Amyloid-beta (Aβ)-induced changes in neuronal activity could yield valuable early markers of Alzheimer’s disease (AD). The neurophysiological manifestations associated with early Aβ-pathology in humans are however not well defined. This study investigated the relationship between Aβ-pathology and neurophysiological characteristics in 110 cognitively unimpaired individuals (65.9±5.7 years). All subjects underwent 18F-flutemetamol-PET imaging and resting-state magnetoencephalography (MEG) recording at baseline and 4-year follow-up. We tested associations between baseline Aβ-binding potentials (BPND) and longitudinal MEG characteristics (spectral characteristics, functional connectivity), as well as between Aβ-BPND and MEG change scores, using linear mixed models corrected for age and sex. Higher Aβ-BPND in orbitofrontal-posterior cingulate regions at baseline predicted oscillatory slowing, reflected by a steeper increase in orbitofrontal-posterior cingulate and whole-brain relative theta (4-8Hz) power (p<.001) and decrease in whole-brain relative beta (13-30Hz) power over time (p<.05). In addition, elevated baseline regional Aβ-BPND predicted a reduction in regional functional connectivity over time, as measured by inverted Joint Permutation Entropy (JPEinv) theta (p<.05). An increase in regional Aβ-BPND over time was associated with an increase in regional relative theta power (p<.05) and a reduction in regional (measured by JPEinv theta (p<0.01) and corrected amplitude envelope correlation (AEC-c) alpha (8-13Hz), p<.05)) and whole-brain functional connectivity (measured by AEC-c alpha, p<.001) over time. Disruptions of spectral power and functional connectivity appear to represent early functional consequences of emerging AD pathology in cognitively unimpaired individuals. Not only baseline Aβ-levels, but also temporal changes in Aβ-levels inform us about the trajectory of neurophysiological characteristics over time.