Visual gamma entrainment using sensory stimuli (vGENUS) is a promising non-invasive therapeutic approach for Alzheimer's disease (AD), showing efficacy in improving memory function and physiological biomarkers levels in mice and, in perspective, also human patients. However, its mechanisms of action remain poorly understood. Explanations in terms of boosted neurogenesis or glymphatic clearance have been advanced. Here we probe the alternative hypothesis that this non-invasive and non-pharmacological stimulation acts by increasing the fluidity of brain dynamics. Our hypothesis expands upon previous evidence that fluidity of system’s network dynamics is hampered in AD and aging and that higher fluidity is associated to better cognitive performance. Using young AppNL-F/MAPT double knock-in (dKI) mice, a model of early AD, we examined brain dynamics alterations well before amyloid plaque onset, using high-density EEG recordings during sleep and behavior, as well as resting state fMRI. For fMRI, we assessed fluidity of dynamic functional connectivity (dFC) using metrics of network reconfiguration speed and viscosity. For EEG, we used a symbolized dynamics analysis (microstate sequence extraction), maximum entropy landscape analysis, as a well as a novel dynamic fluidity metric, based on extreme events statistics, previously used in climate physics. We thus revealed that dKI mice exhibit early, reductions in brain dynamics fluidity associated with cognitive deficits in complex memory tasks. Daily vGENUS sessions over two weeks restored brain dynamics fluidity and rescued memory deficits in dKI mice. Importantly, these effects built up during the stimulation protocol and persisted after stimulation ended. Based on these results, we propose a "brain dynamics repair" mechanism for vGENUS that goes beyond current amyloid-centric hypotheses. This dual insight –that brain dynamics are both a target for repair and a potential diagnostic tool– provides new perspectives on early Alzheimer's disease pathophysiology.