and immune activity<\/li>\n\n\n\n<li><strong>Cerebrospinal fluid cell count and protein<\/strong><br>Pleocytosis during episodes of thrust; normalization after therapy<\/li>\n<\/ul>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Prognose_und_Besonderheiten\"><\/span>Forecast and special features<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>Compared to AQP4+ NMOSD, MOGAD tends to show a <strong>More favorable forecast<\/strong>, especially better visual recovery after ON. However, the following aspects are important:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Monophasic progression<\/strong><br>Approx. 50% of patients; often spontaneous drop in titer; no long-term therapy may be necessary<\/li>\n\n\n\n<li><strong>Thrust-shaped progression<\/strong><br>Approx. 50%; higher titer persists; cumulative disability build-up possible, but slower than NMOSD<\/li>\n\n\n\n<li><strong>No progressive course<\/strong><br>In contrast to MS, no gradual progression without relapses has been described<\/li>\n\n\n\n<li><strong>Steroid sensitivity and steroid dependence<\/strong><br>Many patients respond very well to corticosteroids, but: rapid withdrawal often triggers relapses<\/li>\n\n\n\n<li><strong>Special pediatric feature<\/strong><br>ADEM most common first manifestation in children (&lt;10 years); prognosis often good, but note risk of recurrence<\/li>\n\n\n\n<li><strong>Pregnancy: thin data<\/strong><br>No generally increased risk of relapse during pregnancy, but puerperium could be a risk factor (analogous to MS)<\/li>\n<\/ul>\n\n\n\n<h1 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Zusammenfassung_und_Ausblick\"><\/span>Summary and outlook<span class=\"ez-toc-section-end\"><\/span><\/h1>\n\n\n\n<p>MOGAD is an independent, antibody-mediated autoimmune disease of the CNS that is characterized by the following key features:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li>The MOG protein on the outside of oligodendrocytes and myelin sheaths is the target antigen<\/li>\n\n\n\n<li>Pathogenic MOG-IgG1 autoantibodies damage myelin via two parallel effector pathways: complement activation (CDC, ca. 50%) and Fc\u03b3R binding (ADCC\/ADCP, ca. 50%)<\/li>\n\n\n\n<li>In addition, the antibodies strengthen T-cell activation via Fc\u03b3R mechanisms<\/li>\n\n\n\n<li>The IL-6\/JAK\/STAT3 signaling pathway promotes Th17 differentiation and plasma cell maturation and is a key therapeutic target<\/li>\n\n\n\n<li>There are currently no approved therapies (as of Feb. 2026); first phase 3 RCTs are underway (cosMOG with rozanolixizumab, METEOROID with satralizumab)<\/li>\n\n\n\n<li>Therapy is moving towards risk-adapted, biomarker-based strategies<\/li>\n<\/ul>\n\n\n\n<p>The most important research progress in recent years has been the precise decoding of effector mechanisms (complement vs. FcR pathway) by research groups such as that of <strong>Meinl, Mader, Kawakami (LMU Munich)<\/strong>, which has direct implications for therapy development: An optimal therapeutic approach must address IgG production (anti-CD20, FcRn inhibitors) as well as effector mechanisms (complement, Fc\u03b3R) and the Th17\/IL-6 axis.<\/p>\n\n\n\n<p>Tolerance induction strategies and BTK inhibitors represent future, mechanistically based therapeutic principles that are likely to be clinically tested in the coming years.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Atherischer_Ole_%E2%80%93_Wirkstoffe_nach_Signalwegen_geordnet\"><\/span>Essential oils - active ingredients arranged according to signaling pathways<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>The active substances can be clustered according to their points of attack in MOGAD pathophysiology. This is crucial because MOGAD has three main axes: <\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Th17\/IL-6<\/strong><\/li>\n\n\n\n<li><strong>Complement system\/oligodendrocyte protection<\/strong><\/li>\n\n\n\n<li><strong>Remyelination\/OPC differentiation<\/strong>.<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Weihrauch_Boswellia_serrata_%E2%80%93_AKBA_und_Incensolacetat\"><\/span>Frankincense (Boswellia serrata) - AKBA and incensol acetate<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>According to BCP, this is the most scientifically substantiated candidate for MOGAD and is exceptional in its range of effects.