Fig. 4

Label-free quantitative proteomics reveals alterations in the host mouse brain tissue induced by AD human grafts a Principal component analysis of murine proteins identified in control and AD-grafted mouse hippocampi. CHG-MT (control human graft-mouse tissue); ADHG-MT (AD human graft-mouse tissue). b Hierarchical clustering analysis of dysregulated host mouse proteins (Two-tailed t-test; p-value < 0.05; Benjamini–Hochberg FDR < 0.05) using Pearson correlation distance. The abundance of protein groups decreased and increased is represented in blue and red, respectively. c Pathway analysis of the protein clusters in C (p-value < 0.01). p-values are denoted as the –log10 (p-value). The grey color symbolizes the absence of that specific biological pathway. d Interaction network and pathway enrichment of the commonly dysregulated proteins between AD iPSC-derived human grafts and the host mouse tissues (Two-tailed t-test; p-value:0.05; Benjamini–Hochberg FDR:0.05). Decreased and increased proteins are represented in blue and red, respectively. e Mapping of the dysregulated proteins participating in the AD pathway reported in the KEGG database. The analysis was centered on the dysregulated proteins (AD vs. Control) in the ADHG model in comparison to ADHS, ADHPMBT, and ADHG-MT. Protein groups with decreased and increased abundances are represented in blue and red, respectively. Proteins with no significant changes in their abundance and not detected are represented in grayscale