Weber, Martin S.

[["dc.bibliographiccitation.artnumber","863105"],["dc.bibliographiccitation.journal","Frontiers in Neurology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Buttmann, Mathias"],["dc.contributor.author","Meuth, Sven G."],["dc.contributor.author","Dirks, Petra"],["dc.contributor.author","Muros-Le Rouzic, Erwan"],["dc.contributor.author","Eggebrecht, Julius C."],["dc.contributor.author","Hieke-Schulz, Stefanie"],["dc.contributor.author","Leemhuis, Jost"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.date.accessioned","2022-06-01T09:39:52Z"],["dc.date.available","2022-06-01T09:39:52Z"],["dc.date.issued","2022"],["dc.description.abstract","Background Real-world relapsing multiple sclerosis (RMS) and primary progressive MS (PPMS) populations may be more diverse than in clinical trials. Here, we present a first analysis of safety, adherence and persistence data from a real-world cohort of patients newly treated with ocrelizumab. Methods CONFIDENCE (ML39632, EUPAS22951) is an ongoing multicenter, non-interventional post authorization safety study assessing patients with RMS or PPMS newly treated with ocrelizumab or other disease-modifying therapies for up to 10 years. For this analysis, patients newly treated with ocrelizumab were analyzed in subgroups by MS phenotype and age over a mean ~1 year of exposure totaling 2,329 patient years [PY]). Results At data cutoff (14 October 2020), 1,702 patients with RMS and 398 patients with PPMS were treated with ≥1 dose of ocrelizumab. At baseline, the mean ages (SD) of patients with RMS and PPMS were 41.59 (11.24) and 50.95 (9.88) years and the mean EDSS (Expanded Disability Status Scale) was 3.18 (1.87) and 4.41 (1.59), respectively. The most common adverse events (AEs) and serious AEs across both phenotypes were infections and infestations, with infection SAE rates of 2.8 events/100 PY and 1.5 events/100 PY in patients with RMS and PPMS, respectively. Across all phenotypes, ocrelizumab persistence was 92% at 24 months; median time between doses was ~6 months. Conclusions The ocrelizumab safety profile observed in the CONFIDENCE real-world MS population was consistent to the one observed in pivotal clinical trials. High treatment persistence and adherence were observed. Trial Registration ML39632, EUPAS22951"],["dc.identifier.doi","10.3389/fneur.2022.863105"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/108582"],["dc.notes.intern","DOI-Import GROB-572"],["dc.relation.eissn","1664-2295"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Safety, Adherence and Persistence in a Real-World Cohort of German MS Patients Newly Treated With Ocrelizumab: First Insights From the CONFIDENCE Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1019"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","CNS Drugs"],["dc.bibliographiccitation.lastpage","1030"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Geladaris, Anastasia"],["dc.contributor.author","Torke, Sebastian"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2022-11-01T10:17:42Z"],["dc.date.available","2022-11-01T10:17:42Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s40263-022-00951-z"],["dc.identifier.pii","951"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/116880"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-605"],["dc.relation.eissn","1179-1934"],["dc.relation.issn","1172-7047"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Bruton’s Tyrosine Kinase Inhibitors in Multiple Sclerosis: Pioneering the Path Towards Treatment of Progression?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","275"],["dc.contributor.author","Feldmann, Linda"],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T09:33:34Z"],["dc.date.available","2018-11-07T09:33:34Z"],["dc.date.issued","2014"],["dc.format.extent","18"],["dc.identifier.doi","10.1016/j.jneuroim.2014.08.052"],["dc.identifier.isi","000345192100045"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31992"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.conference","12th International Congress of Neuroimmunology (ISNI)"],["dc.relation.eventlocation","Mainz, GERMANY"],["dc.relation.issn","1872-8421"],["dc.relation.issn","0165-5728"],["dc.title","Following anti-CD20 treatment, compartment-specific repletion with immune-competent B cells depends on activation of reappearing B cells"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1083"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1099"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Menzfeld, Christiane"],["dc.contributor.author","John, Michael"],["dc.contributor.author","van