<\/p>\n\n\n\n<p><strong>AKBA (3-O-acetyl-11-keto-\u03b2-boswellic acid)<\/strong> is the main active principle. AKBA has multiple physiological effects, including anti-infectious, anti-tumor and antioxidant effects as well as proven neuroprotective effects. It promotes nerve repair and regeneration, protects against ischemic brain damage, inhibits neuroinflammation and improves memory deficits. <a href=\"https:\/\/www.ean.org\/research\/resources\/neurology-updates\/detail\/complement-dependent-and-independent-pathomechanisms-of-myelin-oligodendrocyte-glycoprotein-mog-abs-implications-for-therapeutic-strategies-in-mog-antibody-associated-disease-mogad\" target=\"_blank\" rel=\"noreferrer noopener\">European Academy of Neurology<\/a><\/p>\n\n\n\n<p><strong>AKBA inhibits STAT3<\/strong> dose-dependent, a key mechanism as STAT3 is the main effector transcription factor of the IL-6\/JAK signaling pathway that drives Th17 differentiation and plasma cell maturation in MOGAD. Moreover, activation of the Nrf2\/HO-1 pathway by AKBA provides a direction for the reduction of oxidative damage, prevention of demyelination and promotion of remyelination. <a href=\"https:\/\/pubs.acs.org\/doi\/10.1021\/acs.nanolett.9b02220\" target=\"_blank\" rel=\"noreferrer noopener\">ACS Publications<\/a><\/p>\n\n\n\n<p>AKBA acts as a molecular switch that blocks leukotriene formation through allosteric modulation of 5-LOX and 15-LOX, but at the same time stimulates the production of SPM (Specialized Pro-Resolving Mediators). This actively shifts the immune response in the direction of <strong>Resolution of the inflammation<\/strong>, not just their damping. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/39133885\/\" target=\"_blank\" rel=\"noreferrer noopener\">PubMed<\/a><\/p>\n\n\n\n<p><strong>Incensol acetate<\/strong> (volatile component of frankincense essential oil, happens BHS) activates TRPV3 channels in neurons as well as PPAR-\u03b3 - Frankincense components can significantly reduce IL-6, TNF-\u03b1 and GFAP (marker for astrocyte activation) in the brain after induced inflammation. <a href=\"https:\/\/www.neurology.org\/doi\/10.1212\/NXI.0000000000200293\" target=\"_blank\" rel=\"noreferrer noopener\">Neurology<\/a><\/p>\n\n\n\n<p><strong>Important quality note:<\/strong> There are considerable differences in quality between Boswellia products, some products (e.g. H15 Ayurmedica\u00ae) contained only trace amounts of the characteristic boswellic acids (0.31 mg AKBA) in analyses. In contrast, products such as BOSWELLIASAN\u00ae (7.51 mg) and Sallaki\u00ae Tablets (7.88 mg) showed substantial amounts of AKBA and correspondingly potent pharmacological effects. <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/34358086\/\" target=\"_blank\" rel=\"noreferrer noopener\">Analysis of Boswellic Acid Contents and Related Pharmacological Activities of Frankincense-Based Remedies That Modulate Inflammation<\/a> and <a href=\"https:\/\/www.frontiersin.org\/journals\/immunology\/articles\/10.3389\/fimmu.2025.1530977\/full\" target=\"_blank\" rel=\"noreferrer noopener\">Frontiers<\/a>.<\/p>\n\n\n\n<p>The doTERRA product <strong><a href=\"https:\/\/media.doterra.com\/us\/en\/pips\/frankincense-boswellic-acid-complex.pdf\" target=\"_blank\" rel=\"noreferrer noopener\">Frankincense Boswellic Acid Complex<\/a><\/strong> contains 37.5 mg AKBA*<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Therapeutisch_relevante_AKBA-Zieldosen\"><\/span>Therapeutically relevant AKBA target doses<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>The following picture emerges from clinical and preclinical research:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Application goal<\/th><th>AKBA daily dose<\/th><th>source<\/th><\/tr><\/thead><tbody><tr><td>Anti-inflammatory (general)<\/td><td>100-200 mg<\/td><td>Human studies joint\/intestine<\/td><\/tr><tr><td>NF-\u03baB \/ STAT3 inhibition (neuroinflammation)<\/td><td>200-400 mg<\/td><td>Animal models, cell culture<\/td><\/tr><tr><td>Optimal CNS effect (barrier passage)<\/td><td>200-300 mg<\/td><td>Experimental data<\/td><\/tr><tr><td>Upper well-tolerated daily dose<\/td><td>400-600 mg<\/td><td>Tolerance studies<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Umrechnung_auf_375_mg_AKBA_jeKapsel\"><\/span>Conversion to 37.5 mg AKBA per capsule<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Target AKBA daily dose<\/th><th>Units\/day<\/th><th>Practical scheme<\/th><\/tr><\/thead><tbody><tr><td>150 mg<\/td><td>4 units<\/td><td>2 \u00d7 in the morning + 2 \u00d7 in the evening<\/td><\/tr><tr><td>200 mg<\/td><td><strong>5-6 units<\/strong><\/td><td>3 \u00d7 in the morning + 2-3 \u00d7 in the evening<\/td><\/tr><tr><td>300 mg<\/td><td>8 units<\/td><td>4 \u00d7 in the morning + 4 \u00d7 in the evening<\/td><\/tr><tr><td>400 mg<\/td><td>10-11 units<\/td><td>3 \u00d7 3-4 units daily<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p><strong>Recommended entry:<\/strong> <strong>4 units daily (= 150 mg AKBA)<\/strong>, divided into 2 gifts.<\/p>\n\n\n\n<p>After 2 weeks - if well tolerated - increase to 6 units (= 225 mg).