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5. Siponimod versus placebo in secondary progressive multiple sclerosis (EXPAND): a double-blind, randomised, phase 3 study

Author

Achiron, Anat, Achtnichts, Lutz, Agan, Kadriye, Akman-Demir, Gulsen, Allen, Alison B, Antel, Jack P, Antiguedad, Alfredo Rodriguez, Apperson, Michelle, Applebee, Angela M, Ayuso, Guillermo Izquierdo, Baba, Masayuki, Bajenaru, Ovidiu, Balasa, Rodica, Balci, Belgin Petek, Barnett, Michael, Bass, Ann, Becker, Veit U, Bejinariu, Mihaela, Bergh, Florian Then, Bergmann, Arnfin, Bernitsas, Evanthia, Berthele, Achim, Bhan, Virender, Bischof, Felix, Bjork, Randall John, Blevins, Gregg, Boehringer, Matthias, Boerner, Thomas, Bonek, Robert, Bowen, James D, Bowling, Allen, Boyko, Alexey N, Boz, Cavit, Bracknies, Vera, Braune, Stefan, Brescia Morra, Vincenzo, Brochet, Bruno, Brola, Waldemar, Brownstone, Paul Kenneth, Brozman, Miroslav, Brunet, Donald, Buraga, Ioan, Burnett, Margaret, Buttmann, Mathias, Butzkueven, Helmut, Cahill, Jonathan, Calkwood, Jonathan C, Camu, William, Cascione, Mark, Castelnovo, Giovani, Centonze, Diego, Cerqueira, Joao, Chan, Andrew, Cimprichova, Andrea, Cohan, Stanley, Comi, Giancarlo, Conway, Jill, Cooper, Joanna A, Corboy, John, Correale, Jorge, Costell, Brian, Cottrell, David A, Coyle, Patricia K, Craner, Matthew, Cui, Liying, Cunha, Luis, Czlonkowska, Anna, da Silva, Ana Martins, de Sa, Joao, de Seze, Jérôme, Debouverie, Marc, Debruyne, Jan, Decoo, Danny, Defer, Gilles, Derfuss, Tobias, Deri, Norma H, Dihenia, Bhupesh, Dioszeghy, Peter, Donath, Vladimir, Dubois, Benedicte, Duddy, Martin, Duquette, Pierre, Edan, Gilles, Efendi, Husnu, Elias, Stanton, Emrich, Peter J, Estruch, Bonaventura Casanova, Evdoshenko, Evgeniy P, Faiss, Juergen, Fedyanin, Alexander S, Feneberg, Wolfgang, Fermont, Jiske, Fernandez, Oscar Fernandez, Ferrer, Francisco Coret, Fink, Katharina, Ford, Helen, Ford, Corey, Francia, Ada, Freedman, Mark, Frishberg, Benjamin, Galgani, Simonetta, Garmany, George P, Gehring, Klaus, Gitt, Jeffrey, Gobbi, Claudio, Goldstick, Lawrence P, Gonzalez, Rafael Arroyo, Grandmaison, Francois, Grigoriadis, Nikolaos, Grigorova, Olga, Grimaldi, Luigi Maria Edoardo, Gross, Jeffrey, Gross-Paju, Katrin, Gudesblatt, Mark, Guillaume, Daniel, Haas, Judith, Hancinova, Viera, Hancu, Anca, Hardiman, Orla, Harmjanz, Arndt, Heidenreich, Fedor R, Hengstman, G J D, Herbert, Joseph, Herring, Mark, Hodgkinson, Suzanne, Hoffmann, Olaf M, Hofmann, Werner E, Honeycutt, William D, Hua, Le Hanh, Huang, Dehui, Huang, Yining, Huang, DeRen, Hupperts, Raymond, Imre, Piroska, Jacobs, Alan Keith, Jakab, Gabor, Jasinska, Elzbieta, Kaida, Kenichi, Kalnina, Jolanta, Kaprelyan, Ara, Karelis, Guntis, Karussis, Dimitrios, Katz, Amos, Khabirov, Farit A, Khatri, Bhupendra, Kimura, Takashi, Kister, Ilya, Kizlaitiene, Rasa, Klimova, Eleonora, Koehler, Juergen, Komatineni, Aparna, Kornhuber, Anselm, Kovacs, Krisztina, Koves, Agnes, Kozubski, Wojciech, Krastev, Georgi, Krupp, Lauren