• Korean Journal of Psychosomatic Medicine
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• v.4 no.1
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• pp.124-137
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• 1996

As the society becomes more industrialized and modernized, we have more chances to experience a serious traumatic event. Post-traumatic stress disorder (PTSD) has 3 major categories of symptoms such as memory disturbance, hyperarousal and avoidance or numbness. I reviewed the psychobiological evidences in 3 main categories of symptoms and the biological treatment after a brief review of the epidemiology, psychosocial etiology and diagnosis of PTSD. The memory disturbance of PTSD might be developed by the potentiation of the memory pathway mediated by norepinephrine. PTSD induces HPA axis abnormality, it might also develop hippocampal dysfunction, which might contribute to the memory disturbance. The kindling effect develops desensitization, which might develop reexperiencing of the traumatic events and hyperarousal state. Chronic aroused state of locus ceruleus with resultant chronic maladaptive state of norepinephrine system, might develop hyperarousal state. Social avoidance and physical numbing state in PTSD might be caused by serotnin or opiate system. Stress induced analgesia might be developed by opiate reliesed against the acute stress. The biologic research results would help the selective treatment of PTSD.

• 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).

• 한국약용작물학회:학술대회논문집
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• 2011.09a
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• pp.31-45
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• 2011

The amyloid ${\beta}$-peptide ($A{\beta}$), which originates from the proteolytic cleavage of amyloid precursor protein (APP), plays a central role in the pathogenesis of Alzheimer's disease (AD). Mounting evidence indicates that different species of $A{\beta}$, such as $A{\beta}$ oligomers and fibrils, may contribute to AD pathogenesis via distinct mechanisms at different stages of the disease. Importantly, elevation and accumulation of soluble $A{\beta}$ oligomers closely correlate with cognitive decline and/or disease progression in animal models of AD. In agreement with these studies, oligomers of $A{\beta}$ have been shown to directly affect synaptic plasticity, a neuronal process that is known to be essential for memory formation. Our previous studies showed that $A{\beta}$ induces the breakdown of phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2), a phospholipid that regulates key aspects of neuronal function. PI(4,5)P2 breakdown was found to be a key step toward synaptic and memory dysfunction in a mouse model of AD. To this end, we seek to identify small molecules that could elevate the levels of PI(4,5)P2 and subsequently block $A{\beta}$ oligomer-induced breakdown of PI(4,5)P2 and synaptic dysfunction.. We found that (20S)Rg3, an active triterpene glycoside from heat-processed ginseng, serves as an agonist for phosphatidylinositol 4-kinase IIalpha (PI4KIIalpha), which is a lipid kinase that mediates a rate-limiting step in PI(4,5)P2 synthesis. Consequently, (20S)Rg3 stimulates PI(4,5)P2 synthesis by directly stimulating the activity of PI4KIIalpha. Interestingly, treatment of a mouse model of AD with (20S)Rg3 leads to reversal of memory deficits. Our data suggest that the PI(4,5)P2-promoting effects of (20S)Rg3 may help mitigate the cognitive symptoms associated with AD.

• 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.

• The Journal of Korean Medicine
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• v.21 no.4
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• pp.236-241
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• 2000

Background and Purpose : Cerebrovascular accident is a serious neurologic event. It can have temporary or permanent effects on survivors, including memory, cognition and volitional control of voiding. The purpose of this study is to evaluate the clinical effect of moxibustion in patients with voiding dysfunction after a cerebrovascular accident. Methods : Twenty patients with post-stroke voiding dysfunction were studied. All patients had computerized tomography(CT) and magnetic resonance imaging(MRI) to localize the lesion in the central nervous system. They were randomly divided into two groups : the control and moxibustion group. Ten of twenty patients underwent moxibustion treatment by randomization. The moxibustion group receieved moxibustion at three points : Chung-guk (Conception Vessel CV3), Kuanwon (CV4) Kihae (CV6). Residual urine volume evaluation was undertaken in all patients. Results : 1. IIn the balanced bladder time, the moxibustion group had the shorter time than non moxibustion group. But there was no significiant difference between the moxibustion group and non-moxibustion group. 2. In the residual urine volume, the moxibustion group and non-moxibustion group showed a tendency to decrease. But there was no significiant difference between the moxibustion group and non-moxibustion group. Conclusions : Though further study is needed, our findings suggested that the time of achieving balanced voiding was shorter with moxibustion than in the control group.

