• Korean Journal of Medicinal Crop Science
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• v.28 no.2
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• pp.85-94
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• 2020

Background: Alzheimer's disease (AD) is caused by various factors, such as cholinergic dysfunction, regulation of neurotrophic factor expression, and accumulation of amyloid-beta. We investigated whether or not a combination of Carthamus tinctorius L. seed and Taraxacum coreanum (CT) has a protective effect on scopolamine-induced memory impairment in a mouse model. Methods and Results: Mice were orally pretreated with CT (50, 100 and 200 mg/kg/day) for 14 days, and scopolamine (1 mg/kg/day) was injected intraperitoneally before subjecting them to behavior tests. CT-administered mice showed better novel object recognition and working memory ability than scopolamine-treated control mice. In T-maze and Morris water maze tests, CT (100 and 200 mg/kg/day) significantly increased space perceptive ability and occupancy to the target quadrant, respectively. In addition, 100 and 200 mg/kg/day of CT attenuated cholinergic dysfunction through inhibition of butyryl cholinesterase in brain tissue. Furthermore, CT-administered mice showed higher cyclic adenosine monophosphate-response element-binding protein (CREB) levels and lower amyloid precursor protein (APP) levels compared to scopolamine-treated control mice. Conclusions: CT improved scopolamine-induced memory impairment through inhibition of cholinergic dysfunction, up-regulation of CREB, and down-regulation of APP. Therefore, CT could be a useful therapeutic agent for AD with protective effects on cognitive impairment.

• The Korean Journal of Physiology and Pharmacology
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• v.21 no.1
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• pp.55-64
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• 2017

Progressive memory impairment such as that associated with depression, stroke, and Alzheimer's disease (AD) can interfere with daily life. In particular, AD, which is a progressive neurodegenerative disorder, prominently features a memory and learning impairment that is related to changes in acetylcholine and abnormal ${\beta}$-amyloid ($A{\beta}$) deposition in the brain. In the present study, we investigated the effects of dehydroevodiamine HCl (DHED) on cognitive improvement and the related mechanism in memory-impaired rat models, namely, a scopolamine-induced amnesia model and a $A{\beta}_{1-42}$-infused model. The cognitive effects of DHED were measured using a water maze test and a passive avoidance test in the memory-impaired rat models. The results demonstrate that DHED (10 mg/kg, p.o.) and Donepezil (1 mg/kg, p.o.) ameliorated the spatial memory impairment in the scopolamine-induced amnestic rats. Moreover, DHED significantly improved learning and memory in the $A{\beta}_{1-42}$-infused rat model. Furthermore, the mechanism of these behavioral effects of DHED was investigated using a cell viability assay, reactive oxygen species (ROS) measurement, and intracellular calcium measurement in primary cortical neurons. DHED reduced neurotoxicity and the production of $A{\beta}$-induced ROS in primary cortical neurons. In addition, similar to the effect of MK801, DHED decreased intracellular calcium levels in primary cortical neurons. Our results suggest that DHED has strong protective effects against cognitive impairments through its antioxidant activity and inhibition of neurotoxicity and intracellular calcium. Thus, DHED may be an important therapeutic agent for memory-impaired symptoms.

• Journal of Physiology & Pathology in Korean Medicine
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• v.34 no.2
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• pp.81-87
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• 2020

Cognitive impairment is symptoms of dementia, a degenerative brain disease that is drawing attention in a rapidly aging society. This study was conducted to investigate the improvement of cognitive function of Leonurus japonicus on scopolamine-induced memory impairment in mice and the effect and mechanism of memory recovery. In vivo studies were conducted on mice orally pretreated with L. japonicus in doses of 50, 100 and 200 mg/kg (p.o.) and scopolamine (1 mg/kg, i.p.) were injected 30 min before the behavioral task. Antioxidant activity was assessed by 2,2-diphenyl-1-picryl hydrazyl (DPPH) assay and 2,2-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) assay, and acetylcholinesterase (AChE) inhibition activity evaluated by Ellman's method. In behavior studies showed that L. japonicus has an improved the memory of scopolamine-treated mice in Y-maze, passive avoidance and Morris water maze test. In addition, L. japonicus was also exerted free radical scavenging activity and inhibited acetyl cholinesterase activity. These results suggest that L. japonicus improves short-term and long-term memory in scopolamine-induced memory decline model and prevents scopolamine-induced memory impairments through in reduced oxidative stress and acetyl cholinesterase inhibition effect. Thus, L. japonicus is related to functional medicinal materials for prevention and treatment of human dementia patients.

