Fig. 1: Multivariate assessment of reactive astrocytes.

a, Reactive astrocyte proliferation in the vicinity of blood vessels assessed by co-staining for BrdU (green; arrows), DAPI (blue), GFAP (white), and CD31 (red) after stab injury of the mouse cortex. Scale bar, 15 µm. Unpublished image from authors S.S. and M.G. b, Human cortical protoplasmic astrocytes in a surgical specimen injected with Lucifer yellow (arrow, injection site) that traverses the gap junctions into neighboring astrocytes. Scale bar, 45 µm. Courtesy of Drs. Xu, Sosunov, and McKhann, Columbia University Department of Neurosurgery. c, Event-based determination of Ca²⁺ responses in a GCaMP6-expressing astrocyte (surrounded by a dashed line) in mouse cortical slices using astrocyte quantitative analysis (AQuA)¹²⁰. Colors indicate AQuA events occurring in a single 1-s frame of a 5-min movie. Scale bar, 10 μm. d, Activation of the transcription factor STAT3 (green) assessed by nuclear accumulation in GFAP⁺ reactive astrocytes (red) surrounding an amyloid plaque (blue, arrow) in a mouse AD model. Scale bar, 20 µm. Adapted from ref. ¹²¹, Society for Neuroscience. e, ScRNAseq in the remission phase of a mouse model of MS reveals several transcriptional astrocyte clusters. These astrocyte sub-populations may be validated with spatial transcriptomics, as shown in f in a model of AD. Adapted from ref. ⁴⁰, Nature Publishing Group. f, Distribution of 87 astrocytic (green), neuronal (red), microglial (yellow), and oligodendroglial (blue) genes with in situ multiplex gene sequencing in a coronal section from a mouse model of AD. The method ‘reads’ barcodes of antisense DNA probes that simultaneously target numerous mRNAs. Scale bar, 800 μm. Boxed area is magnified in bottom image, showing 6E10⁺ amyloid-β plaques (white; arrows). Adapted from ref. ⁹⁶, Cell Press.