An alternative explanation of the compensatory mechanism may be that damage to a specific network enhances connectivity within regions that normally feature an anticorrelated relation to the damaged network [12]. However, since theta connectivity correlated with the MMSE scores, suggesting a worsening of increased activity with the progression of memory decline, the possibility that higher connectivity in a slow band (i.e., theta band) relates to pathology or dysfunctionality (e.g., excitotoxicity or neuronal failure) rather than to compensation cannot be ruled out. EEG reports showing a negative correlation between slow wave global synchronization and AD severity provide support to this view [76], [77]. Altogether, our findings and those of recent EEG/MEG studies indicate that increased theta synchronization between certain brain regions in AD does not represent a paradoxical phenomenon, suggesting a role for increases in functional connectivity in AD pathophysiology.
