Objective: Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disorder, with patients often exhibiting social withdrawal at an early stage. Its primary pathological hallmarks include abnormal β-amyloid (Aβ) deposition, glial hyperactivation, synaptic impairment, and myelin dysfunction. Recently, the enriched environment (EE), a non-pharmacological intervention, has garnered attention for its potential to enhance neuroplasticity. However, research on the effects of EE on social behavior and related neuropathological changes in the early stages of AD remains insufficient. This study utilized the 5×FAD mouse model to systematically investigate the impact of EE on early pathological progression in AD, providing new evidence to support the application of EE in the prevention and treatment of AD. Methods: Two-month-old 5×FAD mice were randomly assigned to a standard environment (SE) group or an EE group (5 mice per cage) and maintained in their respective housing conditions for 4 weeks. Behavioral tests, including the Y-maze, open field, elevated plus maze, and three-chamber social interaction assays, were conducted. Histopathological analyses of the medial prefrontal cortex (mPFC) were performed to evaluate neuropathological changes. Results: EE did not affect short-term spatial memory or anxiety-like behaviors in 5×FAD mice but significantly enhanced their social interaction capabilities. Pathologically, 5×FAD mice exhibited marked Aβ deposition and glial activation in the mPFC. Compared to the SE group, EE mice showed significantly reduced Aβ accumulation and glial activation in the mPFC. Furthermore, EE improved myelin structural integrity in this region, while no significant effects were observed on synaptic proteins, synaptic ultrastructure, or neuronal survival. Conclusion: This study demonstrates that EE effectively mitigates AD-related pathology in 5×FAD mice and alleviates social behavioral deficits, highlighting its potential for addressing AD-associated social dysfunction. These findings suggest that environmental interventions may exert neuroprotective effects by modulating neuroinflammation, reducing Aβ deposition, and preserving myelin homeostasis during AD progression.Keywords: Enriched Physical Environment; Social Behavioral Deficits; Medial Prefrontal Cortex