Rossum, Denise"],["dc.contributor.author","Regen, Tommy"],["dc.contributor.author","Scheffel, Joerg"],["dc.contributor.author","Janova, Hana"],["dc.contributor.author","Goetz, Alexander A."],["dc.contributor.author","Ribes, Sandra"],["dc.contributor.author","Nau, Roland"],["dc.contributor.author","Borisch, Angela"],["dc.contributor.author","Boutin, Philippe"],["dc.contributor.author","Neumann, Konstantin"],["dc.contributor.author","Bremes, Vanessa"],["dc.contributor.author","Wienands, Juergen"],["dc.contributor.author","Reichardt, Holger Michael"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Tischner, Denise"],["dc.contributor.author","Waetzig, Vicky"],["dc.contributor.author","Herdegen, Thomas"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Greig, Iain"],["dc.contributor.author","Mueller, Michael"],["dc.contributor.author","Pukrop, Tobias"],["dc.contributor.author","Mildner, Alexander"],["dc.contributor.author","Kettenmann, Helmut"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Rotshenker, Shlomo"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Hanisch, Uwe-Karsten"],["dc.date.accessioned","2018-11-07T09:56:53Z"],["dc.date.available","2018-11-07T09:56:53Z"],["dc.date.issued","2015"],["dc.description.abstract","The putative protein tyrosine kinase (PTK) inhibitor tyrphostin AG126 has proven beneficial in various models of inflammatory disease. Yet molecular targets and cellular mechanisms remained enigmatic. We demonstrate here that AG126 treatment has beneficial effects in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. AG126 alleviates the clinical symptoms, diminishes encephalitogenic Th17 differentiation, reduces inflammatory CNS infiltration as well as microglia activation and attenuates myelin damage. We show that AG126 directly inhibits Bruton's tyrosine kinase (BTK), a PTK associated with B cell receptor and Toll-like receptor (TLR) signaling. However, BTK inhibition cannot account for the entire activity spectrum. Effects on TLR-induced proinflammatory cytokine expression in microglia involve AG126 hydrolysis and conversion of its dinitrile side chain to malononitrile (MN). Notably, while liberated MN can subsequently mediate critical AG126 features, full protection in EAE still requires delivery of intact AG126. Its anti-inflammatory potential and especially interference with TLR signaling thus rely on a dual mechanism encompassing BTK and a novel MN-sensitive target. Both principles bear great potential for the therapeutic management of disturbed innate and adaptive immune functions. GLIA 2015;63:1083-1099"],["dc.identifier.doi","10.1002/glia.22803"],["dc.identifier.isi","000353244400011"],["dc.identifier.pmid","25731696"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37056"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Tyrphostin AG126 Exerts Neuroprotection in CNS Inflammation by a Dual Mechanism"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","161"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Therapeutic Advances in Neurological Disorders"],["dc.bibliographiccitation.lastpage","173"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Lehmann-Horn, Klaus"],["dc.contributor.author","Kronsbein, Helena C."],["dc.contributor.author","Weber, Martin S."],["dc.date.accessioned","2018-11-07T09:25:50Z"],["dc.date.available","2018-11-07T09:25:50Z"],["dc.date.issued","2013"],["dc.description.abstract","Recent years have substantially broadened our view on the pathogenesis of multiple sclerosis (MS). While earlier concepts focused predominantly on T lymphocytes as the key cell type to mediate inflammatory damage within central nervous system (CNS) lesions, emerging evidence suggests that B lymphocytes may play a comparably important role both as precursors of antibody-secreting plasma cells and as antigen-presenting cells (APCs) for the activation of T cells. With greater appreciation of this pathogenic B-cell function in MS, B-cell-directed therapies, and in particular B-cell-depleting monoclonal antibodies targeting the CD20 molecule, have gained enormous interest over recent years. Clinical trials demonstrated that anti-CD20 treatment, which depletes immature and mature B cells but spares CD20 negative plasma cells, rapidly reduces formation of new inflammatory CNS lesions. While these findings clearly corroborate a pathogenic contribution of B cells, recent experimental but also clinical