Ginseng has been shown to produce a cognitive improvement effect. The key molecular components in ginseng that produce pharmacological effects are ginsenosides. Previous studies reported a memory improvement effect of a few major ginsenosides. However, the identity of specific minor ginsenosides mediating such function remains unknown. Here, we report that a minor ginsenoside F1 improves memory function in APPswe/PSEN1dE9 (APP/PS1) double-transgenic Alzheimer’s disease (AD) model mice. After 8-wk oral administration of F1 jelly, we observed that spatial working memory, but not context-dependent fear memory, was restored in AD mice. To search for a possible underlying molecular and cellular mechanism, we investigated the effect of F1 on Aβ plaque. We observed F1 administration reduced the Aβ plaque area and density in the cortex, but not in the hippocampus of AD mice. Next, we tested for the effect of F1 on the expression level of key molecules involved in learning and memory. Results from Western blot assay revealed that an abnormally reduced level of a phosphorylated form of CREB in the hippocampus of AD mice was restored to a normal level by F1 administration. Moreover, in the same animals, BDNF level was augmented in the cortex. Our results, therefore, suggest that minor ginsenoside F1 constitutes a promising target to develop therapeutic agents for AD. Electronic supplementary material The online version of this article (10.1186/s13041-019-0495-7) contains supplementary material, which is available to authorized users.
The present study aimed to analyze and compare the prognostic performances of the Revised Trauma Score (RTS), Injury Severity Score (ISS), Shock Index (SI), and Modified Early Warning Score (MEWS) for in-hospital mortality in patients with traumatic brain injury (TBI). This retrospective observational study included severe trauma patients with TBI who visited the emergency department between January 2018 and December 2020. TBI was considered when the Abbreviated Injury Scale was 3 or higher. The primary outcome was in-hospital mortality. In total, 1108 patients were included, and the in-hospital mortality was 183 patients (16.3% of the cohort). Receiver operating characteristic curve analyses were performed for the ISS, RTS, SI, and MEWS with respect to the prediction of in-hospital mortality. The area under the curves (AUCs) of the ISS, RTS, SI, and MEWS were 0.638 (95% confidence interval (CI), 0.603–0.672), 0.742 (95% CI, 0.709–0.772), 0.524 (95% CI, 0.489–0.560), and 0.799 (95% CI, 0.769–0.827), respectively. The AUC of MEWS was significantly different from the AUCs of ISS, RTS, and SI. In multivariate analysis, age (odds ratio (OR), 1.012; 95% CI, 1.000–1.023), the ISS (OR, 1.040; 95% CI, 1.013–1.069), the Glasgow Coma Scale (GCS) score (OR, 0.793; 95% CI, 0.761–0.826), and body temperature (BT) (OR, 0.465; 95% CI, 0.329–0.655) were independently associated with in-hospital mortality after adjustment for confounders. In the present study, the MEWS showed fair performance for predicting in-hospital mortality in patients with TBI. The GCS score and BT seemed to have a significant role in the discrimination ability of the MEWS. The MEWS may be a useful tool for predicting in-hospital mortality in patients with TBI.
How memory is organized in cell ensembles when an event is repeated is not well-understood. Recently, we found that retraining 24 h after the initial fear conditioning (FC) event induces turnover of neurons in the lateral amygdala (LA) that encodes fear memory. Excitability-dependent competition between eligible neurons has been suggested as a rule that governs memory allocation. However, it remains undetermined whether excitability is also involved in the allocation of a repeated event. By increasing excitability in a subset of neurons in the LA before FC, we confirmed that these neurons preferentially participated in encoding fear memory as previously reported. These neurons, however, became unnecessary for memory recall after retraining 24 h following initial FC. Consistently, the initial memory-encoding neurons became less likely to be reactivated during recall. This reorganization in cell ensembles, however, was not induced and memory was co-allocated when retraining occurred 6 h after the initial FC. In 24-h retraining condition, artificially increasing excitability right before retraining failed to drive memory co-allocation. These results suggest a distinct memory allocation mechanism for repeated events distantly separated in time.
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