Downregulation of co-expression network modules enriched for TGF-beta, EGFR, angiogenesis, Notch signalling, focal adhesion, adherens and tight junction gene pathways encoding proteins involved in the maintenance of BBB with AD (e.g., RAC1, RASAL237) in association with increased expression of Module 1287 enriched for interleukin-/NFκB and interleukin-2 pathways suggests an inflammatory trigger for loss of BBB integrity (Fig. 2F). This evidence concerns the gene EGFR and Alzheimer disease.