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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Deep proteomic network analysis of Alzheimer’s disease brain reveals alterations in RNA binding proteins and RNA splicing associated with disease

Fig. 3

Protein Abundance Changes in AD Adjusted for Cell Type Changes. ae The abundance of cell type-specific protein markers of astrocytes, microglia, neurons, and oligodendrocytes (oligos) was used to calculate the percentage of each cell type in control, asymptomatic AD (AsymAD), and AD brain tissue (a). b The number of proteins with significantly different levels among control (CT), AsymAD, and AD prior to adjustment for cell type populations changes observed in AsymAD and AD. The number of total proteins with differential abundance for AD, AsymAD, and CT is given in parentheses. c The number of proteins with differential abundance after adjustment for changes in cell type population by cell type deconvolution (regression). The circles in (b, c) are not drawn to scale. d Gene ontology (GO) network analysis of the AsymAD vs. AD proteins shown in (b), prior to cell type regression. e GO network analysis of the AsymAD vs. AD proteins in (c), after cell type regression. The nonspecific GO terms “cytoplasm” and “cytosol” were removed from the network. The RNA binding protein subnetwork is highlighted in green. An enlarged version of the network is given in Additional file 16: Figure S9, with a complete list of GO terms provided in Additional file 4: Table S4. P values in (a) were calculated after one-way ANOVA. Significance of each GO term in (d, e) is indicated by false discovery rate (FDR, or Q value). GO network analysis of AsymAD vs. control is provided in Additional file 15: Figure S8

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