Most authors proposed that increased resting-state functional connectivity in AD might reflect a compensatory mechanism in an attempt to counteract the inefficiency of memory networks and make up for the decrease in cognitive functions caused by the disease [36], [69], [71]. This argument is mainly based on evidence of increased connectivity in resting fMRI, particularly in prefrontal networks and in anterior/medial temporal regions, which are sites of early pathological changes in AD. Reports of hyperconnectivity in MEG recordings of patients with amnestic mild cognitive impairment, a disorder considered as a prodromal stage of AD, provides support to this view [72], [73]. Our findings and evidence of enhanced theta activity in association with cognitive-task induced activation in humans [74], and with recovery of memory function [75] in rats further suggest that increased phase synchronization in theta band may represent the underlying neural activity of a compensatory network in AD.
