Marc Ehrlich
Max Planck Society
16 Papers
64 Citations
Marc Ehrlich is an academic researcher from Max Planck Society. The author has contributed to research in topics: Cellular differentiation & Induced pluripotent stem cell. The author has an hindex of 9, co-authored 16 publications. Previous affiliations of Marc Ehrlich include University of Münster.
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Papers
Modeling Parkinson’s disease in midbrain-like organoids
Lisa M. Smits,Lydia Reinhardt,Lydia Reinhardt,Peter Reinhardt,Peter Reinhardt,Michael Glatza,Michael Glatza,Anna S. Monzel,Nancy Stanslowsky,Marcelo D. Rosato-Siri,Alessandra Zanon,Paul Antony,Jessica Bellmann,Sarah Nicklas,Kathrin Hemmer,Xiaobing Qing,Emanuel Berger,Norman Kalmbach,Marc Ehrlich,Silvia Bolognin,Andrew A. Hicks,Florian Wegner,Jared Sterneckert,Jared Sterneckert,Jens Christian Schwamborn +24 more
TL;DR: It is demonstrated that three-dimensional differentiation of expandable midbrain floor plate neural progenitor cells (mfNPCs) leads to organoids that resemble key features of the human midbrain that investigate PD-relevant patho-mechanisms.
Rapid and efficient generation of oligodendrocytes from human induced pluripotent stem cells using transcription factors.
Marc Ehrlich,Sabah Mozafari,Michael Glatza,Laura Starost,Sergiy Velychko,Anna Lena Hallmann,Qiao Ling Cui,Axel Schambach,Kee-Pyo Kim,Corinne Bachelin,Antoine Marteyn,Gunnar Hargus,Radia M. Johnson,Jack P. Antel,Jared Sterneckert,Holm Zaehres,Holm Zaehres,Hans R. Schöler,Hans R. Schöler,Anne Baron-Van Evercooren,Tanja Kuhlmann +20 more
TL;DR: iPSC-derived OL disperse and myelinate the CNS of Mbpshi/shi Rag−/− mice during development and after demyelination, are suitable for in vitro myelination assays, disease modeling, and screening of pharmacological compounds potentially promoting oligodendroglial differentiation.
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BCAS1 expression defines a population of early myelinating oligodendrocytes in multiple sclerosis lesions
Maryam K. Fard,Franziska van der Meer,Paula Sánchez,Ludovico Cantuti-Castelvetri,Sunit Mandad,Sunit Mandad,Sarah Jäkel,Eugenio F. Fornasiero,Sebastian Schmitt,Marc Ehrlich,Marc Ehrlich,Laura Starost,Laura Starost,Tanja Kuhlmann,Christina Sergiou,Verena Schultz,Claudia Wrzos,Wolfgang Brück,Henning Urlaub,Henning Urlaub,Leda Dimou,Leda Dimou,Christine Stadelmann,Mikael Simons +23 more
TL;DR: This work identifies a means to map ongoing myelin formation in health and disease and presents a potential cellular target for remyelination therapies in MS.
Distinct Neurodegenerative Changes in an Induced Pluripotent Stem Cell Model of Frontotemporal Dementia Linked to Mutant TAU Protein
Marc Ehrlich,Marc Ehrlich,Anna Lena Hallmann,Anna Lena Hallmann,Peter Reinhardt,Peter Reinhardt,Marcos J. Araúzo-Bravo,Marcos J. Araúzo-Bravo,Sabrina Korr,Albrecht Röpke,Olympia E. Psathaki,Petra Ehling,Sven G. Meuth,Adrian L. Oblak,Jill R. Murrell,Bernardino Ghetti,Holm Zaehres,Hans R. Schöler,Jared Sterneckert,Jared Sterneckert,Tanja Kuhlmann,Gunnar Hargus,Gunnar Hargus +22 more
TL;DR: In this article, the authors derived induced pluripotent stem cells (iPSCs) from individuals with FTD-associated MAPT mutations and differentiated them into mature neurons, which demonstrated pronounced TAU pathology with increased fragmentation and phospho-TAU immunoreactivity, decreased neurite extension, and increased but reversible oxidative stress response to inhibition of mitochondrial respiration.
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Astrocyte pathology in a human neural stem cell model of frontotemporal dementia caused by mutant TAU protein.
Anna-Lena Hallmann,Marcos J. Araúzo-Bravo,Lampros Mavrommatis,Lampros Mavrommatis,Marc Ehrlich,Marc Ehrlich,Albrecht Röpke,Johannes Brockhaus,Markus Missler,Jared Sterneckert,Hans R. Schöler,Tanja Kuhlmann,Holm Zaehres,Holm Zaehres,Gunnar Hargus,Gunnar Hargus,Gunnar Hargus +16 more
TL;DR: This study utilized CRISPR/Cas9 genome editing in human induced pluripotent stem (iPS) cell-derived neural progenitor cells (NPCs) to repair the FTD-associated N279K MAPT mutation and highlights the utility of iPS cell- derived NPCs to elucidate the role of astrocytes in the pathogenesis of FTD.