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Fig. 5 | Acta Neuropathologica Communications

Fig. 5

From: Complement 3+-astrocytes are highly abundant in prion diseases, but their abolishment led to an accelerated disease course and early dysregulation of microglia

Fig. 5

Analyses of immune cell and astrocyte marker expression. a Fold change induction of reactive astrocyte specific transcripts split to Pan-, A1-, and A2-specific cassettes for all experimental groups including age matched control groups. Data are mean +/−SEM using Nanostring nCounter data. b Fold change induction of reactive astrocyte specific transcripts split to Pan-, A1-, and A2-specific cassettes showing significant differences between infected WT- and TKO-mice. Data are mean +/−SEM using microfluidic qPCR. c Heatmap of transcripts of Nanostring encounter expression analysis from terminally sick prion infected WT- and TKO-mice. Although subtle, there are clustering differences between infected WT- versus TKO-mice. d PCA plot of Nanostring expression data. Unit variance scaling is applied to rows; singular value decomposition with imputation is used to calculate principal components. X and Y axis show principal component 1 and principal component 2 that explain 50.6 and 12% of the total variance, respectively. All control animals regardless of genotype cluster closely together, while prion infected animals are clustered according to genotype; n = 3 individual animals per group for all analyses

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