In light of these findings, we can postulate a similar scenario in our study, where the increased centrality associated with aging in APOE4 presence (red pattern in Fig. 3) may serve as a compensatory mechanism to preserve normal cognitive function despite presence of AD brain pathology, while decreased centrality in the right insular and frontal opercular brain regions could reflect local distress of affected neuronal populations. This evidence concerns the gene APOE and Alzheimer disease.