Carolin Baade‐Büttner

ORCID: 0009-0000-3098-5961
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Research Areas
  • Autoimmune Neurological Disorders and Treatments
  • Genetics and Neurodevelopmental Disorders
  • Neuroinflammation and Neurodegeneration Mechanisms
  • RNA regulation and disease
  • Peripheral Neuropathies and Disorders
  • Ion channel regulation and function
  • Chronic Lymphocytic Leukemia Research
  • Neurogenesis and neuroplasticity mechanisms
  • DNA Repair Mechanisms
  • Genetic Neurodegenerative Diseases
  • Cellular transport and secretion
  • Genomics and Rare Diseases
  • Neonatal and fetal brain pathology
  • Carcinogens and Genotoxicity Assessment
  • Immunodeficiency and Autoimmune Disorders
  • Genomic variations and chromosomal abnormalities
  • Neuroscience and Neuropharmacology Research
  • Immune Response and Inflammation

Jena University Hospital
2022-2024

Leipzig University
2019

Franziska S. Thaler Luise Zimmermann Stefan Kammermeier Christine Strippel Marius Ringelstein and 95 more Andrea Kraft Kurt‐Wolfram Sühs Jonathan Wickel Christian Geis Robert Markewitz Christian Urbanek Claudia Sommer Kathrin Doppler Loana Penner Jan Lewerenz Rosa Rößling Carsten Finke Harald Prüß Nico Melzer Klaus‐Peter Wandinger Frank Leypoldt Tania Kümpfel Michael Adelmann Luise Appeltshauser Ilya Ayzenberg Carolin Baade‐Büttner Andreas van Baalen Sebastian Baatz Bettina Balint Sebastian Bauer Annette Baumgärtner Sonka Benesch Robert L. Berger Sascha Berning Sarah Bernsen Christian G. Bien Corinna I. Bien Andreas Binder Stefan Bittner Daniel Bittner Franz Blaes Astrid Blaschek Justina Dargvainiene Andre Dik Mona Dreesmann Friedrich Ebinger Lena Edelhoff Sven Ehrlich Katharina Eisenhut Dominique Endres Marina Entscheva Jürgen Faiss Walid Fazeli Alexander Finke Dirk Fitzner Marina Flotats‐Bastardas Friedemann Paul Manuel A. Friese Marco Gallus M. M. Gebhard Christian Geis Anna Gorsler Armin Grau Oliver Grauer Catharina C. Groß Halime Gül Robert Handreka Niels Hansen Martin Häusler Joachim Havla Chung Ha-Yeun Wolfgang Heide Valentin Held Kerstin Hellwig Philip Hillebrand Frank Hoffmann Ulrich Hofstadt‐van Oy Fatme Seval Ismail Martina Jansen Max Kaufmann Christoph Kellinghaus Susanne Knake Peter Körtvélyessy Stjepana Kovac Markus Krämer Christos Krogias Christoph Lehrich Andreas Linsa Jan D. Lünemann Michael P. Malter Kristin Stefanie Melzer Til Menge Sven G. Meuth Gerd Meyer zu Hörste Constanze Mönig Marie‐Luise Mono Michael Nagel Tobias Neumann‐Haefelin Jost Obrocki Thomas Pfefferkorn

<h3>Background and Objectives</h3> To determine the real-world use of rituximab in autoimmune encephalitis (AE) to correlate treatment with long-term outcome. <h3>Methods</h3> Patients 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 GErman Network for Research on AuToimmune Encephalitis who had received at least 1 dose a control cohort non–rituximab-treated patients...

10.1212/nxi.0000000000001088 article EN cc-by-nc-nd Neurology Neuroimmunology & Neuroinflammation 2021-10-01

Sepsis-associated encephalopathy (SAE) is a severe and frequent complication of sepsis causing delirium, coma, long-term cognitive dysfunction. We identified microglia C1q complement activation in hippocampal autopsy tissue patients with increased C1q-mediated synaptic pruning murine polymicrobial model. Unbiased transcriptomics isolated derived from septic mice revealed an involvement the innate immune system, activation, up-regulation lysosomal pathways during SAE parallel to neuronal...

10.1126/sciadv.abq7806 article EN cc-by-nc Science Advances 2023-05-26
Patrik Greguletz Maria Plötz Carolin Baade‐Büttner Christian G. Bien Katharina Eisenhut and 95 more Christian Geis Robert Handreka Jaqueline Klausewitz Peter Körtvélyessy Stjepana Kovac Andrea Kraft Jan Lewerenz Michael P. Malter Michael Nagel Felix von Podewils Harald Prüß Anna Rada Johanna Maria Helena Rau Sebastian Rauer Rosa Rößling Thomas Seifert Kai Siebenbrodt Kurt‐Wolfram Sühs Simone C. Tauber Franziska S. Thaler Judith Wagner Jonathan Wickel Frank Leypoldt Heike L. Rittner Claudia Sommer Carmen Villmann Kathrin Doppler Michael Adelmann Luise Appeltshauser Ilya Ayzenberg Andreas van Baalen Sebastian Baatz Oliver Bähr Bettina Balint Sebastian Bauer Annette Baumgärtner Stefanie Becker Sonka Benesch Robert L. Berger Birgit S. Berger Martin Berghoff Sascha Berning Sarah Bernsen Achim Berthele Christian G. Bien Corinna I. Bien Andreas Binder Stefan Bittner Daniel Bittner Franz Blaes Astrid Blaschek Amelie Bohn Sergio Castro‐Gomez Justina Dargvainiene Timo Deba Julia Maren Decker Andre Dik Juliane Dominik Mona Dreesmann Friedrich Ebinger Lena Edelhoff Laura Ehrhardt Sven Ehrlich Alexander Emmer Dominique Endres Marina Entscheva Daniela Esser Thorleif Etgen Jürgen Faiss Kim Kristin Falk Walid Fazeli Alexander Finke Carsten Finke Dirk Fitzner Marina Flotats‐Bastardas Mathias Fousse Tobias Freilinger Friedemann Paul Manuel A. Friese Marco Gallus M. M. Gebhard Anna Gorsler Armin Grau Oliver Grauer Britta Greshake Catharina C. Groß Thomas Grüter Aiden Haghikia Niels Hansen Jens Harmel Antonia Harms Yetzenia Dubraska Haro Alizo Martin Häusler Joachim Havla Chung Ha-Yeun

