Fig. 2: The top 98 EAML genes are connected to GWAS genes, dysregulated in AD patients, and capable of separating AD and healthy control samples.
From: Functional variants identify sex-specific genes and pathways in Alzheimer’s Disease
A Diffusions from the top 98 EAML genes from the full cohort to the 25 GWAS genes. AUC-ROC curve, x: False Positive Rate, y: True Positive Rate. This AUC-ROC curve represents the predictive power of 97 EAML genes to prioritize the 25 GWAS genes. Density distribution of randomly generated 100 AUCs based on randomly selected genes. The arrow indicates the AUC calculated from Fig. 2A. B (left) Integration of EAML candidates with expression networks dysregulated in AD. EAML candidates mapped into the AD consensus modules network (organic distribution) based on gene co-expression analysis75,76,78. The main function enriched in each module75,76,78 is indicated. Darker, thicker edges connect genes that are more highly correlated. Genes with a red ring are dysregulated in at least one brain region in AD vs control. (right) Heat map indicating which of the genes in the “immune system” module are dysregulated in AD brains. Also shown is the cell type in which their expression is enriched in the brain. C Risk prediction that based on the EAML genes for the full cohort. The box plot indicates minimum and maximum (lower and upper) whiskers, median (horizontal line), and first and third quartile (box). The mean AUCs of two groups (APOE vs. 98 FDR genes) and p-value of standard t-test (two sided) are shown.
