Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory. However, the mechanism underlying these symptoms remains unclear. The best correlation between cognitive decline and pathological changes is in synaptic dysfunction. Histopathological hallmarks of AD are the abnormal aggregation of A beta and Tau. Evidence suggests that A beta and Tau oligomers contribute to synaptic loss in AD. Recently, direct links between epigenetic alterations, such as dysfunction in non-coding RNAs (ncRNAs), and synaptic pathologies have emerged, raising interest in exploring the potential roles of ncRNAs in the synaptic deficits in AD. In this paper, we summarize the potential roles of A beta, Tau, and epigenetic alterations (especially by ncRNAs) in the synaptic dysfunction of AD and discuss the novel findings in this area.