Taking into account the neurobiological basis of AD (e.g., axonal disruption, synaptic loss and cholinergic deficits) and its implications for the disconnection hypothesis in this disorder, increased connectivity in patients with AD has been seen as a paradoxical phenomenon in several fMRI studies, based on BOLD signal changes as an indirect measure of neural activity [15], [16], [36], [70], [71]. Increases in neural synchronization in AD have been reported in a few resting-state functional connectivity studies using EEG or MEG techniques, which measure neural activity (i.e., postsynaptic potentials) directly and noninvasively [18], [20], [22]. For instance, an MEG report on AD connectivity by Stam et al. using synchronization likelihood indicated a loss of long-distance alpha interactions with concomitant increase in parietal lobe connectivity [22]. More recently, another resting-state MEG report suggested both decreases and increases in functional couplings in different frequency bands, as indicated by logistic regressions on linear and nonlinear connectivity values. However, the topographic distribution of these connectivity deficits was not explored [20]. Sankari et al. using a comprehensive EEG coherence analysis found decreased temporo-parieto-central functional connections along