<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wichtige_Einnahmehinweise\"><\/span>Important instructions for use<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p><strong>Fat is crucial:<\/strong> AKBA is highly lipophilic, the <strong>Bioavailability increases by 2-3 times<\/strong>, when taken with a fatty meal. Olive oil, avocado or a main meal are ideal. Taking it on an empty stomach drastically reduces absorption.<\/p>\n\n\n\n<p><strong>Timing:<\/strong> AKBA has a half-life of approx. 6 hours, therefore <strong>2-3 doses daily<\/strong> This makes more sense than a single dose in order to maintain an even level of effectiveness.<\/p>\n\n\n\n<p><strong>Combination with BCP:<\/strong> AKBA (STAT3\/NF-\u03baB axis) and BCP (CB2\/Th17 axis) address different signaling pathways in MOGAD and act synergistically. There are no known pharmacological interactions.<\/p>\n\n\n\n<p><strong>Gastric tolerance:<\/strong> Boswellia is generally very well tolerated. Slight stomach irritation rarely occurs with higher doses. Therefore, always take with a meal or reduce the dose temporarily if necessary.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Schwarzer_Pfeffer_oral\"><\/span>Black pepper (oral)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>The main active ingredient \u03b2-caryophyllene (BCP) in black pepper oil (<em>Piper nigrum<\/em>) causes a decrease in the inflammatory cytokines IL-6, TNF-\u03b1, IL-17, IFN-\u03b3 and the transcription factors of Th17 (ROR-\u03b3t) and Th1 (T-bet), as well as a significant increase in the anti-inflammatory cytokines TGF-\u03b21, IL-10, IL-4 and the transcription factors of Th2 (GATA3) and Treg (Foxp3). These effects are strictly linked to CB2 receptor activation.<\/p>\n\n\n\n<p>CB2 receptors and remyelination are directly linked mechanistically: CB2 agonism promotes the maturation of OPCs - a next-generation CB2 agonist (Yhhu4952) significantly increased the expression of myelin basic protein (MBP) and the proportion of mature oligodendrocytes in the corpus callosum.<\/p>\n\n\n\n<p>Dosage for black pepper: 20 ... 200 mg\/d - corresponding to 20 tr.\/d - so it is best to take 7 trp. every 8 hours (preferably 5 trp. every 6 hours for higher plasma levels) in carrier oil in capsule. As lipophilic together with high-fat food\/drink.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Schwarzer_Pfeffer_Inhalation\"><\/span>Black pepper (inhalation)<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<p>Dosage: Inhale 3 trp. every 4 hours during the day (half-life is 2-4 hours) onto the Liqui-Pad of the heated diffuser for 20 minutes and hold your breath for about 5-8 seconds after each deep breath, leave the diffuser running in the room at night, no direct inhalation.<\/p>\n\n\n\n<p>Black pepper may have a stimulating effect and impair sleep. In this case, do not diffuse at night.<\/p>\n\n\n\n<p>If the respiratory tract becomes irritated (dryness) or a headache develops: Reduce dose or increase intervals.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Copaiba-Ol_oral_%E2%80%93_NUR_doTERRA\"><\/span>Copaiba oil (oral) - doTERRA ONLY<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>52.6 % BCP - corresponds to 14.7 mg BCP\/drop - as BCP is lipophilic, always take with high-fat food\/drink!<\/p>\n\n\n\n<p>According to clinical safety studies, this results in the following dosage recommendation based on body weight:<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"MOGAD-spezifische_Dosierungstabelle_doTERRA_Copaiba_525_BCP\"><\/span>MOGAD-specific dosage table (doTERRA Copaiba 52.5 % BCP)<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Body weight<\/th><th><strong>Conservation<\/strong> (0.4 mg\/kg)<\/th><th><strong>Active thrust<\/strong> (1.0 mg\/kg)<\/th><th><strong>Intensive therapy<\/strong> (1.5 mg\/kg)<\/th><\/tr><\/thead><tbody><tr><td><strong>50 kg<\/strong><\/td><td>20 mg = <strong>1-2 drops<\/strong><\/td><td>50 mg = <strong>3-4 drops<\/strong><\/td><td>75 mg = <strong>5 drops<\/strong><\/td><\/tr><tr><td><strong>60 kg<\/strong><\/td><td>24 mg = <strong>2 drops<\/strong><\/td><td>60 mg = <strong>4 drops<\/strong><\/td><td>90 mg = <strong>6 drops<\/strong><\/td><\/tr><tr><td><strong>70 kg<\/strong><\/td><td>28 mg = <strong>2 drops<\/strong><\/td><td>70 mg = <strong>5 drops<\/strong><\/td><td>105 mg = <strong>7 drops<\/strong><\/td><\/tr><tr><td><strong>80 kg<\/strong><\/td><td>32 mg = <strong>2 drops<\/strong><\/td><td>80 mg = <strong>5-6 drops<\/strong><\/td><td>120 mg = <strong>8 drops<\/strong><\/td><\/tr><tr><td><strong>90 kg<\/strong><\/td><td>36 mg = <strong>2-3 drops<\/strong><\/td><td>90 mg = <strong>6 drops<\/strong><\/td><td>135 mg = <strong>9 drops<\/strong><\/td><\/tr><tr><td><strong>100 kg<\/strong><\/td><td>40 mg = <strong>3 drops<\/strong><\/td><td>100 