findings indicate that not all B cells contribute in an equally pathogenic manner and that certain subsets may in contrast mediate anti-inflammatory effects. In this review, we summarize current findings in support of pathogenic B-cell function in MS, including the encouraging clinical data which derived from anti-CD20 MS trials. Further, we review novel findings suggestive of regulatory properties of B-cell subsets which may be collaterally abolished by pan-CD20 depletion. In conclusion, we aim to provide an outlook on how this currently differentiating concept of pro- and anti-inflammatory B-cell function could be harnessed to further improve safety and effectiveness of B-cell-directed therapeutic approaches in MS."],["dc.identifier.doi","10.1177/1756285612474333"],["dc.identifier.isi","000335824800002"],["dc.identifier.pmid","23634189"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30154"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.relation.issn","1756-2864"],["dc.relation.issn","1756-2856"],["dc.title","Targeting B cells in the treatment of multiple sclerosis: recent advances and remaining challenges"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e913"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neurology - Neuroimmunology Neuroinflammation"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Kümpfel, Tania"],["dc.contributor.author","Thiel, Sandra"],["dc.contributor.author","Meinl, Ingrid"],["dc.contributor.author","Ciplea, Andrea I."],["dc.contributor.author","Bayas, Antonios"],["dc.contributor.author","Hoffmann, Frank"],["dc.contributor.author","Hofstadt-van Oy, Ulrich"],["dc.contributor.author","Hoshi, Muna"],["dc.contributor.author","Kluge, Jakob"],["dc.contributor.author","Ringelstein, Marius"],["dc.contributor.author","Aktas, Orhan"],["dc.contributor.author","Stoppe, Muriel"],["dc.contributor.author","Walter, Annette"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Ayzenberg, Ilya"],["dc.contributor.author","Hellwig, Kerstin"],["dc.date.accessioned","2021-04-14T08:29:55Z"],["dc.date.available","2021-04-14T08:29:55Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1212/NXI.0000000000000913"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83036"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2332-7812"],["dc.title","Anti-CD20 therapies and pregnancy in neuroimmunologic disorders"],["dc.title.alternative","A cohort study from Germany"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","JCI Insight"],["dc.contributor.author","Greenfield, Ariele L."],["dc.contributor.author","Dandekar, Ravi"],["dc.contributor.author","Ramesh, Akshaya"],["dc.contributor.author","Eggers, Erica L."],["dc.contributor.author","Wu, Hao"],["dc.contributor.author","Laurent, Sarah"],["dc.contributor.author","Harkin, William"],["dc.contributor.author","Pierson, Natalie S."],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Henry, Roland G."],["dc.contributor.author","Bischof, Antje"],["dc.contributor.author","Cree, Bruce A.C."],["dc.contributor.author","Hauser, Stephen L."],["dc.contributor.author","Wilson, Michael R."],["dc.contributor.author","von Büdingen, H.-Christian"],["dc.date.accessioned","2020-12-10T18:38:20Z"],["dc.date.available","2020-12-10T18:38:20Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1172/jci.insight.126599"],["dc.identifier.eissn","2379-3708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77274"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Longitudinally persistent cerebrospinal fluid B-cells can resist treatment in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e19598"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","JMIR Research Protocols"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Ziemssen, Tjalf"],["dc.contributor.author","Hoffmann, Olaf"],["dc.contributor.author","Klotz, Luisa"],["dc.contributor.author","Schreiber, Herbert"],["dc.contributor.author","Weber, Martin S"],["dc.contributor.author","Rauser, Benedict"],["dc.date.accessioned","2021-06-01T10:48:38Z"],["dc.date.available","2021-06-01T10:48:38Z"],["dc.date.issued","2020"],["dc.description.abstract","Background A high proportion of patients with relapsing remitting multiple sclerosis convert to secondary progressive multiple sclerosis (SPMS) characterized by irreversibly progressing disability and cognitive decline. Siponimod (Mayzent), a selective sphingosine-1-phosphate receptor modulator, was recently approved by the European Medicines Agency for the treatment of adult SPMS patients