• Journal of Korean Academy of Nursing
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• v.49 no.3
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• pp.317-328
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• 2019

Purpose: The purpose of this study was to identify the effect of ghrelin on memory impairment in a rat model of vascular dementia induced by chronic cerebral hypoperfusion. Methods: Randomized controlled groups and the posttest design were used. We established the representative animal model of vascular dementia caused by bilateral common carotid artery occlusion and administered $80{\mu}g/kg$ ghrelin intraperitoneally for 4 weeks. First, behavioral studies were performed to evaluate spatial memory. Second, we used molecular biology techniques to determine whether ghrelin ameliorates the damage to the structure and function of the white matter and hippocampus, which are crucial to learning and memory. Results: Ghrelin improved the spatial memory impairment in the Y-maze and Morris water maze test. In the white matter, demyelination and atrophy of the corpus callosum were significantly decreased in the ghrelin-treated group. In the hippocampus, ghrelin increased the length of hippocampal microvessels and reduced the microvessels pathology. Further, we confirmed angiogenesis enhancement through the fact that ghrelin treatment increased vascular endothelial growth factor (VEGF)-related protein levels, which are the most powerful mediators of angiogenesis in the hippocampus. Conclusion: We found that ghrelin affected the damaged myelin sheaths and microvessels by increasing angiogenesis, which then led to neuroprotection and improved memory function. We suggest that further studies continue to accumulate evidence of the effect of ghrelin. Further, we believe that the development of therapeutic interventions that increase ghrelin may contribute to memory improvement in patients with vascular dementia.

• Biomolecules & Therapeutics
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• v.26 no.4
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• pp.368-373
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• 2018

Rapid eye movement (REM) sleep has an essential role in the process of learning and memory in the hippocampus. It has been reported that linalool, a major component of Lavandula angustifolia, has antioxidant, anti-inflammatory, and neuroprotective effects, along with other effects. However, the effect of linalool on the cognitive impairment and behavioral alterations that are induced by REM-sleep deprivation has not yet been elucidated. Several studies have reported that REM-sleep deprivation-induced memory deficits provide a well-known model of behavioral alterations. In the present study, we examined whether linalool elicited an anti-stress effect, reversing the behavioral alterations observed following REM-sleep deprivation in mice. Furthermore, we investigated the underlying mechanism of the effect of linalool. Spatial memory and learning memory were assessed through Y maze and passive avoidance tests, respectively, and the forced swimming test was used to evaluate anti-stress activity. The mechanisms through which linalool improves memory loss and behavioral alterations in sleep-deprived mice appeared to be through an increase in the serotonin levels. Linalool significantly ameliorated the spatial and learning memory deficits, and stress activity observed in sleep-deprived animals. Moreover, linalool led to serotonin release, and cortisol level reduction. Our findings suggest that linalool has beneficial effects on the memory loss and behavioral alterations induced by REM-sleep deprivation through the regulation of serotonin levels.

• Dementia and Neurocognitive Disorders
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• v.17 no.3
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• pp.120-129
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• 2018

Background and Purpose: Prospective memory (PM) has a known relationship with frontal function, and PM decline has been observed in amnestic mild cognitive impairment (aMCI). Cerebral small vessel disease, as evidenced by white matter hyperintensities (WMHs), is linked to frontal dysfunction. This study was undertaken to evaluate the relationship between PM decline and WMHs in patients with aMCI. Methods: Of 74 enrollees with aMCI, 69 completed this prospective study. We compared total scores and sub-scores of the Prospective and Retrospective Memory Questionnaire (PRMQ) administered at baseline and 3 months later, stratifying patients by degree of WMHs. Results: A significant decline was seen in PRMQ total scores and PM scores at the 3-month mark in patients with moderate (vs. mild) degrees of WMHs ($-2.8{\pm}7.2$ vs. $0.2{\pm}7.1$; p=0.032). In addition, patients with moderate (vs. mild) degrees of deep WMHs (DWMHs) showed greater PM decline, whereas PM loss in patients with mild, moderate, or severe degrees of periventricular WMHs (PVWMHs) did not differ significantly. Conclusions: Findings of this study indicate that the burden of WMHs is consistently implicated in PM deterioration experienced by patients with aMCI, and signifies greater PM decline, especially in instances of extensive DWMHs. Greater attention to the change of PM is therefore needed in aMCI patients with WMHs.