B, Kurca, Egon, Lassek, Christoph, Laureys, Guy, Lee, Liesly, Lensch, Eckart, Leutmezer, Fritz, Li, Hongzeng, Linker, Ralf A, Linnebank, Michael, Liskova, Petra, Llanera, Cristina, Lu, Jiahong, Lutterotti, Andreas, Lycke, Jan, Macdonell, Richard, Maciejowski, Maciej, Maeurer, Mathias, Magzhanov, Rim V, Maida, Eva-Maria, Malciene, Lina, Mao-Draayer, Yang, Marfia, Girolama Alessandra, Markowitz, Clyde, Mastorodimos, Vasileios, Matyas, Klotild, Meca-Lallana, Jose, Merino, Juan Antonio Garcia, Mihetiu, Ioan Gheorghe, Milanov, Ivan, Miller, Aaron E, Millers, Andrejs, Mirabella, Massimiliano, Mizuno, Masanori, Montalban, Xavier, Montoya, Lilina, Mori, Masahiro, Mueller, Stefanie, Nakahara, Jin, Nakatsuji, Yuji, Newsome, Scott, Nicholas, Richard, Nielsen, A Scott, Nikfekr, Esmaeil, Nocentini, Ugo, Nohara, Chiyoko, Nomura, Kyoichi, Odinak, Miroslav M, Olsson, Tomas, van Oosten, B W, Oreja-Guevara, Celia, Oschmann, Patrick, Overell, James, Pachner, Andrew, Panczel, Gyula, Pandolfo, Massimo, Papeix, Caroline, Patrucco, Liliana, Pelletier, Jean, Piedrabuena, Raul, Pless, Misha, Polzer, Udo, Pozsegovits, Krisztian, Rastenyte, Daiva, Rauer, Sebastian, Reifschneider, Gerd, Rey, Roberto, Rizvi, Syed A, Robertson, Derrick, Rodriguez, Jose Martinez, Rog, David, Roshanisefat, Homayoun, Rowe, Vernon, Rozsa, Csilla, Rubin, Susan, Rusek, Stanislaw, Saccà, Francesco, Saida, Takahiko, Salgado, Antonio Vasco, Sanchez, Victoria Eugenia Fernandez, Sanders, Kalina, Satori, Maria, Sazonov, Denis V, Scarpini, Elio Angelo, Schlegel, Eugen, Schluep, Myriam, Schmidt, Stephan, Scholz, Erich, Schrijver, H M, Schwab, Matthias, Schwartz, Raymond, Scott, James, Selmaj, Krzysztof, Shafer, Stuart, Sharrack, Basil, Shchukin, Ivan A, Shimizu, Yuko, Shotekov, Penko, Siever, Arno, Sigel, Karl-Otto, Silliman, Scott, Simo, Magdolna, Simu, Mihaela, Sinay, Vladimiro, Siquier, Antonio Escartin, Siva, Aksel, Skoda, Ondrej, Solomon, Andrew, Stangel, Martin, Stefoski, Dusan, Steingo, Brian, Stolyarov, Igor D, Stourac, Pavel, Strassburger-Krogias, Katrin, Strauss, Erik, Stuve, Olaf, Tarnev, Ivaylo, Tavernarakis, Antonios, Tello, Cristina Ramo, Terzi, Murat, Ticha, Veronika, Ticmeanu, Marina, Tiel-Wilck, Klaus, Toomsoo, Toomas, Tubridy, Niall, Tullman, Mark J, Tumani, Hayrettin, Turcani, Peter, Turner, Ben, Uccelli, Antonio, Urtaza, Francisco Javier Olascoaga, Vachova, Marta, Valikovics, Attila, Walter, Silke, Van Wijmeersch, Bart, Vanopdenbosch, Ludo, Weber, Joerg R, Weiss, Sara, Weissert, Robert, Vermersch, Patrick, West, Timothy, Wiendl, Heinz, Wiertlewski, Sandrine, Wildemann, Brigitte, Willekens, Barbara, Visser, L H, Vorobeychik, Galina, Xu, Xianhao, Yamamura, Takashi, Yang, Yi N, Yelamos, Sergio Martinez, Yeung, Michael, Zacharias, Alan, Zelkowitz, Marvin, Zettl, Uwe, Zhang, Meini, Zhou, Hongyu, Zieman, Ulf, Ziemssen, Tjalf, Kappos, Ludwig, Bar-Or, Amit, Cree, Bruce A C, Fox, Robert J, Giovannoni, Gavin, Gold, Ralf, Arnold, Douglas L, Arnould, Sophie, Scherz, Tatiana, Wolf, Christian, Wallström, Erik, and Dahlke, Frank