with active disease, as evidenced by relapses or magnetic resonance imaging features of ongoing inflammatory activity. Approval by the Food and Drug Administration covers a broader range of indications, comprising clinically isolated syndrome, relapsing remitting multiple sclerosis, and active SPMS. However, treatment effects of siponimod have not been assessed in a structured setting in clinical routine so far. Objective The objectives of AMASIA (impAct of Mayzent [siponimod] on secondAry progressive multiple Sclerosis patients in a long-term non-Interventional study in GermAny), a prospective noninterventional study, are to assess the long-term effectiveness and safety of siponimod in clinical routine and to evaluate the impact of disease burden on quality of life and socioeconomic conditions. Here, we report the study design of AMASIA. Methods Treatment effects of siponimod will be evaluated in 1500 SPMS patients during a 3-year observational phase. According to the genetic polymorphism of CYP2C9, the initial dose will be titrated to the maintenance dose of 1 mg (CYP2C9 1 3 and 2 3) or 2 mg (all other polymorphisms of CYP2C9 except 3 3, which is contraindicated) taken orally once daily. Primary endpoint is the 6-month confirmed disability progression, as assessed by a functional composite endpoint comprising the Expanded Disability Status Scale and symbol digit modalities test to take appropriate account of cognitive changes and increase sensitivity. Further measures including multiple sclerosis activity data; assessments of functional domains; questionnaires addressing the patients’, physicians’, and relatives’ perspectives of disability progression; cognitive worsening; quality of life; and socioeconomic aspects will be documented using the multiple sclerosis documentation system MSDS3D. Results AMASIA is being conducted between February 2020 and February 2025 in up to 250 neurological centers in Germany. Conclusions AMASIA will complement the pivotal phase III–derived efficacy and safety profile of siponimod with real-world data and will further evaluate several individual treatment aspects such as quality of life and socioeconomic conditions of patients and caregivers. It might help to establish siponimod as a promising option for the treatment of SPMS patients in clinical routine. International Registered Report Identifier (IRRID) DERR1-10.2196/19598"],["dc.identifier.doi","10.2196/19598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86001"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1929-0748"],["dc.title","Gaining First Insights on Secondary Progressive Multiple Sclerosis Patients Treated With Siponimod in Clinical Routine: Protocol of the Noninterventional Study AMASIA"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Journal of the Neurological Sciences"],["dc.bibliographiccitation.volume","375"],["dc.contributor.author","Fereidan-Esfahani, Mahboobeh"],["dc.contributor.author","Mahmudi, Farhad"],["dc.contributor.author","Jahansouz, Mohamadmostafa"],["dc.contributor.author","Weber, Martin S."],["dc.contributor.author","Rodriguez, Moses"],["dc.date.accessioned","2018-11-07T10:24:59Z"],["dc.date.available","2018-11-07T10:24:59Z"],["dc.date.issued","2017"],["dc.format.extent","129"],["dc.identifier.doi","10.1016/j.jns.2017.01.055"],["dc.identifier.isi","000398752000023"],["dc.identifier.pmid","28320114"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42761"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1878-5883"],["dc.relation.issn","0022-510X"],["dc.title","Biomarkers in radiologically isolated syndrome: The missing piece in the puzzle of treatment indication?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","286"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Nephron"],["dc.bibliographiccitation.lastpage","292"],["dc.bibliographiccitation.volume","69"],["dc.contributor.author","Brack, M."],["dc.contributor.author","Weber, M."],["dc.date.accessioned","2022-10-06T13:26:01Z"],["dc.date.available","2022-10-06T13:26:01Z"],["dc.date.issued","2008"],["dc.identifier.doi","10.1159/000188472"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114977"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-602"],["dc.relation.eissn","2235-3186"],["dc.relation.issn","1660-8151"],["dc.relation.orgunit","Deutsches Primatenzentrum"],["dc.title","Ultrastructural and Histochemical Mesangial Alterations in Callitrichid IgM Nephropathy (Primates: Platyrrhina)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]