Aging and Alzheimer’s disease (AD) are characterized by common pathological features associated with alterations in neuronal connections. These inevitably affect the functioning of specific brain areas and their interrelations, leading to questions about neuronal plasticity and the compensatory mechanisms associated with dopaminergic (DA) mediation. In this study on twelve-month-old freely moving 5XFAD-transgenic mice, serving as a model of AD, and their wild-type (WT) littermates, we analyze electroencephalograms (EEGs) from the motor cortex (MC), putamen (Pt) and the DA-producing ventral tegmental area (VTA) and substantia nigra (SN). Baseline EEGs in the transgenic mice were characterized by delta 2 activity enhancements in VTA and alpha attenuation in VTA and SN. In contrast to WT mice, which lack differences in EEG from these brain areas, 5XFAD mice showed theta–alpha attenuation and delta 2 and beta 2 enhancements in EEG from both VTA and SN vs. MC. In 5XFAD mice, a DA mimetic, apomorphine, lowered (vs. saline) the theta oscillations in Pt, VTA and SN and enhanced alpha in MC, Pt, VTA and beta 1 in all brain areas. These results and those obtained earlier in younger (six-month-old) mice suggest that the age-related characteristics of cerebral adaptive mechanisms affected by AD might be associated with modification of dopaminergic mediation in the mechanisms of intracerebral dynamic interrelations between different brain areas.