Published
2018
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11. Nervous system‐related tropism of SARS‐CoV‐2 and autoimmunity in COVID‐19 infection.

Author

Weissert, Robert

Subjects
COVID-19, POST-acute COVID-19 syndrome, AUTOIMMUNE diseases, SARS-CoV-2, VIRAL tropism, MOLECULAR mimicry
Abstract

The effects of SARS‐CoV‐2 in COVID‐19 on the nervous system are incompletely understood. SARS‐CoV‐2 can infect endothelial cells, neurons, astrocytes, and oligodendrocytes with consequences for the host. There are indications that infection of these CNS‐resident cells may result in long‐term effects, including emergence of neurodegenerative diseases. Indirect effects of infection with SARS‐CoV‐2 relate to the induction of autoimmune disease involving molecular mimicry or/and bystander activation of T‐ and B cells and emergence of autoantibodies against various self‐antigens. Data obtained in preclinical models of coronavirus‐induced disease gives important clues for the understanding of nervous system‐related assault of SARS‐CoV‐2. The pathophysiology of long‐COVID syndrome and post‐COVID syndrome in which autoimmunity and immune dysregulation might be the driving forces are still incompletely understood. A better understanding of nervous‐system‐related immunity in COVID‐19 might support the development of therapeutic approaches. In this review, the current understanding of SARS‐CoV‐2 tropism for the nervous system, the associated immune responses, and diseases are summarized. The data indicates that there is viral tropism of SARS‐CoV‐2 in the nervous system resulting in various disease conditions. Prevention of SARS‐CoV‐2 infection by means of vaccination is currently the best strategy for the prevention of subsequent tissue damage involving the nervous system. [ABSTRACT FROM AUTHOR]

Published
2024
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21. Additional file 1 of Early remission in multiple sclerosis is linked to altered coherence of the Cerebellar Network

Author

Tahedl, Marlene, Levine, Seth M., Weissert, Robert, Kohl, Zacharias, Lee, De-Hyung, Linker, Ralf A., and Schwarzbach, Jens V.

Abstract

Additional file 1: Figure S1. Probability that a given network is the “original network”, whose functional coherence is changed in MS patients following their entrance into remission. Open circles are data from individual patients; closed circles depict the mean, and error bars are SEM. (A) Results from the first set of 9 patients. (B) Results from the second set of 9 patients. Note that in both cases the cerebellar network is, by far, the most likely network to change its functional coherence.

