Alzheimer's disease (AD) is characterized by a high prevalence, which imposes a heavy burden on families and society. Recently, many studies in animals have shown that chronic stress-induced elevation of glucocorticoid (GC) level and dysfunction of GC receptor (GR) are involved in the pathological process of AD. The involved mechanisms include increased deposition of β-amyloid (Aβ), hyperphosphorylation of tau protein, damaged synaptic plasticity, and co-mediation of chronic inflammation with microglia. Treatment with GR antagonists can improve the cognitive performance of animal models of AD. This article reviews the possible mechanisms of GC and GR in AD pathology, providing new insights and approaches for the research and treatment of AD.