Recent studies in individuals at increased risk of Alzheimer’s disease suggest that impairments in path integration may represent one of the earliest cognitive deficits, emerging before broader memory decline. The medial entorhinal cortex and hippocampus are central to spatial memory and navigation, with grid cells playing a crucial role in path integration. We therefore hypothesised that dysfunction within medial entorhinal–hippocampal circuits contributes to the early decline in path integration, and that Tau hyperphosphorylation in these areas could be among the earliest molecular events driving these abnormalities. To test this hypothesis, we employed a novel early-stage (pre-tangle) Tauopathy mouse model (S305N KI) to determine whether Tau hyperphosphorylation can recapitulate key path-integration deficits seen in humans and to identify the associated alterations in cellular and network activity underlying these early impairments.