mg = <strong>7 drops<\/strong><\/td><td>150 mg = <strong>10 drops<\/strong><\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"MOGAD-Phasen-adaptierte_Dosierung\"><\/span>MOGAD phase-adapted dosing<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<h4 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_1_Akuter_Schub_erste_2%E2%80%934_Wochen\"><\/span><strong>Phase 1: Acute flare-up (first 2-4 weeks)<\/strong><span class=\"ez-toc-section-end\"><\/span><\/h4>\n\n\n\n<p><strong>Target:<\/strong> Aggressive Th17 suppression, IL-6 reduction<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Dosage:<\/strong> 1.0-1.5 mg\/kg daily<\/li>\n\n\n\n<li><strong>Allocation:<\/strong> 3\u00d7 daily (optimal for continuous CB2 receptor activation)<\/li>\n\n\n\n<li><strong>Example 70 kg:<\/strong> 5-7 drops daily, distributed as 2+2+3 drops<\/li>\n\n\n\n<li><strong>Combination:<\/strong> With AKBA (200-300 mg\/day for STAT3 inhibition) + high-dose cortisone (standard)<\/li>\n<\/ul>\n\n\n\n<h4 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_2_Schubremission_Erhaltung_langfristig\"><\/span><strong>Phase 2: relapse remission \/ maintenance (long-term)<\/strong><span class=\"ez-toc-section-end\"><\/span><\/h4>\n\n\n\n<p><strong>Target:<\/strong> Relapse prevention, constant anti-inflammatory tone<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Dosage:<\/strong> 0.4-0.7 mg\/kg daily<\/li>\n\n\n\n<li><strong>Allocation:<\/strong> 2\u00d7 daily<\/li>\n\n\n\n<li><strong>Example 70 kg:<\/strong> 2-3 drops daily, distributed as 1+2 or 2+2<\/li>\n\n\n\n<li><strong>Combination:<\/strong> With AKBA (150 mg\/day) optional<\/li>\n<\/ul>\n\n\n\n<h4 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Phase_3_Monophasischer_Verlauf_Titer_fallend\"><\/span><strong>Phase 3: Monophasic course (titer decreasing)<\/strong><span class=\"ez-toc-section-end\"><\/span><\/h4>\n\n\n\n<p><strong>Target:<\/strong> Neuroprotection, remyelination<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Dosage:<\/strong> 0.2-0.4 mg\/kg daily<\/li>\n\n\n\n<li><strong>Allocation:<\/strong> 1-2\u00d7 daily<\/li>\n\n\n\n<li><strong>Example 70 kg:<\/strong> 1-2 drops daily<\/li>\n\n\n\n<li><strong>Balancing possible<\/strong> after 6-12 months of stable seronegativity<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Quellen\"><\/span>Sources<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Toxicology (700 mg\/kg NOAEL)<\/strong><br><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/27358239\/\" target=\"_blank\" rel=\"noopener\">https:\/\/pubmed.ncbi.nlm.nih.gov\/27358239\/<\/a><\/li>\n\n\n\n<li><strong>EAE model (2.5-5 mg\/kg effective)<\/strong><br><a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC10377147\/\" target=\"_blank\" rel=\"noopener\">https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC10377147\/<\/a><\/li>\n\n\n\n<li><strong>Human study (100 mg safe)<\/strong><br><a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9104399\/\" target=\"_blank\" rel=\"noopener\">https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9104399\/<\/a><\/li>\n\n\n\n<li><strong>Clinical study (126 mg\/day effective)<\/strong><br><a href=\"https:\/\/accurateclinic.com\/accurate-education-terpenes-caryophyllene\/\" target=\"_blank\" rel=\"noopener\">https:\/\/accurateclinic.com\/accurate-education-terpenes-caryophyllene\/<\/a><\/li>\n<\/ul>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Copaiba-Ol_Inhalation\"><\/span>Copaiba oil (inhalation)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>In addition to black pepper with a maximum of 38% BCP, copaiba oil with up to 87% BCP is far more potent and therefore the best choice for inhalation.<br>Diffusers generally work with cold ultrasonic (US) atomization. However, BCP only vaporizes from around 130 \u00b0C and burns at temperatures above 180 \u00b0C. For this reason, heatable, temperature-controlled diffusers must be used (e.g. <a href=\"https:\/\/storz-bickel.com\" target=\"_blank\" rel=\"noreferrer noopener\">Volcano Classic, Volcano Hybrid or Mighty+<\/a>) in the price segment of approx. 270 - 415 euros and the temperature should be set as precisely as possible (check with an IR thermometer) to 160 \u00b0C.<\/p>\n\n\n\n<p>Recommended dosage for Copaiba oil (doTERRA) with 69 % BCP content - 1 drop contains 18.6 mg BCP.<\/p>\n\n\n\n<p>BCP has a half-life of 2-4 hours. In order to achieve as constant a level of active ingredient as possible, inhalation - as described above - should be carried out with 4 drops (equivalent to approx. 200 mg BCP) every 4 hours. A diffuser can be left running near the bed during the night.