Published
2022
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22. Neurofilament ELISA validation

Author

Petzold, Axel, Altintas, Ayse, Andreoni, Laura, Bartos, Ales, Berthele, Achim, Blankenstein, Marinus A., Buee, Luc, Castellazzi, Massimiliano, Cepok, Sabine, Comabella, Manuel, Constantinescu, Cris S., Deisenhammer, Florian, Deniz, Gunnur, Erten, Gaye, Espiño, Mercedes, Fainardi, Enrico, Franciotta, Diego, Freedman, Mark S., Giedraitis, Vilmantas, Gilhus, Nils Erik, Giovannoni, Gavin, Glabinski, Andrzej, Grieb, Pawel, Hartung, Hans-Peter, Hemmer, Bernhard, Herukka, Sanna-Kaisa, Hintzen, Rogier, Ingelsson, Martin, Jackson, Samuel, Jacobsen, Steve, Jafari, Naghmeh, Jalosinski, Marcin, Jarius, Sven, Kapaki, Elisabeth, Kieseier, Bernd C., Koel-Simmelink, Marleen J.A., Kornhuber, Johannes, Kuhle, Jens, Kurzepa, Jacek, Lalive, Patrice H., Lannfelt, Lars, Lehmensiek, Vera, Lewczuk, Piotr, Livrea, Paolo, Marnetto, Fabiana, Martino, Davide, Menge, Til, Norgren, Niklas, Papuć, Eva, Paraskevas, George P., Pirttilä, Tuula, Rajda, Cecília, Rejdak, Konrad, Ricny, Jan, Ripova, Daniela, Rosengren, Lars, Ruggieri, Maddalena, Schraen, Susanna, Shaw, Gerry, Sindic, Christian, Siva, Aksel, Stigbrand, Torgny, Stonebridge, Iva, Topcular, Baris, Trojano, Maria, Tumani, Hayrettin, Twaalfhoven, Harry A.M., Vécsei, László, Van Pesch, Vincent, Vanderstichele, Hugo, Vedeler, Christian, Verbeek, Marcel M., Villar, Luisa Maria, Weissert, Robert, Wildemann, Brigitte, Yang, Cui, Yao, Karen, and Teunissen, Charlotte E.

Published
2010
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26. Oligoclonal bands predict multiple sclerosis in children with optic neuritis

Author

Heussinger, Nicole, Kontopantelis, Evangelos, Gburek-Augustat, Janina, Jenke, Andreas, Vollrath, Gesa, Korinthenberg, Rudolf, Hofstetter, Peter, Meyer, Sascha, Brecht, Isabel, Kornek, Barbara, Herkenrath, Peter, Schimmel, Mareike, Wenner, Kirsten, Häusler, Martin, Lutz, Soeren, Karenfort, Michael, Blaschek, Astrid, Smitka, Martin, Karch, Stephanie, Piepkorn, Martin, Rostasy, Kevin, Lücke, Thomas, Weber, Peter, Trollmann, Regina, Klepper, Jörg, Häussler, Martin, Hofmann, Regina, Weissert, Robert, Merkenschlager, Andreas, and Buttmann, Mathias

Published
2015
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28. Brain atrophy in acute ischaemic stroke patients treated with reperfusion therapy: a systematic review.

Author

Rastogi, Aarushi, Weissert, Robert, and Bhaskar, Sonu MM

Subjects
*CEREBRAL atrophy, *ISCHEMIC stroke, *REPERFUSION, *THROMBOLYTIC therapy, *THROMBECTOMY
Abstract

