Extended Data Fig. 10: Additional snRNA-seq analysis.
From: Glycocalyx dysregulation impairs blood–brain barrier in ageing and disease
a) UMAP of 69,250 nuclei from pooled cortical and hippocampal tissues of young AAV-EGFP, aged AAV-EGFP, and aged AAV-B3GNT3 groups (n = 3 mice per group), colored by experimental group. b) UMAP of 69,250 nuclei from the cortex and hippocampus of young AAV-EGFP, aged AAV-EGFP, and aged AAV-B3GNT3 groups (n = 3 mice per group), colored by cluster. c) Summary quantification of the proportion of captured cell types by treatment group. d) Summary of the number of DEGs across comparisons of aged AAV-EGFP, aged AAV-B3GNT3, and young AAV-EGFP for each major cell type. e) Venn diagram of the number and examples of excitatory neuronal DEGs upregulated with AAV-B3GNT3 treatment in aged mice and with reverse aging. f) Network analysis of shared excitatory neuronal pathways upregulated with aged AAV-B3GNT3 and in reverse aging. g) Volcano plot of DEGs in oligodendrocytes induced by AAV-B3GNT3 treatment in aged mice (genes upregulated with AAV-B3GNT3 treatment in orange and genes downregulated with AAV-B3GNT3 treatment in yellow). h) Comparison of log2-transformed fold changes of DEGs with B3GNT3 overexpression (Aged B3GNT3/Aged EGFP) and reverse aging (Young EGFP/Aged EGFP). Areas in which AAV-B3GNT3 treatment causes changes in the opposite direction of aging are highlighted. i) Top downregulated pathways in oligodendrocytes based on DEGs shared between AAV-B3GNT3 treatment and reverse aging (bottom left quadrant in (h)).