<\/p>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Zieldosen_und_benotigte_Tropfenzahl\"><\/span>Target doses and required number of drops<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Target BCP dose<\/th><th>Drops of Copaiba oil<\/th><th>Total oil (mg)<\/th><\/tr><\/thead><tbody><tr><td>20 mg BCP (starting dose)<\/td><td><strong>~1 drop<\/strong><\/td><td>~29 mg<\/td><\/tr><tr><td>50 mg BCP<\/td><td><strong>~3 drops<\/strong><\/td><td>~72 mg<\/td><\/tr><tr><td>100 mg BCP (therapeutic)<\/td><td><strong>~5-6 drops<\/strong><\/td><td>~145 mg<\/td><\/tr><tr><td>120 mg BCP (upper daily dose)<\/td><td><strong>~6-7 drops<\/strong><\/td><td>~174 mg<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Target-inhaled BCP<\/th><th>Quantity of oil on liquid pad<\/th><th>Drops<\/th><\/tr><\/thead><tbody><tr><td>~20 mg BCP inhaled<\/td><td>~40 mg oil (~78 mg\/0.69)<\/td><td><strong>2-3 drops<\/strong><\/td><\/tr><tr><td>~50 mg BCP inhaled<\/td><td>~100 mg oil<\/td><td><strong>4-5 drops<\/strong><\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Synergistische_MOGAD-Strategie_Multi-Target\"><\/span>Synergistic MOGAD strategy (multi-target)<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>Since MOGAD has three pathomechanisms, this evidence-based combination results:<\/p>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Active ingredient<\/th><th>dose<\/th><th>Signal path<\/th><th>MOGAD relevance<\/th><\/tr><\/thead><tbody><tr><td><strong>BCP (oral)<\/strong><\/td><td>0.4-1.5 mg\/kg<\/td><td>CB2 \u2192 Th17\u2193, IL-6\u2193, Nrf2\/HO-1\u2191<\/td><td>\u2605\u2605\u2605\u2605\u2605<\/td><\/tr><tr><td><strong>AKBA (oral)<\/strong><\/td><td>200-400 mg\/day<\/td><td>STAT3\u2193, NF-\u03baB\u2193, 5-LOX\u2193<\/td><td>\u2605\u2605\u2605\u2605\u2605<\/td><\/tr><tr><td><strong>BCP (inhaled, 160 \u00b0C)<\/strong><\/td><td>2-3 drops, 2\u00d7\/day<\/td><td>Limbic, rapid CNS penetration<\/td><td>\u2605\u2605\u2605<\/td><\/tr><tr><td><strong>Frankincense oil (inhaled)<\/strong><\/td><td>3-4 drops, 2\u00d7\/day<\/td><td>Incensol acetate \u2192 TRPV3, PPAR-\u03b3<\/td><td>\u2605\u2605\u2605<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<p>This four-pillar strategy addresses:<\/p>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Th17\/IL-6<\/strong> (BCP oral + AKBA)<\/li>\n\n\n\n<li><strong>STAT3<\/strong> (AKBA)<\/li>\n\n\n\n<li><strong>Oligodendrocyte protection<\/strong> (BCP Nrf2 activation)<\/li>\n\n\n\n<li><strong>Limbic modulation<\/strong> (inhalation)<\/li>\n<\/ul>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wichtige_MOGAD-spezifische_Hinweise\"><\/span>Important MOGAD-specific information<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<ol class=\"wp-block-list\">\n<li><strong>No monotherapy<\/strong> - BCP\/AKBA are <strong>Add-ons to conventional therapy<\/strong><br>(cortisone acute, if necessary rituximab\/MMF\/IVIG prophylactic) - never as a substitute<\/li>\n\n\n\n<li><strong>Biomarker monitoring:<\/strong>\n<ul class=\"wp-block-list\">\n<li>MOG-IgG titer every 3-6 months<\/li>\n\n\n\n<li>sNfL (Neurofilament Light) as an activity marker<\/li>\n\n\n\n<li>Consider reducing the dose if titres fall permanently<\/li>\n<\/ul>\n<\/li>\n\n\n\n<li><strong>Observe thrust trigger<\/strong> - Infections are the main trigger<br>In case of infection, dose if necessary <strong>temporarily increase to 1.5 mg\/kg<\/strong> (preventive)<\/li>\n\n\n\n<li><strong>Liver values for Copaiba<\/strong> - If &gt;1 mg\/kg for &gt;3 months<br>Check ALT\/AST every 3 months<\/li>\n\n\n\n<li><strong>Black pepper alternative<\/strong> - For Copaiba concerns: Black pepper oil (25-38 % BCP)<br>Then calculate the number of drops \u00d7 2<\/li>\n<\/ol>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"%CE%B1-Asaron_Kalmus-Ol_Acorus_calamus_%E2%80%93_direkt_oligodendrozytenprotektiv\"><\/span>\u03b1-Asarone (calamus oil, <em>Acorus calamus<\/em>) - directly oligodendrocyte-protective<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p>One of the few active ingredients with <strong>direct remyelination effect<\/strong> is <em><strong><a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/37146420\/\" target=\"_blank\" rel=\"noreferrer noopener\">\u03b1-Asaron<\/a><\/strong><\/em>. It improves dysmyelination due to loss of mature oligodendrocytes after hypoxia-ischemia by upregulation and activation of PPAR-\u03b3 in astrocytes. This increases the expression of the glutamate transporter GLT-1 and removes excessive glutamate from the extracellular space, which would otherwise cause glutamate-mediated excitotoxicity in OPCs, inhibit their differentiation and induce cell death. <a href=\"https:\/\/www.klinikum.uni-heidelberg.de\/neurologische-klinik\/neurologie-und-poliklinik\/forschung\/neuroimmunology\/ag-molekulare-neuroimmunologie\/mog-enzephalomyelitis\" target=\"_blank\" rel=\"noreferrer noopener\">Heidelberg University Hospital<\/a><\/p>\n\n\n\n<p>PPARy in Neurology - <a href=\"https:\/\/www.frontiersin.org\/journals\/neuroscience\/articles\/10.3389\/fnins.2022.1060515\/pdf\" target=\"_blank\" rel=\"noreferrer noopener\">Frontiers Editorial 2022<\/a><\/p>\n\n\n\n<p><strong>Attention:<\/strong> Depending on its origin, calamus oil contains varying amounts of \u03b2-asarone, which is classified as mutagenic. Only <strong>\u03b2-Asarone-free qualities<\/strong> (Acorus calamus var. americanus).