Background: Brain atrophy (BA) may have a role in acute ischemic stroke (AIS) in mediating outcomes after reperfusion therapy. The extent of this association is not well understood. Purpose: : To examine the impact of pre-existing BA on functional outcome, survival, symptomatic intracerebral hemorrhage (sICH), and early neurological change in patients with AIS treated with intravenous thrombolysis (IVT) and/or endovascular thrombectomy (EVT). Material and Methods: PubMed, EMBASE, and the Cochrane library were searched for studies on BA in AIS receiving reperfusion therapy. Studies were included if: (i) patients were aged ≥18 years; (ii) patients had been diagnosed with AIS; (iii) patients received IVT and/or EVT; (iv) studies reported on BA; (v) studies reported on post-reperfusion outcomes; and (vi) studies had a sample size of >25 patients. Results: A total of 4444 patients from eight studies were included. Four out of seven studies reporting on 90-day functional outcome found pre-existing BA to be significantly associated with poor functional outcome. Moreover, two out of four studies found BA to be a significant predictor of 90-day mortality. None of the included studies reported a significant association of BA with sICH or early neurological deterioration. Conclusion: This systematic review indicates a potential prognostic role of BA in AIS. Quantitative analysis of association of BA with outcomes in AIS is not possible given the heterogeneity in BA assessment and reporting across studies. Future studies using standardized BA assessment are warranted to clarify its association with clinical and safety outcomes in AIS. [ABSTRACT FROM AUTHOR]

Published
2023
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34. Effects of Alemtuzumab on (Auto) antigen-Specific Immune Responses

Author

Weissert, Robert, Hilger, Clara, Riedhammer, Christine, and Orsó, Evelyn

Subjects
Adult, CD4-Positive T-Lymphocytes, Male, lcsh:Immunologic diseases. Allergy, immunotherapy, mechanism of action, multiple sclerosis, alemtuzumab, autoantigen, T cell, CD4, MHC ligandome, Immunology, 610 Medizin, Autoimmunity, multiple sclerosis, Autoantigens, Interferon-gamma, Antineoplastic Agents, Immunological, Multiple Sclerosis, Relapsing-Remitting, alemtuzumab, Humans, Original Research, MHC ligandome, B-Lymphocytes, ddc:610, T cell, Progression-Free Survival, CD4, autoantigen, CD4 Lymphocyte Count, Killer Cells, Natural, Female, immunotherapy, Peptides, lcsh:RC581-607, Follow-Up Studies, mechanism of action
Abstract

Alemtuzumab (anti-CD52 mAb) leads to a long-lasting disease activity suppression in patients with relapsing forms of multiple sclerosis (MS). In this study, we examined the change of the immune cell repertoire and the cellular reactivity after treatment with alemtuzumab. We analyzed the number of IFN-gamma-secreting cells in presence of several peptides which had been eluted from the central nervous system (CNS) of MS patients and are possible targets of autoreactive T cells in MS. The patients showed a stabilized disease activity measured in clinical parameters and lesion formation after the treatment. We detected a reduction of the number of IFN-gamma-secreting cells in the presence of every tested self-antigen. The number of IFN-gamma-secreting cells was also reduced in the presence of non-self-antigens. We also found a clear change in the immune cell repertoire. After an almost complete depletion of all lymphocytes, the cell specificities showed different reconstitution patterns, resulting in different cell fractions. The percentage of CD4+ T cells was clearly reduced after therapy, whereas the fractions of B and NK cells were elevated. When we evaluated the number of IFN-gamma-secreting cells in relation to the number of present CD4+ T cells, we still found a significant reduction. We conclude that the reduction of IFN-gamma-secreting cells by alemtuzumab is not only due to a reduction of the CD4+ T cell fraction within the peripheral blood mononuclear cell (PBMC) compartment but might also be caused by functional changes or a shift in the distribution of different subtypes in the CD4+ T cell pool.

Published
2020

37. Identification of HLA-DR-bound peptides presented by human bronchoalveolar lavage cells in sarcoidosis

Author

Wahlstrom, Jan, Dengjel, Jorn, Persson, Bengt, Duyar, Huseyin, Rammensee, Hans-Georg, Stevanovic, Stefan, Eklund, Anders, Weissert, Robert, and Grunewald, Johan

Subjects
Histocompatibility antigens -- Identification and classification, Histocompatibility antigens -- Research, HLA histocompatibility antigens -- Identification and classification, HLA histocompatibility antigens -- Research, Peptides -- Health aspects, Sarcoidosis -- Diagnosis, Sarcoidosis -- Drug therapy, Sarcoidosis -- Research
Abstract

Sarcoidosis is an inflammatory disease of unknown etiology, most commonly affecting the lungs. Activated [CD4.sup.+] T cells accumulate in the lungs of individuals with sarcoidosis and are considered to be [...]