Abstract Autoantibodies against contactin-associated protein 2 (Caspr2) not only induce limbic autoimmune encephalitis but are also associated with pain conditions. Here, we analyzed clinical data on in a large cohort of patients included into the German Network for Research Autoimmune Encephalitis. Out 102 our cohort, was frequent symptom (36% all patients), often severe (63.6% pain) and/or even major (55.6% pain). Pain phenotypes differed between patients. Cluster analysis revealed two...

10.1007/s00415-024-12224-4 article EN cc-by Journal of Neurology 2024-02-22
Christine Strippel Marisol Herrera-Rivero Mareike Wendorff Anja K. Tietz Frauke Degenhardt and 95 more Anika Witten Christina B. Schroeter Christopher Nelke Kristin S. Golombeck Marie Madlener Theodor Rüber Leon Ernst Áttila Rácz Tobias Baumgartner Guido Widman Kathrin Doppler Franziska S. Thaler Kai Siebenbrodt Andre Dik Constanze Kerin Saskia Räuber Marco Gallus Stjepana Kovac Oliver Grauer Alexander Grimm Harald Prüß Jonathan Wickel Christian Geis Jan Lewerenz Norbert Goebels Marius Ringelstein Til Menge Björn Tackenberg Christoph Kellinghaus Christian G. Bien Andrea Kraft Uwe K. Zettl Fatme Seval Ismail Ilya Ayzenberg Christian Urbanek Kurt‐Wolfram Sühs Simone C. Tauber Sigrid Mues Peter Körtvélyessy Robert Markewitz Asterios Paliantonis Christian E. Elger Rainer Surges Claudia Sommer Tania Kümpfel Catharina C. Groß Holger Lerche Jörg Wellmer Carlos Martínez Quesada Florian Then Bergh Klaus‐Peter Wandinger Albert J. Becker Wolfram S. Kunz Gerd Meyer zu Hörste Michael P. Malter Felix Rosenow Heinz Wiendl Gregor Kuhlenbäumer Frank Leypoldt Wolfgang Lieb André Franke Sven G. Meuth Monika Stoll Nico Melzer Michael Adelmann Luise Appeltshauser Ilya Ayzenberg Carolin Baade‐Büttner Andreas van Baalen Sebastian Baatz Bettina Balint Sebastian Bauer Annette Baumgärtner Sonka Benesch R. Berger Sascha Berning Sarah Bernsen Christian G. Bien Corinna I. Bien Andreas Binder Stefan Bittner Daniel Bittner Franz Blaes Astrid Blaschek Justina Dargvainiene Julia Maren Decker Andre Dik Kathrin Doppler Mona Dreesmann Friedrich Ebinger Lena Edelhoff Sven Ehrlich Katharina Eisenhut Dominique Endres Marina Entscheva

Abstract Autoimmune neurological syndromes (AINS) with autoantibodies against the 65 kDa isoform of glutamic acid decarboxylase (GAD65) present limbic encephalitis, including temporal lobe seizures or epilepsy, cerebellitis ataxia, and stiff-person-syndrome overlap forms. Anti-GAD65 are also detected in autoimmune diabetes mellitus, which has a strong genetic susceptibility conferred by human leukocyte antigen (HLA) non-HLA genomic regions. We investigated predisposition patients anti-GAD65...

10.1093/brain/awac119 article EN cc-by-nc Brain 2022-03-25

Microglia are innate immune cells in the brain and show exceptional heterogeneity. They key players physiological development regulating synaptic plasticity shaping neuronal networks. In pathological disease states, microglia-induced pruning mediates loss targeting microglia was proposed as a promising therapeutic strategy. However, effect of depletion subsequent repopulation on dendritic spine density function adult is largely unknown. this study, we investigated whether pharmacological...

10.1002/glia.24541 article EN Glia 2024-05-23

MRE11, RAD50, and NBS1 form the MRN complex in response to DNA damage activate ATM, a gene responsible for Ataxia-Telangiectasia (A-T). Loss of any components compromises cell life. Mutations cause human genomic instability syndromes Ataxia-Telangiectasia-like disorder (A-TLD), NBS-like (NBSLD), Nijmegen Breakage Syndrome (NBS), respectively. Among other pathologies, neuronal deficits, including microcephaly, intellectual disabilities, progressive cerebellar degeneration, are common these...

10.3389/fnagi.2021.786199 article EN cc-by Frontiers in Aging Neuroscience 2022-01-28

Abstract Background Deciphering the monogenetic causes of neurodevelopmental disorders (NDD) is an important milestone to offer personalized care. But plausibility reported candidate genes in exome studies often remains unclear, which slows down progress field. Methods We performed sequencing (ES) 198 cases NDD. Cases that remained unresolved (n=135) were re-investigated a research setting. established scoring system (CaSc) based on 12 different parameters reflecting variant and gene...

10.1101/588517 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2019-03-26
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