Inhibitory deficits and an excitation/inhibition(E/I) imbalance arising from loss of inhibitory synapses may predispose to subclinical-epileptiform-activity and contribute to the earliest stages of Alzheimer’s disease(AD), and progressively lead to macroscopic neuronal network dysfunction. The classical brain-criticality-hypothesis posits that neuronal-systems operate at a continuous, second-order phase-transition with E/I-balance serving as primary control parameter. However, we have recently found neuronal systems in vivo may also operate at a discontinuous, first-order phase-transition and exhibit bistable-critical-synchronization dynamics. This bistability may be regulated by slow positive feedback or activity-dependent depletion mechanisms, and through control parameters beyond classical E/I. While moderate-bistability is associated with good cognition, excessive-bistability is a salient biomarker for epileptiform-brain-tissue. The trajectory of bistable dynamics across the continuum of AD disease progression, i.e., from subjective-cognitive-decline(SCD) to mild-cognitive-impairment(MCI) to AD, has remained unclear. We analysed resting-state magnetoencephalography(MEG) data of 85 SCD, 142 MCI, 14 AD patients, and 116 healthy controls(HC). MEG recordings were transformed into individual source-space and parcellated using Schaefer’s atlas into 400 cortical-parcels. Bistability-index (BiS) was calculated for 32 wavelets ranging from 2−90 Hz. We found progressive breakdown of moderate-BiS for SCD, MCI and AD compared to HC over the spectrum of 7–40 Hz. Importantly, BiS differentiated early-disease-stages and had frequency-specific between-cohort differences. The results suggest already earliest stages of AD are associated with deficits in the neuronal control of bistable synchronization dynamics. This bistability breakdown was progressive through disease-timeline suggesting that it may constitute a novel mechanistic biomarker for early AD and potentially serve AD-diagnosis and prognosis.