Achieving early diagnosis in Alzheimer's disease (AD) is a crucial objective in preclinical and clinical AD research, since it represents a therapeutic window during which interventions can be initiated before the onset of severe cognitive decline. Accumulation of amyloid-beta (Aß) in the prefrontal cortex is linked to rapid forgetting in this prodromal AD stage. Thus, early forgetting becomes a potential target for preclinical studies seeking to prevent/delay the onset of severe forms of AD. We used mouse models to identify early alterations in memory formation. Our findings indicate that Aβ1-42 accumulation within the anterior cingulate cortex during the prodromal AD stage disrupts memory consolidation processes essential for the formation of remote memory. This disruption may not arise from its impact on the encoding process, because mice are able to initiate memory formation. In contrast, Aβ1-42 accumulation disturbs the early post-encoding of memories, leading to accelerated forgetting. Our results suggest that the proper plasticity of the intrinsic excitability of engram cells plays a permissive role in the formation of long-term memories. Anomalies in this plasticity may serve as a crucial mechanism for defective consolidation in AD, resulting in memory dysfunction. To test this, we visualized neurons specifically engaged in encoding long-term memory by employing a c-fos-dependent labeling system. Whole-cell recordings from these putative engram neurons allowed us to characterize learning-specific intrinsic excitability changes and explore their potential alterations in AD. We further investigated the functional relevance of these plasticity changes in AD by modulating the excitability of these putative engram neurons.