Published
2007

49. Rituximab Treatment and Long-term Outcome of Patients With Autoimmune Encephalitis

Author

Thaler, Franziska S, Zimmermann, Luise, Urbanek, Christian, Pfefferkorn, Thomas, Philipsen, Alexandra, Piepgras, Johannes, von Podewils, Felix, Priller, Josef, Pröbstel, Anne-Katrin, Helena Rau, Johanna Maria, Räuber, Saskia Jania, Reimann, Gernot, Reinecke, Raphael, Sommer, Claudia, Ringelstein, Marius, Rohner, Hendrik, Rosenow, Felix, Rostásy, Kevin, Rüegg, Stephan, Schaumberg, Jens, Schmidt, Jens, Schmütz, Ina-Isabelle, Schreiber, Stephan, Schreyer, Gesa, Doppler, Kathrin, Schröder, Ina, Schuster, Simon, Seidel, Günter, Senel, Makbule, Siebenbrodt, Kai, Stammel, Oliver, Stangel, Martin, Stolze, Henning, Stoppe, Muriel, Storm Van's Gravesande, Karin, Penner, Loana, Sybre, Steffen, Tauber, Simone, Bergh, Florian Then, Trebst, Corinna, Trendelenburg, George, Trollmann, Regina, Tumani, Hayrettin, Türedi, Methab, von Mering, Matthias, Wagner, Judith, Lewerenz, Jan, Weissert, Robert, Wiendl, Heinz, Wildemann, Brigitte, Witt, Karsten, Wöpking, Sigrid, Wunderlich, Benjamin, Zieger, Lara, Roessling, Rosa, Finke, Carsten, Prüß, Harald, Melzer, Nico, Wandinger, Klaus-Peter, Kammermeier, Stefan, Leypoldt, Frank, Kümpfel, Tania, Encephalitis, German Network for Research on Autoimmune, Adelmann, Michael, Appeltshauser, Luise, Ayzenberg, Ilya, Baade-Büttner, Carolin, van Baalen, Andreas, Baatz, Sebastian, Balint, Bettina, Strippel, Christine, Bauer, Sebastian, Baumgartner, Annette, Benesch, Sonka, Berger, Robert, Berning, Sascha, Bernsen, Sarah, Bien, Christian, Bien, Corinna, Binder, Andreas, Bittner, Stefan, Bittner, Daniel, Blaes, Franz, Blaschek, Astrid, Dargvainiene, Justina, Dik, Andre, Dreesmann, Mona, Ebinger, Friedrich, Edelhoff, Lena, Ehrlich, Sven, Eisenhut, Katharina, Kraft, Andrea, Endres, Dominique, Entscheva, Marina, Faiss, Jürgen Hartmut, Fazeli, Walid Ahmad, Finke, Alexander, Fitzner, Dirk, Flotats-Bastardas, Marina, Paul, Friedemann, Friese, Manuel, Gallus, Marco, Sühs, Kurt-Wolfram, Gebhard, Marcel, Geis, Christian, Gorsler, Anna, Grau, Armin, Grauer, Oliver, Groß, Catharina, Gül, Halime, Handreka, Robert, Hansen, Niels, Häusler, Martin, Wickel, Jonathan, Havla, Joachim, Ha-Yeun, Chung, Heide, Wolfgang, Held, Valentin, Hellwig, Kerstin, Hillebrand, Philip, Hoffmann, Frank, Oy, Ulrich Hofstadt-van, Ismail, Fatme Seval, Jansen, Martina, Kaufmann, Max, Kellinghaus, Christoph, Knake, Susanne, Körtvelyessy, Peter, Kovac, Stjepana, Krämer, Markus, Krogias, Christos, Lehrich, Christoph, Linsa, Andreas, Lünemann, Jan, Markewitz, Robert, Malter, Michael, Melzer, Kristin Stefanie, Menge, Til, Meuth, Sven, Meyer Zu Hörste, Gerd, Mönig, Constanze, Mono, Marie-Luise, Nagel, Michael, Neumann-Haefelin, Tobias, and Obrocki, Jost

