• Molecules and Cells
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• v.37 no.11
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• pp.767-776
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• 2014

Alzheimer's disease (AD) is clinically characterized with progressive memory loss and cognitive decline. Synaptic dysfunction is an early pathological feature that occurs prior to neurodegeneration and memory dysfunction. Mounting evidence suggests that aggregation of amyloid-${\alpha}$ ($A{\alpha}$) and hyperphosphorylated tau leads to synaptic deficits and neurodegeneration, thereby to memory loss. Among the established genetic risk factors for AD, the ${\varepsilon}4$ allele of apolipoprotein E (APOE) is the strongest genetic risk factor. We and others previously demonstrated that apoE regulates $A{\alpha}$ aggregation and clearance in an isoform-dependent manner. While the effect of apoE on $A{\alpha}$ may explain how apoE isoforms differentially affect AD pathogenesis, there are also other underexplored pathogenic mechanisms. They include differential effects of apoE on cerebral energy metabolism, neuroinflammation, neurovascular function, neurogenesis, and synaptic plasticity. ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain. Although there are a few conflicting findings and the underlying mechanism is still unclear, several lines of studies demonstrated that apoE4 leads to synaptic deficits and impairment in long-term potentiation, memory and cognition. In this review, we summarize current understanding of apoE function in the brain, with a particular emphasis on its role in synaptic plasticity and the underlying cellular and molecular mechanisms, involving low-density lipoprotein receptor-related protein 1 (LRP1), syndecan, and LRP8/ApoER2.

• Preventive Nutrition and Food Science
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• v.19 no.4
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• pp.343-347
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• 2014

The present study investigated the effects of Vaccinium uliginosum L. (bilberry) on the learning and memory impairments induced by amyloid-${\beta}$ protein ($A{\beta}P$) 1-42. ICR Swiss mice were divided into 4 groups: the control ($A{\beta}40$-1A), control with 5% bilberry group ($A{\beta}40$-1B), amyloid ${\beta}$ protein 1-42 treated group ($A{\beta}1$-42A), and $A{\beta}1$-42 with 5% bilberry group ($A{\beta}1$-42B). The control was treated with amyloid ${\beta}$-protein 40-1 for placebo effect, and Alzheimer's disease (AD) group was treated with amyloid ${\beta}$-protein 1-42. Amyloid ${\beta}$-protein 1-42 was intracerebroventricular (ICV) micro injected into the hippocampus in 35% acetonitrile and 0.1% trifluoroacetic acid. Although bilberry added groups tended to decrease the finding time of hidden platform, no statistical significance was found. On the other hand, escape latencies of $A{\beta}P$ injected mice were extended compared to that of $A{\beta}40$-1. In the Probe test, bilberry added $A{\beta}1$-42B group showed a significant (P<0.05) increase of probe crossing frequency compared to $A{\beta}1$-42A. Administration of amyloid protein ($A{\beta}1$-42) decreased working memory compared to $A{\beta}40$-1 control group. In passive avoidance test, bilberry significantly (P<0.05) increased the time of staying in the lighted area compared to AD control. The results suggest that bilberry may help to improve memory and learning capability in chemically induced Alzheimer's disease in experimental animal models.

• Biomolecules & Therapeutics
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• v.25 no.3
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• pp.249-258
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• 2017

To examine the effect of biflorin, a component of Syzygium aromaticum, on memory deficit, we introduced a scopolamine-induced cognitive deficit mouse model. A single administration of biflorin increased latency time in the passive avoidance task, ameliorated alternation behavior in the Y-maze, and increased exploration time in the Morris water maze task, indicating the improvement of cognitive behaviors against cholinergic dysfunction. The biflorin-induced reverse of latency in the scopolamine-treated group was attenuated by MK-801, an NMDA receptor antagonist. Biflorin also enhanced cognitive function in a naïve mouse model. To understand the mechanism of biflorin for memory amelioration, we performed Western blot. Biflorin increased the activation of protein kinase C-${\zeta}$ and its downstream signaling molecules in the hippocampus. These results suggest that biflorin ameliorates drug-induced memory impairment by modulation of protein kinase C-${\zeta}$ signaling in mice, implying that biflorin could function as a possible therapeutic agent for the treatment of cognitive problems.

