Fig. 5: Altered synaptic signatures are prominent features in postmortem CTE brains and HF-HI mice. | Nature Communications

Fig. 5: Altered synaptic signatures are prominent features in postmortem CTE brains and HF-HI mice.

From: High-frequency head impact causes chronic synaptic adaptation and long-term cognitive impairment in mice

Fig. 5: Altered synaptic signatures are prominent features in postmortem CTE brains and HF-HI mice.

a Venn diagram of significant differentially expressed genes from HF-HI brains and all weighted gene correlation network analysis (WGCNA) clusters from postmortem human CTE brains identifies 134 overlapping genes. b Circos plot depicting overlapping differentially expressed genes in human CTE brains and HF-HI mice (FDR < 0.1) and how they associated with neurodegenerative diseases or cognitive traits as identified in GWAS studies. The proportion of the circle’s circumference allocated to each disease represents the number of genes associated with that disease that are also differentially expressed in both human CTE brain and HF-HI mice. The lines connecting genes within the circle indicate which genes were shared amongst disease and trait signatures. c Gene sets obtained by functional enrichment of WGCNA–neuron cluster from postmortem human CTE brains using gene ontology (GO) to display significant biological processes (BP), cellular components (CCs), and Kyoto encyclopedia of genes and genomes (KEGG) functional enrichment show changes to synaptic compartments. d Venn diagram demonstrating overlap of differentially expressed genes in human CTE WGNCA–neuron cluster and mouse HF-HI brains. e Venn diagram demonstrating overlapping KEGG pathways between human CTE WGNCA–neuron cluster and HF-HI brains. The ten overlapping pathways are listed. f Inflammatory pathways analyzed from the postmortem CTE WGCNA–Inflammation cluster using gene ontology BP analysis, and g Venn diagram comparison of inflammatory genes compared to HF-HI mice show no overlap between CTE and HF-HI mice.

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