Ginseng berry exhibits a diverse range of pharmacological activities. The present study aimed to examine the neuroprotective effects of ginseng berry aqueous extract (GBE) against oxidative stress and to assess the impact of GBE on memory impairment in mice. In HT-22 cells, GBE pretreatment significantly inhibited glutamate-and hydrogen peroxide-mediated cytotoxicity in a concentration-dependent manner, while treatment with up to 100 µg/ml GBE alone did not change cell viability. In a murine model of scopolamine (SCP)-induced memory impairment, results from the passive avoidance test and the Morris water maze test indicated that GBE administration for 4 weeks prolonged step-through latency time and shortened escape latency time, suggesting that GBE can attenuate deficits in long-term memory induced by SCP. Additionally, GBE prevented SCP-induced reductions in acetylcholine by decreasing acetylcholinesterase activity and upregulating choline acetyltransferase mRNA levels in the hippocampus. GBE mitigated SCP-mediated mRNA decreases in brain-derived neurotrophic factor levels and its associated signaling molecules. Furthermore, GBE administration significantly suppressed malondialdehyde production and increased glutathione levels, catalase activity and superoxide dismutase activity in SCP-induced memory impaired mice. Therefore, the results of the current study indicated that ginseng berry may be a potential candidate for treating or preventing memory deficits that are associated with neurodegenerative disorders.

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We report that curcumin spray powder (CM-SD) alleviated scopolamine-induced memory impairment by suppressing scopolamine-induced ACh levels and upregulating hippocampal ChAT and memory susceptibility genes, including, BDNF, PI3K, Akt, ERK1/2, CREB, and CaMK IV in C57BL/6 mice. Previous studies have reported that scopolamine treatment in C57BL/6 mice significantly decreased step-through latency in the passive avoidance task test, hippocampus ACh contents, ChAT mRNA expression, and the expressions of memory susceptibility genes. In the present study, scopolamine treatment increased escape latency times in the Morris water maze test, the activity of hippocampal AChE in C57BL/6 mice, and disrupted the cerebral cortex anti-oxidant defense system. However, CM-SD, treatment dose-dependently reduced these effects in our scopolamine-induced C57BL/6 mouse model of amnesia. Our findings indicate CM-SD is a potential medicinal food ingredient that might ameliorate various types of memory impairment.