• Journal of the Korea Convergence Society
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• v.10 no.9
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• pp.167-172
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• 2019

The purpose of this study was to investigate the effect of computer based cognitive rehabilitation program on the generative naming. Twenty - one patients were assigned to the CoTras program and eight were treated with traditional face - to - face language rehabilitation such as paper and table activities. The experimental group and the control group performed sequential language recall memory training, association memory recall training, language categorization memory training, and language integrated memory training for 12 weeks. The Welch's robust ANCOVA showed significant differences in mean fluency and MMSE-K changes (p<0.05). On the other hand, phonemic fluency increased significantly after 12 weeks of treatment compared to baseline in both experimental and control groups, but there was no statistically significant difference between treatment groups. The results of this study suggest that the computer based cognitive rehabilitation program may be more effective in improving the semantic fluency than the conventional cognitive-linguistic rehabilitation.

• Journal of Physiology & Pathology in Korean Medicine
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• v.36 no.1
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• pp.18-22
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• 2022

To investigate effects of cognitive function improvement whether against Taegeuk ginseng on scopolamine-induced memory impairment in rats. All experiments were conducted in three groups: the control group (CTR), the scopolamine 0.4mg/kg (SCP), and the scopolamine (SCP+T) treated with Taegeuk ginseng 100 mg/kg. Taegeuk ginseng 100 mg/kg daily was orally administered for one month and treated with scopolamine was only for 7 consecutive days on the Morris water maze task. 3 weeks after oral administration of Taegeuk ginseng, subjects were performed the Morris water maze test for 8 days and then the open-field exploration test which to assessed for cognitive function improvement. After behavioral testing, subjects were sacrificed and microdissected brains for neurochemical analysis. In the cognitive-behavioral test, long-term administration of Taegeuk ginseng improved spatial navigation learning task compared with the impeded by scopolamine treatment. In neurochemistry, the expression of the synaptic marker PSD95 (postsynaptic density protein 95) was increased in the hippocampus compared to the scopolamine group. Also, brain-derived neurotrophic factor (BDNF) expression was significantly increased in the taegeuk ginseng administration group. These data suggested that long-term administration of taegeuk ginseng might improve cognitive-behavioral functions on hippocampal related spatial learning memory, and it was correlated with neurotropic and synaptic reinforcement. In conclusion, treatment with taegeuk ginseng may positive outcome on learning and memory deficit disorders.

• Journal of Physiology & Pathology in Korean Medicine
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• v.36 no.1
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• pp.11-17
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• 2022

In this study, we investigated the effects of Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng extracts (FRG) on cognitive function in scopolamine-induced memory-impaired mice. We measured the effects of G, R, and FRG on the improvement of memory and cognition via behavior analysis. In addition, we measured the acetylcholinesterase (AChE) activity in the hippocampus of each group of mice. The expression of β-amyloid, Tau, and BDNF in the brain tissues were observed through immunohistochemical staining. Ginseng Radix (G) and Fermented red-ginseng (FRG) have effectively improved cognitive function in the water maze test. Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) have improved the willingness of mice to explore the new environment, as confirmed by Y maze test. In addition, immunohistochemical staining revealed that Ginseng Radix (G) decreased the expression of β-amyloid and Tau in the hippocampus. In addition, fermented red-ginseng (FRG) increased the expression of BDNF. Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) have decreased the concentration of acetylcholinesterase in the hippocampus as compared with the control group of mice. In conclusion, Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) are considered to have the potential for development as candidate drugs to control the progression of Alzheimer's disease (AD).