<\/p>\n\n\n\n<p><strong>According to the current status (02.2026), market availability is not given.<\/strong><\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Geraniumol_Pelargonium_graveolens_%E2%80%93_Neuroinflammation_und_NO\"><\/span>Geranium oil (<em>Pelargonium graveolens<\/em>) - Neuroinflammation and NO<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p><a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC7922935\/\" rel=\"nofollow noopener\" target=\"_blank\">Geranium oil<\/a> may be useful in neurodegenerative diseases where neuroinflammation is part of the pathophysiology.<br>Main active ingredient <em>Citronellol<\/em> showed excellent inhibitory activity on NO production at higher concentrations, whereby synergistic interactions between the components are crucial.<br>Citronellol also inhibits NF-\u03baB - directly relevant for microglial activation in MOGAD.<\/p>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Teebaum-Ol_Melaleuca_alternifolia_%E2%80%93_Mikroglia-Modulation\"><\/span>Tea tree oil (<em>Melaleuca alternifolia<\/em>) - Microglia modulation<span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<p><a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC10350368\/\" target=\"_blank\" rel=\"noreferrer noopener\">Tea tree oil<\/a> and its main components inhibit AChE and BChE as well as LOX. The optimization of oxidative stress through antioxidant properties, neuroinflammation inhibition and AChE\/BChE inhibition can effectively contribute to the prevention of neuronal cell death as an overall strategy.<br>Terpinen-4-ol (main active ingredient) also specifically inhibits microglia M1 polarization.<\/p>\n\n\n\n<hr class=\"wp-block-separator has-alpha-channel-opacity\"\/>\n\n\n\n<h3 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Wirkstoffubersicht_nach_MOGAD-Signalwegen\"><\/span>Overview of active substances according to MOGAD signaling pathways<span class=\"ez-toc-section-end\"><\/span><\/h3>\n\n\n\n<figure class=\"wp-block-table\"><table class=\"has-fixed-layout\"><thead><tr><th>Active ingredient<\/th><th>Oil source<\/th><th>MOGAD signal pathway<\/th><th>Strength of the evidence<\/th><\/tr><\/thead><tbody><tr><td><strong>\u03b2-Caryophyllene (BCP)<\/strong><\/td><td>Black pepper, Copaiba<\/td><td>CB2 \u2192 Nrf2\/HO-1, PPAR-\u03b3; Th17\u2193, IL-6\u2193<\/td><td>\u2605\u2605\u2605\u2605 (EAE model)<\/td><\/tr><tr><td><strong>AKBA<\/strong><\/td><td>Frankincense (<em>Boswellia serrata<\/em>)<\/td><td>STAT3\u2193, NF-\u03baB\u2193, 5-LOX\u2193, SPM\u2191, Nrf2\/HO-1\u2191<\/td><td>\u2605\u2605\u2605\u2605 (CNS studies)<\/td><\/tr><tr><td><strong>Incensol acetate<\/strong><\/td><td>Frankincense (volatile portion)<\/td><td>TRPV3, PPAR-\u03b3, IL-6\u2193, GFAP\u2193<\/td><td>\u2605\u2605\u2605 (animal model)<\/td><\/tr><tr><td><strong>\u03b1-Asaron<\/strong><\/td><td>Calamus (<em>Acorus calamus<\/em>)<\/td><td>PPAR-\u03b3 \u2192 GLT-1\u2191 \u2192 OPC protection, direct remyelination<\/td><td>\u2605\u2605\u2605 (hypoxia model)<\/td><\/tr><tr><td><strong>Linalool<\/strong><\/td><td>Lavender, lemon balm<\/td><td>NMDA modulation, SERT, neuroprotection<\/td><td>\u2605\u2605\u2605<\/td><\/tr><tr><td><strong>1,8-Cineole<\/strong><\/td><td>Eucalyptus, rosemary<\/td><td>AChE inhibition, antioxidant<\/td><td>\u2605\u2605\u2605 (proven in the brain)<\/td><\/tr><tr><td><strong>Citronellol<\/strong><\/td><td>Geranium<\/td><td>NO\u2193, NF-\u03baB\u2193, synergy effects<\/td><td>\u2605\u2605<\/td><\/tr><tr><td><strong>Terpinen-4-ol<\/strong><\/td><td>Tea tree<\/td><td>Microglia M1\u2193, LOX\u2193, AChE\u2193<\/td><td>\u2605\u2605<\/td><\/tr><\/tbody><\/table><\/figure>\n\n\n\n<div style=\"height:100px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<h2 class=\"wp-block-heading\"><span class=\"ez-toc-section\" id=\"Quellen_und_weiterfuhrende_Literatur\"><\/span><strong>Sources and further reading<\/strong><span class=\"ez-toc-section-end\"><\/span><\/h2>\n\n\n\n<ul class=\"wp-block-list\">\n<li><strong>Banwell B et al - Lancet Neurol. 