| First Author | Upīte J | Year | 2020 |
| Journal | Brain Res | Volume | 1746 |
| Pages | 147022 | PubMed ID | 32707043 |
| Mgi Jnum | J:300834 | Mgi Id | MGI:6503062 |
| Doi | 10.1016/j.brainres.2020.147022 | Citation | Upite J, et al. (2020) Subchronic administration of auranofin reduced amyloid-beta plaque pathology in a transgenic APP(NL-G-F/NL-G-F) mouse model. Brain Res 1746:147022 |
| abstractText | Alzheimer's disease (AD) is the most common cause of dementia. Neuropathological processes, including the accumulation of amyloid-beta (Abeta) 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 Abeta 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, Abeta 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 Abeta deposition in the hippocampus and the number of Abeta 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. |