• Journal of Yeungnam Medical Science
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• v.36 no.3
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• pp.183-191
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• 2019

Some patients with type 1 and type 2 diabetes mellitus (DM) present with cognitive dysfunctions. The pathophysiology underlying this complication is not well understood. Type 1 DM has been associated with a decrease in the speed of information processing, psychomotor efficiency, attention, mental flexibility, and visual perception. Longitudinal epidemiological studies of type 1 DM have indicated that chronic hyperglycemia and microvascular disease, rather than repeated severe hypoglycemia, are associated with the pathogenesis of DM-related cognitive dysfunction. However, severe hypoglycemic episodes may contribute to cognitive dysfunction in high-risk patients with DM. Type 2 DM has been associated with memory deficits, decreased psychomotor speed, and reduced frontal lobe/executive function. In type 2 DM, chronic hyperglycemia, long duration of DM, presence of vascular risk factors (e.g., hypertension and obesity), and microvascular and macrovascular complications are associated with the increased risk of developing cognitive dysfunction. The pathophysiology of cognitive dysfunction in individuals with DM include the following: (1) role of hyperglycemia, (2) role of vascular disease, (3) role of hypoglycemia, and (4) role of insulin resistance and amyloid. Recently, some investigators have proposed that type 3 DM is correlated to sporadic Alzheimer's disease. The molecular and biochemical consequences of insulin and insulin-like growth factor resistance in the brain compromise neuronal survival, energy production, gene expression, plasticity, and white matter integrity. If patients claim that their performance is worsening or if they ask about the effects of DM on functioning, screening and assessment are recommended.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2008.04a
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• pp.169-169
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• 2008

• Journal of Life Science
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• v.9 no.5
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• pp.548-555
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• 1999

Long-term effects of Ganoderma lucidum (GL) on memory and oxidative stress of senescence-accelerated mice (SAM) were investigated. Senescence-resistant (R1) and prone (P8) strains of SAM were fed GL diets, premixed with low (20 mg/kg/day, T1) or high (200 mg/kg/day, T2) levels of GL powder for 9 months starting from young (3 months of age) or for 5 months starting from old (7 months of age). After the final feeding at 12 months of age, all animals were subjected to passive avoidance test for the evaluation of memory function. In addition, the changes in hepatic thiobarbituric acid-reactive substance (TBARS) and glutathione were analyzed. SAMP8 fed GL diets from old age (7 months) exhibited the improvement of memory, although GL rather inhibited the memory function of both SAMR1 and SAMP8 mice fed diets from young (3 months of age). Hepatic TBARS contents were decreased in SAMP8 fed high GL diet for 9 months and in SAMR1 fed low GL diet for 5 months. Hepatic glutathione content was also remarkably increased in SAMR1 following both feeding periods, and less extent in SAMP8 fed diet for 5 months of age. Taken together, it is proposed that GL extracts may play an anti-aging role through antioxidant action, and thereby may improve the senescence-related memory dysfunction.

• Korean Journal of Pharmacognosy
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• v.41 no.3
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• pp.196-203
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• 2010

Black sesame (Sesami semen nigrum) has been used to treat dizziness, earnoise, constipation in the traditional Chinese medicine. In the present study, we assessed memory enhancing properties of 70% ethanolic extract of black sesame (EBS70) and its ameliorating activities on learning and memory impairments induced by scopolamine. Drug-induced amnesia was made by scopolamine treatment (1 mg/kg, i.p.). Single EBS70 (200 mg/kg, p.o.) administration significantly enhanced cognitive function and attenuated scopolamine-induced cognitive impairments as determined by the passive avoidance and Y-maze tasks (P<0.05) and also reduced escape-latency on the Morris water maze task (P<0.05). In addition, EBS70 increased BDNF expression in hippocampus 4 h after its administration (P<0.05). These results suggest that EBS70 enhances learning and memory in normal state and attenuates amnesic state caused by cholinergic dysfunction.

• Journal of Oriental Neuropsychiatry
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• v.10 no.2
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• pp.105-113
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• 1999

The purpose of this study was to investigate the effect of Sunhyangjungkisan on the learning and memory ability in rats. For this purpose we have evoked cerebral dysfunction in rats with NOS inhibitor and then performed the Morris water maze task for each rat. We have found that Sunghyangjungkisan have some improving effedts on impaired learning and memort ability in the NOS inhibitor treated rat. In these improving effects, memory effect was more evident then learning effect. This result implies that Sunghyangjungkisan may be one of useful prescriptions for treatment of vascular dementia after cerebral ischemia.