S
Stefan A. Grathwohl
Researcher at University of Tübingen
Publications - 11
Citations - 1562
Stefan A. Grathwohl is an academic researcher from University of Tübingen. The author has contributed to research in topics: Microglia & Amyloid. The author has an hindex of 9, co-authored 11 publications receiving 1353 citations. Previous affiliations of Stefan A. Grathwohl include German Center for Neurodegenerative Diseases.
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Journal ArticleDOI
Formation and maintenance of Alzheimer's disease |[beta]|-amyloid plaques in the absence of microglia
Stefan A. Grathwohl,Roland E. Kälin,Tristan Bolmont,Tristan Bolmont,Stefan Prokop,Georg Winkelmann,Stephan A. Kaeser,Stephan A. Kaeser,Jörg Odenthal,Jörg Odenthal,Rebecca Radde,Rebecca Radde,Therese Eldh,Sam Gandy,Adriano Aguzzi,Matthias Staufenbiel,Paul M. Mathews,Paul M. Mathews,Hartwig Wolburg,Frank L. Heppner,Mathias Jucker,Mathias Jucker +21 more
TL;DR: This work crossed two distinct APP transgenic mouse strains with CD11b-HSVTK mice, in which nearly complete ablation of microglia was achieved for up to 4 weeks after ganciclovir application, suggesting that neither amyloid plaque formation and maintenance nor amyloids-associated neuritic dystrophy depended on the presence ofmicroglia.
Journal ArticleDOI
Novel pentameric thiophene derivatives for in vitro and in vivo optical imaging of a plethora of protein aggregates in cerebral amyloidoses
Andreas Åslund,Christina J. Sigurdson,Therése Klingstedt,Stefan A. Grathwohl,Tristan Bolmont,Dara L. Dickstein,Eirik Glimsdal,Stefan Prokop,Mikael Lindgren,Peter Konradsson,David M. Holtzman,Patrick R. Hof,Frank L. Heppner,Sam Gandy,Mathias Jucker,Adriano Aguzzi,Per Hammarström,K. Peter R. Nilsson,K. Peter R. Nilsson +18 more
TL;DR: The chemical design of pentameric thiophene derivatives, denoted luminescent conjugated oligothiophenes (LCOs), which could be used for real-time visualization of cerebral protein aggregates in transgenic mouse models of neurodegenerative diseases by multiphoton microscopy are reported.
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Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE.
Samira Parhizkar,Thomas Arzberger,Matthias Brendel,Gernot Kleinberger,Maximilian Deussing,Carola Focke,Brigitte Nuscher,Monica Xiong,Alireza Ghasemigharagoz,Natalie Katzmarski,Susanne Krasemann,Stefan F. Lichtenthaler,Stephan A. Müller,Stephan A. Müller,Alessio Colombo,Laura Sebastian Monasor,Sabina Tahirovic,Jochen Herms,Jochen Herms,Michael Willem,Nadine Pettkus,Oleg Butovsky,Peter Bartenstein,Dieter Edbauer,Axel Rominger,Ali Ertürk,Stefan A. Grathwohl,Jonas J. Neher,Jonas J. Neher,David M. Holtzman,Melanie Meyer-Luehmann,Christian Haass,Christian Haass +32 more
TL;DR: Findings suggest that in the absence of functional Trem2, early amyloidogenesis is accelerated due to reduced phagocytic clearance of amyloids seeds despite reduced plaque-associated ApoE.
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Microglial repopulation model reveals a robust homeostatic process for replacing CNS myeloid cells
Nicholas H. Varvel,Nicholas H. Varvel,Stefan A. Grathwohl,Stefan A. Grathwohl,Frank Baumann,Frank Baumann,Christian Liebig,Christian Liebig,Andrea Bosch,Andrea Bosch,Bianca Brawek,Dietmar Rudolf Thal,Israel F. Charo,Frank L. Heppner,Adriano Aguzzi,Olga Garaschuk,Richard M. Ransohoff,Mathias Jucker,Mathias Jucker +18 more
TL;DR: It is shown that microglia-depleted brain regions of CD11b-HSVTK transgenic mice are repopulated with new Iba-1-positive cells within 2 wk and engrafted myeloid cells expressed high levels of CD45 and CCR2 and appeared in a wave-like pattern frequently associated with blood vessels, suggesting the engrafted cells were peripheral monocytes.
Journal ArticleDOI
Formation and maintenance of Alzheimer’s disease beta-amyloid plaques in the absence of microglia
Stefan A. Grathwohl,Roland E. Kälin,Tristan Bolmont,Stefan Prokop,Georg Winkelmann,Stephan A. Kaeser,Jörg Odenthal,Rebecca Radde,Therese Eldh,Sam Gandy,Adriano Aguzzi,Matthias Staufenbiel,Paul M. Mathews,Hartwig Wolburg,Frank L. Heppner,Mathias Jucker +15 more
TL;DR: In Alzheimer's disease, microglia cluster around beta-amyloid deposits, suggesting that these cells are important for amyloid plaque formation, maintenance and/or clearance as mentioned in this paper.