Subjects
Adult, Male, medicine.medical_specialty, immunology [Anti-N-Methyl-D-Aspartate Receptor Encephalitis], anti-GAD65 autoantibody, Disease, Real world evidence, Gastroenterology, immunology [Autoimmune Diseases of the Nervous System], pharmacology [Immunosuppressive Agents], anti-CASPR2 autoantibody, administration & dosage [Rituximab], Modified Rankin Scale, Internal medicine, Outcome Assessment, Health Care, immunology [Autoantibodies], Humans, Medicine, In patient, ddc:610, Registries, immunology [Encephalitis], anti-NMDA receptor autoantibody, Aged, Autoantibodies, Autoimmune encephalitis, pharmacology [Rituximab], biology, business.industry, Middle Aged, drug therapy [Encephalitis], Neurology, Cohort, administration & dosage [Immunosuppressive Agents], anti-leucine-rich glioma-inactivated 1 autoantibody, biology.protein, drug therapy [Autoimmune Diseases of the Nervous System], Female, Rituximab, Neurology (clinical), Antibody, drug therapy [Anti-N-Methyl-D-Aspartate Receptor Encephalitis], business, Immunosuppressive Agents, Follow-Up Studies, medicine.drug
Abstract

Background and ObjectivesTo determine the real-world use of rituximab in autoimmune encephalitis (AE) and to correlate rituximab treatment with the long-term outcome.MethodsPatients with NMDA receptor (NMDAR)-AE, leucine-rich glioma-inactivated-1 (LGI1)- AE, contactin-associated protein-like-2 (CASPR2)-AE, or glutamic acid decarboxylase 65 (GAD65) disease from the GErman Network for Research on AuToimmune Encephalitis who had received at least 1 rituximab dose and a control cohort of non–rituximab-treated patients were analyzed retrospectively.ResultsOf the 358 patients, 163 (46%) received rituximab (NMDAR-AE: 57%, CASPR2-AE: 44%, LGI1-AE: 43%, and GAD65 disease: 37%). Rituximab treatment was initiated significantly earlier in NMDAR- and LGI1-AE (median: 54 and 155 days from disease onset) compared with CASPR2-AE or GAD65 disease (median: 632 and 1,209 days). Modified Rankin Scale (mRS) scores improved significantly in patients with NMDAR-AE, both with and without rituximab treatment. Although being more severely affected at baseline, rituximab-treated patients with NMDAR-AE more frequently reached independent living (mRS score ≤2) (94% vs 88%). In LGI1-AE, rituximab-treated and nontreated patients improved, whereas in CASPR2-AE, only rituximab-treated patients improved significantly. No improvement was observed in patients with GAD65 disease. A significant reduction of the relapse rate was observed in rituximab-treated patients (5% vs 13%). Detection of NMDAR antibodies was significantly associated with mRS score improvement. A favorable outcome was also observed with early treatment initiation.DiscussionWe provide real-world data on immunosuppressive treatments with a focus on rituximab treatment for patients with AE in Germany. We suggest that early and short-term rituximab therapy might be an effective and safe treatment option in most patients with NMDAR-, LGI1-, and CASPR2-AE.Class of EvidenceThis study provides Class IV evidence that rituximab is an effective treatment for some types of AE.

Published
2021
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