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