Additional file 1: of Modulation of astrocyte reactivity improves functional deficits in mouse models of Alzheimer’s disease Kelly Ceyzériat Lucile Ben Haim Audrey Denizot Dylan Pommier Marco Matos Océane Guillemaud Marie-Ange Palomares Laurene Abjean Fanny Petit Pauline Gipchtein Marie-Claude Gaillard Martine Guillermier Sueva Bernier Mylène Gaudin Gwenaëlle Aurégan Charlène Joséphine Nathalie Déchamps Julien Veran Valentin Langlais Karine Cambon Alexis Bemelmans Jan Baijer Gilles Bonvento Marc Dhenain Jean-François Deleuze Stéphane Oliet Emmanuel Brouillet Philippe Hantraye Maria-Angeles Carrillo-de Sauvage Robert Olaso Aude Panatier Carole Escartin 10.6084/m9.figshare.7210595.v1 https://springernature.figshare.com/articles/figure/Additional_file_1_of_Modulation_of_astrocyte_reactivity_improves_functional_deficits_in_mouse_models_of_Alzheimer_s_disease/7210595 Figure S1. AAV infect astrocytes selectively. To validate astrocyte tropism of the AAVs used in our study, an AAV2/9 encoding GFP was injected in the hippocampus of WT mice. GFP+ cells co-express the astrocytic marker GFAP and S100β, but not NeuN, IBA1, Olig2 and MBP, which are markers of neurons, microglial cells, cells of the oligodendrocyte lineage and myelinating oligodendrocytes, respectively. Astrocyte tropism of these vectors was confirmed in AD mice as well (See colocalization of GFP with GFAP in Figs. 1b and S2). (TIF 14477 kb) 2018-10-16 05:00:00 Reactive astrocytes Alzheimer’s disease JAK2-STAT3 pathway Signaling cascades Viral vectors Neuroinflammation Mouse models