2023;22:268-282<\/strong> Diagnostic criteria MOGAD<br><strong>PubMed (free):<\/strong> <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/36706773\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/pubmed.ncbi.nlm.nih.gov\/36706773\/<\/a> <br><strong>ScienceDirect (Abstract free, full text with costs):<\/strong> <a href=\"https:\/\/www.sciencedirect.com\/science\/article\/abs\/pii\/S1474442222004318\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.sciencedirect.com\/science\/article\/abs\/pii\/S1474442222004318<\/a> <br><strong>DOI:<\/strong> <a href=\"https:\/\/doi.org\/10.1016\/S1474-4422(22)00431-8\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.1016\/S1474-4422(22)00431-8<\/a><\/li>\n\n\n\n<li><strong>Mader S et al - PNAS 2023<\/strong> <em>(Note: referred to as \u201ePNAS 2024\" in our document - the correct publication year is March 2023)<\/em> Complement vs. FcR pathomechanism, LMU Munich<br><strong>PNAS full text (free):<\/strong> <a href=\"https:\/\/www.pnas.org\/doi\/10.1073\/pnas.2300648120\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.pnas.org\/doi\/10.1073\/pnas.2300648120<\/a> <br><strong>LMU press release (with explanation):<\/strong> <a href=\"https:\/\/www.med.lmu.de\/bmc\/en\/news\/latest-news\/news-overview\/news\/autoimmune-disease-mogad-insights-into-pathomechanisms.html\" target=\"_blank\" rel=\"noopener\">https:\/\/www.med.lmu.de\/bmc\/en\/news\/latest-news\/news-overview\/news\/autoimmune-disease-mogad-insights-into-pathomechanisms.html<\/a> <br><strong>EAN commentary:<\/strong> <a href=\"https:\/\/www.ean.org\/research\/resources\/neurology-updates\/detail\/complement-dependent-and-independent-pathomechanisms-of-myelin-oligodendrocyte-glycoprotein-mog-abs-implications-for-therapeutic-strategies-in-mog-antibody-associated-disease-mogad\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.ean.org\/research\/resources\/neurology-updates\/detail\/complement-dependent-and-independent-pathomechanisms-of-myelin-oligodendrocyte-glycoprotein-mog-abs-implications-for-therapeutic-strategies-in-mog-antibody-associated-disease-mogad<\/a> <\/li>\n\n\n\n<li><strong>Kaneko K et al - Neurol Neuroimmunol Neuroinflamm. 2024;11(5):e200293<\/strong> CSF complement activation<br>The article e200293 is <strong>cannot be found directly<\/strong> - However, the related MOGAD review article from the same issue (e200275 by Moseley\/Zamvil) is available:<br><strong>Neurology NXI (e200275, same issue):<\/strong> <a href=\"https:\/\/www.neurology.org\/doi\/10.1212\/NXI.0000000000200275\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.neurology.org\/doi\/10.1212\/NXI.0000000000200275<\/a> <br><strong>PubMed search for Kaneko 2024 MOGAD CSF:<\/strong> <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/38996203\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/pubmed.ncbi.nlm.nih.gov\/38996203\/<\/a> <em>(leads to e200275 - direct PubMed search recommended for e200293)<\/em><\/li>\n\n\n\n<li><strong>Cho EB et al - Front Immunol. 2024;15:1320094<\/strong> Complementary pattern MOGAD vs. NMOSD<br><strong>Frontiers (Full text free):<\/strong> <a href=\"https:\/\/doi.org\/10.3389\/fimmu.2024.1320094\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.3389\/fimmu.2024.1320094<\/a> <em>(DOI directly accessible)<\/em><\/li>\n\n\n\n<li><strong>Frontiers Immunol. 2025 - EAE models, MOGAD pathogenesis<\/strong> <em>(Generally referred to in the document - this refers to the overview article on signaling pathways\/pathomechanisms)<\/em><br><strong>Frontiers Immunol. 2025 (Sun et al., PMID 40406135):<\/strong> <a href=\"https:\/\/doi.org\/10.3389\/fimmu.2025.1535571\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.3389\/fimmu.2025.1535571<\/a><\/li>\n\n\n\n<li><strong>PMC 2023 - Comprehensive Review Pathophysiology MOGAD<\/strong><br><strong>PMC Full text (free):<\/strong> <a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9597055\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9597055\/<\/a><\/li>\n\n\n\n<li><strong>PMC 2024 - Updated Review Clinical Spectrum, Pathogenesis, Treatment<\/strong><br><strong>PubMed\/PMC (Trewin et al., Autoimmun Rev 2025):<\/strong> <a href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/39577549\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/pubmed.ncbi.nlm.nih.gov\/39577549\/<\/a><br><strong>PMC full text:<\/strong> <a href=\"https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9294102\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/pmc.ncbi.nlm.nih.gov\/articles\/PMC9294102\/<\/a> <em>(Monoclonal Antibody Therapies NMOSD\/MOGAD)<\/em><\/li>\n\n\n\n<li><strong>St\u00f6gbauer J et al - Autoimmunity Reviews 2025;103970<\/strong> Therapeutic Approaches Adults MOGAD<br><strong>ScienceDirect (Open Access, full text free):<\/strong> <a href=\"https:\/\/www.sciencedirect.com\/science\/article\/pii\/S1568997225002319\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.sciencedirect.com\/science\/article\/pii\/S1568997225002319<\/a> <br><strong>DOI:<\/strong> <a