Alzheimer’s disease (AD) is the most common cause of dementia. Neuropathological processes, including the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, and neuroinflammation, lead to cognitive impairment at middle and eventually later stages of AD progression. Over the last decade, focused efforts have explored repurposed drug approaches for AD pathophysiological mechanisms. Recently, auranofin, an anti-inflammatory drug, was shown to have therapeutic potential in a number of diseases in addition to rheumatoid arthritis. Surprisingly, no data regarding the effects of auranofin on cognitive deficits in AD mice or the influence of auranofin on Aβ pathology and neuroinflammatory processes are available. In the present study, we used 14-month-old transgenic male APP^{NL-G-F/NL-G-F} mice to assess the effects of subchronic administration of auranofin at low doses (1 and 5 mg/kg, intraperitoneal) on spatial memory, Aβ pathology and the expression of cortical and hippocampal proteins (glial fibrillary acidic protein (GFAP), ionized calcium binding adaptor molecule-1 (Iba-1)) and proteins related to synaptic plasticity (glutamic acid decarboxylase 67 (GAD67), homer proteins homologue-1 (Homer-1)). The data demonstrated that auranofin significantly decreased Aβ deposition in the hippocampus and the number of Aβ plaques in the cingulate cortex, but it did not have memory-enhancing effects or induce changes in the expression of the studied proteins. Our current results highlight the importance of considering further pre-clinical research to investigate the possible beneficial effects of auranofin on the other pathological aspects of AD.

阿尔茨海默病 (AD) 是痴呆症的最常见原因。神经病理学过程，包括淀粉样蛋白 β (Aβ) 斑块和神经原纤维缠结的积累以及神经炎症，会导致 AD 进展中期和最终阶段的认知障碍。在过去的十年中，集中努力探索了 AD 病理生理机制的重新利用药物方法。最近，金诺芬是一种抗炎药，除类风湿性关节炎外，还显示出对许多疾病的治疗潜力。令人惊讶的是，没有关于金诺芬对 AD 小鼠认知缺陷的影响或金诺芬对 Aβ 病理学和神经炎症过程的影响的数据。在本研究中，我们使用了 14 个月大的转基因雄性 APP ^NL-GF/NL-GF小鼠评估亚慢性施用低剂量金诺芬（1 和 5 mg/kg，腹膜内）对空间记忆、Aβ 病理以及皮质和海马蛋白（胶质纤维酸性蛋白 (GFAP)、离子钙结合接头）表达的影响分子 1 (Iba-1)) 和与突触可塑性相关的蛋白质（谷氨酸脱羧酶 67 (GAD67)、荷马蛋白质同源物 1 (Homer-1)）。数据表明，金诺芬显着减少海马中的 Aβ 沉积和扣带回皮层中的 Aβ 斑块数量，但它没有增强记忆的作用或诱导所研究蛋白质表达的变化。