In Alzheimer’s Disease (AD), memory deficits, particularly in spatial tasks, are well-documented. However, integrated memory encompassing both spatial and social information remains less explored. This study investigates early impairments in social recognition in the triple transgenic murine model of AD (3xTgAD) and correlates these deficits with the progression of AD pathology. Female 3xTgAD mice aged 2-4 and 6-8 months underwent a social recognition test, revealing significant impairments in recognizing non-familiar individuals by 6-8 months. Immunofluorescence assays for beta-amyloid and TAU, alongside whole-brain quantification, were performed at 3, 6, 9, and 12 months. Results indicated early intracellular beta-amyloid accumulation in parts of the hippocampus, with abundant extracellular deposits observed by 9-12 months, suggesting a correlation between social recognition deficits and early pathological changes. Further investigation involved calcium imaging to record dCA1 place cell activity during exposure to urinary marks, a critical component of rodent conspecific and territorial recognition. Younger mice demonstrated robust cell activation, whereas 6-8-month-old mice exhibited a marked decrease in dCA1 place cell recruitment, indicating a disruption in integrating social stimuli into hippocampal memory networks. These findings highlight early social recognition deficits in 3xTgAD mice, preceding extensive beta-amyloid deposition. The correlation between diminished dCA1 place cell activity and social recognition impairment underscores potential early biomarkers for AD progression, offering insights into the disease’s impact on integrated memory systems.Funding: Ministry of Science, Innovation and Universitties, PID2022-141733NB-I00/AEI/10.13039/501100011033/ FEDER, UE. A Teruel-Sancis is a predoctoral fellow of the FPU20/02632 program of Spanish