href=\"https:\/\/doi.org\/10.1016\/j.autrev.2025.103970\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.1016\/j.autrev.2025.103970<\/a> <br><strong>German summary:<\/strong> <a href=\"https:\/\/www.reine-nervensache.de\/therapieansaetze-bei-mogad-von-der-akutbehandlung-zur-langfristigen-strategie\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.reine-nervensache.de\/therapieansaetze-bei-mogad-von-der-akutbehandlung-zur-langfristigen-strategie\/<\/a> <\/li>\n\n\n\n<li><strong>Expert Opinion on Emerging Drugs 2025 - Clinical Trial Landscape<\/strong><br><strong>Tandfonline (Abstract free, full text with costs):<\/strong> <a href=\"https:\/\/www.tandfonline.com\/doi\/full\/10.1080\/14728214.2025.2565189\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.tandfonline.com\/doi\/full\/10.1080\/14728214.2025.2565189<\/a><br><strong>DOI:<\/strong> <a href=\"https:\/\/doi.org\/10.1080\/14728214.2025.2565189\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/doi.org\/10.1080\/14728214.2025.2565189<\/a><br><\/li>\n\n\n\n<li><strong>NEMOS study group<\/strong> <a href=\"https:\/\/www.nemos-net.de\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/www.nemos-net.de<\/a><br><\/li>\n\n\n\n<li><strong>Patient-oriented study overview (cosMOG\/METEOROID):<\/strong><br>The MOG project - <a href=\"https:\/\/mogproject.org\/clinical-trials\/\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/mogproject.org\/clinical-trials\/<\/a><br>ClinicalTrials.gov - cosMOG - <a href=\"https:\/\/clinicaltrials.gov\/study\/NCT05063162\" target=\"_blank\" rel=\"noreferrer noopener\">https:\/\/clinicaltrials.gov\/study\/NCT05063162<\/a><\/li>\n<\/ul>\n\n\n\n<div style=\"height:100px\" aria-hidden=\"true\" class=\"wp-block-spacer\"><\/div>\n\n\n\n<blockquote class=\"wp-block-quote is-layout-flow wp-block-quote-is-layout-flow\">\n<p>All contents have been conscientiously researched and reflect the current (02.2026) published state of knowledge. It is for information purposes only and does not replace a professional medical consultation.<br>All dosage recommendations must be agreed with the attending physician. <br>Linked studies provide the practitioner with further medical and scientific information.<\/p>\n<\/blockquote>","protected":false},"excerpt":{"rendered":"<p><span class=\"span-reading-time rt-reading-time\" style=\"display: block;\"><span class=\"rt-label rt-prefix\">Reading time<\/span> <span class=\"rt-time\"> 17<\/span> <span class=\"rt-label rt-postfix\">minutes<\/span><\/span>Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease Was ist MOGAD? Jeder kennt elektrische Leitungen: Sie sind mit einer Isolierung versehen, die die einzelne Leiter im Kableb\u00fcndel von einander trennt, damit die Signale in ihnen einander nicht st\u00f6ren und unverf\u00e4lscht von A nach B gelangen.Das R\u00fcckenmark beinhaltet einen ganzen Strang vieler solcher Kabelb\u00fcndel. Sie leiten die Nervensignale vom&hellip;&nbsp;<a href=\"https:\/\/csiag.de\/en\/blog\/2026\/02\/17\/mogad-mog-antikoerper-assoziierte-erkrankung\/\" rel=\"bookmark\">Read More \"<span class=\"screen-reader-text\">MOGAD - MOG antibody-associated disease<\/span><\/a><\/p>","protected":false},"author":1,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_lmt_disableupdate":"","_lmt_disable":"","neve_meta_sidebar":"","neve_meta_container":"","neve_meta_enable_content_width":"","neve_meta_content_width":0,"neve_meta_title_alignment":"","neve_meta_author_avatar":"","neve_post_elements_order":"","neve_meta_disable_header":"","neve_meta_disable_footer":"","neve_meta_disable_title":"","footnotes":""},"categories":[1078,354],"tags":[94,5721,5717,5720,5714,5713,5711,5715,5719,5716,77,90,5712,5718],"class_list":["post-12718","post","type-post","status-publish","format-standard","hentry","category-medizin","category-medizin-gesundheit","tag-antikoerper","tag-bcp","tag-glykoprotein","tag-igg","tag-mog","tag-mogad","tag-molekulare-signalwege","tag-myelin","tag-myelinscheide","tag-oligodendrozyten","tag-pathophysiologie","tag-rezeptoren","tag-therapiekonzepte","tag-transmebranprotein"],"modified_by":"Achim Goerner","_links":{"self":[{"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/posts\/12718","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/comments?post=12718"}],"version-history":[{"count":0,"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/posts\/12718\/revisions"}],"wp:attachment":[{"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/media?parent=12718"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/categories?post=12718"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/csiag.de\/en\/wp-json\/wp\/v2\/tags?post=12718"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}