(−)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenolic extract in green tea and it has attracted increasing attention for its multiple bioactive effects. However, the mechanisms by which EGCG exerts its neuroprotective actions in Alzheimer’s disease (AD) are presently lacking. In the present study, a sporadic AD transgenic mouse model known as senescence-accelerated mouse prone 8 (SAMP8) was used to investigate whether oral administration of EGCG could improve recognition and memory function through reduction of amyloid β (Aβ) and tau hyperphosphorylation. We also investigated the effects of chronic EGCG treatment on the synaptic dysfunction in the frontal cortex (FC) and the hippocampus (Hip) of AD mice. The results showed that long-term oral consumption of EGCG at a relatively high dose (15 mg/kg) improved memory function in SAMP8 mice in the Y-maze and Morris water maze. The levels of Aβ1–42 and BACE-1 in FC and Hip were significantly reduced by EGCG treatment. EGCG treatment also prevented the hyperphosphorylation of tau and reversed the decreased synaptic protein marker synaptophysin and postsynaptic density protein 95 in FC and Hip of SAMP8 mice. The present study suggests that long-term oral consumption of EGCG ameliorates impairments in spatial learning and memory and rescues the reduction in synaptic proteins observed in an AD mouse model. Thus, EGCG may represent a novel candidate agent for the treatment of neurodegenerative diseases.