• Journal of Digital Convergence
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• v.17 no.2
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• pp.283-292
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• 2019

The loss of semantic knowledge and impairments in semantic associations by semantic category is gaining increasing attention, as indicators of early-stage cognitive decline. As such, we assigned semantic association task (SAT) to normal elderly (NE) and those with subjective memory impairment (SMI) or mild cognitive impairment (MCI) to examine their performance by semantic subcategories and the differences in error patterns. We found a significant difference in the number of correct response and reaction time under the SAT categories among the three groups, with the highest performance observed in 'function' and the lowest performance in 'superordinate' and 'part/whole'. Moreover, the error frequency was the lowest in NE, followed by those with SMI and MCI, with the latter two groups showing a significant increase in no-response. Our findings demonstrate the varying extent and process of impairments in the semantic network by category over different stages of cognitive decline. Thus, we proposed SAT performance as an indicator to detect and follow-up on cognitive decline in elderly with cognitive disorder.

• The Korean Journal of Physiology and Pharmacology
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• v.14 no.5
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• pp.345-352
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• 2010

The present study was undertaken to explore the potential of erythropoietin in memory deficits of mice. Memory impairment was produced by scopolamine (0.5 mg/kg, $i.p.$) and intracerebroventricular streptozotocin (i.c.v STZ, 3 mg/kg, $10{\mu}l$, $1^{st}$ and $3^{rd}$ day) in separate groups of animals. Morris water-maze test was employed to assess learning and memory. The levels of brain thio-barbituric acid reactive species (TBARS) and reduced glutathione (GSH) were estimated to assess degree of oxidative stress. Brain acetylcholinesterase enzyme (AChE) activity was also measured. Scopolamine/streptozotocin administration induced significant impairment of learning and memory in mice as indicated by marked decrease in Morris water-maze performance. Scopolamine/streptozotocin administration also produced a significant enhancement of brain AChE activity and brain oxidative stress (an increase in TBARS and a decrease in GSH) levels. Treatment of erythropoietin (500 and 1,000 IU/Kg i.p.) significantly reversed scopolamine- as well as streptozotocin-induced learning and memory deficits along with attenuation of those-induced rise in brain AChE activity and brain oxidative stress levels. It may be concluded that erythropoietin exerts a beneficial effect in memory deficits of mice possibly through its multiple actions including potential anti-oxidative effect.

• Korean Journal of Cognitive Science
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• v.11 no.3_4
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• pp.33-43
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• 2000

The distinction between short-term store (STS) and long-term store (LTS) has been made in the perspective of information processing. Memory system theorists have argued that memory could be conceived as multiple memory systems beyond the concept of a single LTS. Popular memory system models are Schacter & Tulving (994)'s multiple memory systems and Squire (987)'s the taxonomy of long-term memory. Those m models agree that amnesic patients have intact STS but impaired LTS and have preserved implicit memory. However. there is a debate about the nature of the long-term memory impairment. One model considers amnesic deficit as a selective episodic memory impairment. whereas the other sees the deficits as both episodic and semantic memory impairment. At present, it remains unclear that episodic memory should be distinguished from semantic memory in terms of retrieval operation. The distinction between declarative memory and nondeclarative memory would be the alternative way to reflect explicit memory and implicit memory. The research focused on the function of frontal lobe might give clues to the debate about the nature of LTS.

• CELLMED
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• v.13 no.14
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• pp.14.1-14.9
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• 2023

Administration of Scopolamine can be considered a psychopharmacological model of Alzheimer's disease (AD). We made an animal model of Alzheimer's disease (AD) by administering Scopolamine to Blab/c mice. In this study, we investigated the effects of Resplex Alpha on memory impairment and cognitive function in mice in a mouse animal model of Scopolamine-induced memory impairment. Through Y-mazed and passive avoidance behavioral assays, we observed that Resplex Alpha recovered Scopolamine-induced short-term memory and cognitive functions. The results of our study imply that Resplex Alpha may be beneficial in the prevention of Alzheimer's disease (AD).