阿尔茨海默病（Alzheimer's disease，AD）的高患病率给家庭和社会带来沉重的负担。最近很多动物 研究表明慢性应激导致的糖皮质激素（glucocorticoid，GC）水平增加及其受体功能异常参与AD的病理进 程，其涉及的机制包括增加Aβ沉积与tau蛋白过度磷酸化、损害突触可塑性、与小胶质细胞共同介导慢性炎 症等。给予糖皮质激素受体（glucocorticoid receptor，GR）拮抗剂能够改善AD动物模型的认知表现。本文 综述了GC及GR在AD病理中的可能作用机制，并为AD的研究和治疗提供新的思路与方法。

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.