Alzheimer’s disease (AD) early stages are characterized by amyloid beta oligomers (oAβ) toxicity in the hippocampus, leading to its dysfunction. Previously, we characterized a non-transgenic mouse model of early amyloidosis by a single intracerebroventricular (icv.) injection of oAβ1-42, that showed deficient hippocampal-dependent memory and synaptic plasticity impairment in the CA1–CA3 synapse regardless the sex. Social memory impairments have also been described in AD. However, neuronal oscillatory activity in hippocampal CA2 subfield, a region that plays a crucial role in the formation and integration of social memory, is still poorly understood, and potential sex differences have not been explored yet. In this study, we aimed to characterize the effect of oAβ1-42 on CA2 network activity during social behavior in a non-transgenic mice model of early AD. Male and female animals performed a social memory test in which they had to discriminate between novel and familiar subjects. Simultaneously, CA2 local field potentials (LFPs) were recorded in vivo and oscillatory activity was analyzed during social interactions.Preliminary results showed that a single oAβ1-42 injection impaired social memory in both sexes, without affecting sociability. Disruption in CA2 oscillatory activity in all frequency bands was found, which might underly the social memory impairments observed.This work analyzes for the first time the effect of early amyloidosis on the oscillatory activity of female and male mice during social interactions, providing an electrophysiological substrate to explain social deficits found in early stages of AD.Funding: MICIN, PID2020-115823-GB100/ JCCM, SBPLY/21/180501/000150 and ERDF. AC, NextGenerationEU/PRTR postdoctoral fellowship.