Systems consolidation theory posits that storage and retrieval of recent episodic memory require that plastic changes initially develop in the hippocampus (HIP) and, at later stages, in prefrontal cortex (PFC) which ultimately self-governs storage and retrieval of remote memory. Whether and how systems consolidation develops in mouse models of Alzheimer’s disease (AD) is unknown. We previously reported that 2-month-old pre-symptomatic Tg2576 AD mice trained for contextual fear conditioning (CFC) exhibit intact recent memory without activating the HIP but, instead, over-activating the BLA. Here we examine whether remote CFC memory tested four weeks after CFC training is preserved and, if so, which cortical regions it depends on. By combining retrograde tracing, c-fos detection, and dendritic spine visualization, we observed that remote memory was intact in AD mice but, unlike in Wt mice, was not associated with plastic changes in PFC which, instead, developed in entorhinal cortex (EC). Confirming EC selective involvement in remote memory of AD mice, EC chemogenetic silencing decreased remote memory in AD mice, but did not in Wt mice.Remarkably, application of transcranial direct current stimulation (tDCS) to PFC of AD mice before remote memory recall, reinstated PFC activation and sustained intact memory after chemogenetic silencing of EC, confirming EC disengagement in remote memory of tDCS-AD mice.Our findings suggest that systems consolidation develops in AD mice via activation of a compensatory BLA-EC circuitry that replaces the canonical HIP-PFC and demonstrate the tDCS therapeutic potential of reactivating canonical circuits.