Unique features of 2TG mice help to mark the progression of Aβ accumulation and deposition—loss of functional connectivity in the slow-wave range marks the onset of Aβ accumulation, similarly to what reported in PS1-based AD mice [106], whereas low/high power imbalances characterize Aβ deposition in plaque-seeding mice [108]. Here, PSEN1 is linked to Alzheimer disease.