M
Michael Willem
Researcher at Ludwig Maximilian University of Munich
Publications - 77
Citations - 8042
Michael Willem is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Amyloid precursor protein & Amyloid precursor protein secretase. The author has an hindex of 41, co-authored 69 publications receiving 6845 citations. Previous affiliations of Michael Willem include Max Planck Society & German Center for Neurodegenerative Diseases.
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Journal ArticleDOI
Control of peripheral nerve myelination by the beta-secretase BACE1.
Michael Willem,Alistair N. Garratt,Bozidar Novak,Martin Citron,Steve Kaufmann,Andrea Rittger,Bart DeStrooper,Paul Saftig,Carmen Birchmeier,Christian Haass +9 more
TL;DR: It is found that very high levels of BACE1 were expressed at time points when peripheral nerves become myelinated and correct bundling of axons by Schwann cells, probably through processing of type III NRG1.
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TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis.
Gernot Kleinberger,Yoshinori Yamanishi,Marc Suárez-Calvet,Eva Czirr,Ebba Lohmann,Ebba Lohmann,Ebba Lohmann,Elise Cuyvers,Hanne Struyfs,Nadine Pettkus,Andrea Wenninger-Weinzierl,Fargol Mazaheri,Sabina Tahirovic,Alberto Lleó,Daniel Alcolea,Juan Fortea,Michael Willem,Sven Lammich,José Luis Molinuevo,Raquel Sánchez-Valle,Anna Antonell,Alfredo Ramirez,Michael T. Heneka,Kristel Sleegers,Julie van der Zee,Jean-Jacques Martin,Sebastiaan Engelborghs,Asli Demirtas-Tatlidede,Henrik Zetterberg,Christine Van Broeckhoven,Hakan Gurvit,Tony Wyss-Coray,John Hardy,Marco Colonna,Christian Haass,Christian Haass +35 more
TL;DR: It is reported that missense mutations associated with FTD and FTD-like syndrome reduce TREM2 maturation, abolish shedding by ADAM proteases, and impair the phagocytic activity of TREM1-expressing cells.
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A γ-secretase inhibitor blocks Notch signaling in vivo and causes a severe neurogenic phenotype in zebrafish
TL;DR: It is demonstrated that treatment of zebrafish embryos with a known γ‐secretase inhibitor affects embryonic development in a manner indistinguishable from Notch signaling deficiencies at morphological, molecular and biochemical levels, which indicates severe side‐effects of γ-secretase inhibitors in any Notch‐dependent cell fate decision and demonstrates that the zebra fish is an ideal vertebrate system to validate compounds that selectively affect Aβ production, but not Notch signalling, under in vivo conditions.
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Migratory Activity and Functional Changes of Green Fluorescent Effector Cells before and during Experimental Autoimmune Encephalomyelitis
Alexander Flügel,Tomasz Berkowicz,Thomas Ritter,Marta Labeur,Dieter E. Jenne,Zhaoxia Li,Joachim W. Ellwart,Michael Willem,Hans Lassmann,Hartmut Wekerle +9 more
TL;DR: Homing behavior and function of autoimmune CD4+ T cells in vivo was analyzed before and during EAE, using MBP-specific T cells retrovirally engineered to express the gene of green fluorescent protein.
Journal ArticleDOI
η-Secretase processing of APP inhibits neuronal activity in the hippocampus
Michael Willem,Sabina Tahirovic,Marc Aurel Busche,Marc Aurel Busche,Saak V. Ovsepian,Magda Chafai,Scherazad Kootar,Daniel Hornburg,Lewis D. B. Evans,Steven Moore,Anna Daria,Heike Hampel,Veronika Müller,Camilla Giudici,Brigitte Nuscher,Andrea Wenninger-Weinzierl,Elisabeth Kremmer,Elisabeth Kremmer,Michael T. Heneka,Michael T. Heneka,Dietmar Rudolf Thal,Vilmantas Giedraitis,Lars Lannfelt,Ulrike Müller,Frederick J. Livesey,Felix Meissner,Jochen Herms,Arthur Konnerth,Arthur Konnerth,Hélène Marie,Christian Haass,Christian Haass +31 more
TL;DR: A new physiological APP processing pathway is described, which generates proteolytic fragments capable of inhibiting neuronal activity within the hippocampus, and this finding may also indicate potential translational relevance for therapeutic strategies targeting APP processing.