Tau pathology is a hallmark of Alzheimer's disease (AD); with the medial entorhinal cortex (mEC) and the hippocampus (Hpc) being amongst the earliest affected by the pathology. Interplay between these regions is wellknown to support cognitive abilities related to spatial navigation; in-line with data showing that such detriments are often the earliest seen in individuals who become diagnosed with AD. While such cognitive biomarkers might be able to highlight higher-risk individuals of AD diagnoses, it remains to be elucidated what the neurophysiological signatures of these early perturbations are, their mechanistic underpinnings and how they relate to cognitive impairment. We sought to model this behavioural and neurophysiological phenomenology using the S305N hTauKI mouse-model of early tauopathy, revealing: • S305N mice showed poorer spatial navigation performance •Increased frequency of theta (4–11 Hz) oscillations • Reduced theta–mid-gamma (~40–80 Hz) amplitude modulation Mid-gamma-associated magnification of theta cycle frequency effect size more predictive of poorer spatial navigation performance • Inflexible theta cycle frequency transition dynamics with pathologyassociated spiking and mid-gamma correlates • Theta cycle frequency linked to Layer-III/IIb interneurons exhibiting midgamma modulation gain