Alzheimer disease (AD) is the most common form of dementia in the elderly. Cognitive function can be preserved despite underlying neuropathology. Physical, cognitive, sensory, and social stimulation contribute to this resilience. Environmental enrichment (EE) replicates these effects in animal models through sustained exposure to analogous stimulating conditions. In this study, we assessed spatial learning and memory using the Barnes maze test in 3xTg-AD mice, a transgenic model of AD carrying three key mutated human genes (B6.Cg-Tg(APPSwe,tauP301L)1Lfa Psen1tm1Mpm/J) that typically shows cognitive deficits by 6 months of age. EE was applied to two groups: one up to a presymptomatic stage (4 months, n=10) and another up to a symptomatic stage (6.5 months, n=10). Control mice were housed in standard, non-enriched cages (n=19). At baseline, no significant differences were observed (U=38, p=0.359). After treatment, only the 6-month EE group showed significantly lower escape latency than controls (U=20, p=0.023), indicating better performance. The EE effect hypothesis was confirmed by intra-group analysis (Z=−2.114, p=0.035). These findings suggest that EE can delay cognitive decline in 3xTg-AD mice, highlighting its potential as a non-pharmacological strategy for preserving cognitive function in AD. Further studies aim to explore the CA1-CA3 neuroplastic mechanisms likely underlying this behavioural effect.