We also found that epithelial-mesenchymal transition (EMT) was enriched for the SE events in ELOVL7, SRRM2 and TBC1D5 and was depleted for DRC1 and LINC00665 in GSEA. Recent studies suggest that genes associated with EMT have altered expression levels in the brain of patients with Alzheimer’s disease, which causes chronic neuroinflammation [63]. Other functions significantly enriched or depleted for the identified events included protein folding, chaperone (modulatory process), heat response and heat shock protein, cell-cell adhesion, ECM-receptor signaling pathways, and autoimmune disease (e.g., diabetes).