• Molecules and Cells
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• v.44 no.11
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• pp.795-804
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• 2021

Memory T (T_M) cells play an important role in the long-term defense against pathogen reinvasion. However, it is still unclear how these cells receive the crucial signals necessary for their longevity and homeostatic turnover. To understand how T_M cells receive these signals, we infected mice with lymphocytic choriomeningitis virus (LCMV) and examined the expression sites of neural cadherin (N-cadherin) by immunofluorescence microscopy. We found that N-cadherin was expressed in the surroundings of the white pulps of the spleen and medulla of lymph nodes (LNs). Moreover, T_M cells expressing high levels of killer cell lectin-like receptor G1 (KLRG1), a ligand of N-cadherin, were co-localized with N-cadherin⁺ cells in the spleen but not in LNs. We then blocked N-cadherin in vivo to investigate whether it regulates the formation or function of T_M cells. The numbers of CD127^hiCD62L^hi T_M cells in the spleen of memory P14 chimeric mice declined when N-cadherin was blocked during the contraction phase, without functional impairment of these cells. In addition, when CD127^loKLRG1^hi T_M cells were adoptively transferred into anti-N-cadherin-treated mice compared with control mice, the number of these cells was reduced in the bone marrow and LNs, without functional loss. Taken together, our results suggest that N-cadherin participates in the development of CD127^hiCD62L^hi T_M cells and homing of CD127^loKLRG1^hi T_M cells to lymphoid organs.

• Journal of Physiology & Pathology in Korean Medicine
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• v.38 no.1
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• pp.38-45
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• 2024

To compare and analyze the improvement effects of white ginseng extract, red ginseng extract, and black ginseng extract on cognitive dysfunction and memory impairment caused by scopolamine in rats. In the cognitive behavioral test, the tendency of the SCOP+B group to overcome the escape time delay induced by scopolamine administration was observed, unlike the SCOP group. The frequency on plat form was significantly increased in the group treated with ginseng extracts compared to the SCOP group. As a result of measuring the duration time on goal quadrant, the time spent in the quadrant was significantly increased in the SCOP+B group compared to the SCOP group. In the hippocampus, the SCOP-treated group significantly decreased the activity of AChE compared to the normal group, but the ginseng extract-treated groups significantly increased it compared to the SCOP group. After sacrificing the rats after the behavioral test, the expression of PSD95 protein in the excised brain was significantly decreased in the SCOP group compared to normal, but it was observed that the SCOP+R and SCOP+B groups were significantly increased compared to the SCOP group. CREB1 protein expression was significantly increased in the SCOP+R group, and the expression of Cdk5 was significantly increased in the SCOP+B group. Ginseng extracts significantly restored the memory damaged by scopolamine suggesting that red ginseng increased the expression of CREB1 and PSD95 proteins, and black ginseng increased the protein expression of Cdk5 and PSD95 to induce memory recovery.

• The Journal of Korean society of community based occupational therapy
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• v.6 no.1
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• pp.33-39
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• 2016

Objective : The cognitive rehabilitation were necessary for the elderly has generally decreased memory in order to recovery and maintain. This study showed that effect of memorial strategy program on memory in the elderly. Methods : 20 elderly who has used seniors welfare center in Busan was divided into an experimental group and control group. The control group used program of seniors welfare center, the experimental group participated memorial strategy program twice a week, total of 8 times. We used contextural memory test(CMT) to compared before and after. Results : Immediate recall and delayed recall were no statistically significant difference(p>.05) in both experimental group and control group when compared before and after. But there was statistically significant difference(p<.05) in a experimental group after memorial strategy program. Conclusion : This study shown that memorial strategy program help memory improve in the elderly. Many programs for memory improve in the elderly expect that prevent dementia or mild cognitive impairment.

• Sleep Medicine and Psychophysiology
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• v.3 no.1
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• pp.15-24
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• 1996

After rapid eye movement(REM) sleep was idenified in 1953, a lively interest developed concerning a possible role of this kind of sleep in memory processes. The author reviewed studies relating REM to memory/learning. Many studies in animals and humans gave substantial evidence for relating REM sleep to memory function. The evidence supporting the position taken in this paper comes from experiments showing that : (1) learning session is followed by the significant augmentation of REM sleep : (2) REM sleep deprivation, prior to learning or immediately thereafter, impairs the formation of a permanent memory/learning : (3) there is a vulnerable period of time(eg, REM sleep "window") following succussful learning, during which REM sleep deprivation results in memory impairment : (4) theta rhythm which develops during REM sleep induces long-term potentiation in hippocampus : (5) there are some evidences providing the relationship of neurotransmitter systems to the maintenance of REM sleep and memory storage processes.