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Erschienen in: Acta Neuropathologica 2/2015

01.08.2015 | Original Paper

Microglia inflict delayed brain injury after subarachnoid hemorrhage

verfasst von: Ulf C. Schneider, Anja-Maria Davids, Susan Brandenburg, Annett Müller, Anna Elke, Salima Magrini, Etienne Atangana, Kati Turkowski, Tobias Finger, Angelika Gutenberg, Claire Gehlhaar, Wolfgang Brück, Frank L. Heppner, Peter Vajkoczy

Erschienen in: Acta Neuropathologica | Ausgabe 2/2015

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Abstract

Inflammatory changes have been postulated to contribute to secondary brain injury after aneurysmal subarachnoid hemorrhage (SAH). In human specimens after SAH as well as in experimental SAH using mice, we show an intracerebral accumulation of inflammatory cells between days 4 and 28 after the bleeding. Using bone marrow chimeric mice allowing tracing of all peripherally derived immune cells, we confirm a truly CNS-intrinsic, microglial origin of these immune cells, exhibiting an inflammatory state, and rule out invasion of myeloid cells from the periphery into the brain. Furthermore, we detect secondary neuro-axonal injury throughout the time course of SAH. Since neuronal cell death and microglia accumulation follow a similar time course, we addressed whether the occurrence of activated microglia and neuro-axonal injury upon SAH are causally linked by depleting microglia in vivo. Given that the amount of neuronal cell death was significantly reduced after microglia depletion, we conclude that microglia accumulation inflicts secondary brain injury after SAH.
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Metadaten
Titel
Microglia inflict delayed brain injury after subarachnoid hemorrhage
verfasst von
Ulf C. Schneider
Anja-Maria Davids
Susan Brandenburg
Annett Müller
Anna Elke
Salima Magrini
Etienne Atangana
Kati Turkowski
Tobias Finger
Angelika Gutenberg
Claire Gehlhaar
Wolfgang Brück
Frank L. Heppner
Peter Vajkoczy
Publikationsdatum
01.08.2015
Verlag
Springer Berlin Heidelberg
Erschienen in
Acta Neuropathologica / Ausgabe 2/2015
Print ISSN: 0001-6322
Elektronische ISSN: 1432-0533
DOI
https://doi.org/10.1007/s00401-015-1440-1

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