• Proceedings of the PSK Conference
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• 2003.04a
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• pp.202.1-202.1
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• 2003

Microglial cell can act for phagocytosis against abnormal particles in brain, which means that beta-amyloid produced from APP(amyloid precursor protein) can be phagocytosed by microglia when released. In contrast. when senile plaque has already been formed in brain cortex and hippocamphal region, microglia can also accelerate the AD pathogenesis due to chronic inflammatory action, which lead to neuron cell cytotoxicity. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.141.2-142
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• 2003

beta-Amyloid (A$\beta$) peptide is the major component of senile plaques and considered to have a causal role in the development and progression of Alzheimer's disease. There has been compelling evidence supporting that $A\beta$-induced cytotoxicity is mediated through oxidative and/or nitrosative stress. Recently, considerable attention has been focused on dietary manipulation of oxidative and/or nitrosative damage. L-Egrothioneine (EGT) is a low-molecular weight naturally occurring thiol compound of dietary origin which exists in milimolar concentrations in the brain, liver, kindney, erythrocytes, ocular tissues and in seminal fluids of mammals. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.327.2-327.2
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• 2002

Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of Alzheimer's disease (AD), and nonsteroidal anti-inflammatory drugs have been shown to retard the progress of AD. In this study, we have investigated the molecular mechanisms underlying oxidative and inflammatory cell death induced by beta-amyloid (Abeta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD, in cultured PC12 cells. (omitted)

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.1
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• pp.50-56
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• 2003

This research was done to make the effective prescription and cope with various senile dementia. So Sprague-Dawley rats were injected with ibotenate to make a damage on learning and memory functions. At first acquisition test and retention rest were done in the Morris water maze. And to evaluate the effects of the sample drug(TBM) on choline acetyltranferase and acetylcholine esterase, immunoreactive measurement and enzymatic activity measuring were carried out. The ibotenic acid were injected to hippocampus CA1 and CA3 area. The results were as following. TBM improved the learning ability in the acquisition test and memory function in the retention test significantly. And TBM increased the level of ChAT which is synthesizing acetylcholine in CA3 area, and at the same time it increased the level of AChE which is resolving acetylcholine. These results show that T8M improved the cholinergic catabolism and anabolism, and the increment of metabolic activity of cholinergic system. In other words, it contributes to the recovery of damaged learning and memory function by ibotenic acid. So it can be concluded that TBM will be helpful to cholinergic brain damage induced by primary or senile reduction of acetylcholine secretive activity.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.1
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• pp.190-198
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• 2007

Alzheimer's disease, a representative neurodegenerative disorder, is characterized by the presence of senile plaques and neurofibrillary tangles accompanied by neuronal damages. b-Amyloid peptide is considered to be responsible for the formation of senile plagues that accumulate in the brains of patients with Alzheimer's disease. There has been compelling evidence supporting that b-amyloid-induced cytotoxicity is mediated through generation of reactive oxygen species. In this study, we have investigated the possible protective effect of Rehmannia glutihosaagainst b-amyloid-induced oxidative ceil death in cultured human neuroblastoma SH-SY5Y cells. SH-SY5Y cells treated with b-amyloid underwent apoptotic death as determined by morphological features and positive in situterminal end-labeling (TUNEL staining). Rehmannia glutinosawater extract, wine, and vinegar pretreatments attenuated b-amyloid-induced cytotoxicity and apoptosis. Rehmannia glutinosa vinegar exhibited maximum protective effect by increasing the expression of anti-apoptotic protein, Bcl-2. in addition to oxidative stress, b-amyloid-treatment caused nitrosative stress via marked increase in the levels of nitric oxide, which was effectively blocked by Rehmannia glutinosa. To further explore the possible molecular mechanisms underlying the protective effect of Rehmannia glutinosa, we assessed the mRNA expression of cellular antioxidant enzymes. Treatment of Rehmannia glutinosa vinegar led to up-regulation of heme oxygemase-1 and catalase. These results suggest that Rehmannia glutinosa could modulate oxidative neuronal cell death caused by b-amyloid and may have preventive or therapeutic potential in the management of Alzheimer's disease. Particularly, Rehmannia glutinosa vinegar can augment cellular antioxidant capacity, there by exhibiting higher neuroprotective potential.

• Korean Journal of Cognitive Science
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• v.11 no.2
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• pp.59-68
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• 2000

An increase in senile dementia population has caused social concerns in Korea. The Korean-Boston Naming Test(K-BNT) has been used in assessing naming ability of patients with diffuse brain damage as well as senile dementia. This study was conducted to develop a short from of the K-BNT. to present normative data, and to demonstrate clinical utility of the shortform K-BNT. The participants were 142 healthy elderly adults, ages between 55 and 84, who were sampled in the Seoul-Kyungki area. Twenty patients with mild probable DAT participated in the study. We developed four norms based on education(0∼6 years and more than 6 years) and age(55∼64 and 65∼84 years). The study showed high internal consistency among the items. Further. DAT patients and normal controls showed significant difference in the K-BNT short form scores(F(1, 158) = 23,216, p < .0001). Normative data presented in this study will be useful in evaluating the naming ability of elderly patients in clinical setting.

• IMMUNE NETWORK
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• v.5 no.4
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• pp.252-257
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• 2005

Background: This study was designed to investigate the effect of exercise training on defense mechanism of chronic degenerative disease, aging, and memory impairments of senescence-accelerated mouse (SAM)P8 under the hypothesis that "Senile dementia may be prevented by regular exercises". Methods: To evaluate the effects of exercise training on the defense mechanism of aging and memory impairment, SAMP8 were divided into two groups, the control group and exercise training groups. the exercise training group were performed with low $(\dot{V}O_2max\;25{\sim}33%)$, middle ($\dot{V}O_2max$ 50%) and high $(\dot{V}O_2max\;66{\sim}75%)$ intensity exercise. All SAMP8 mice were fed experimental diet ad libitum until 4, 8 months, and dead period. Results: Median lifespan in middle exercise group resulted in a significantly increased (23.5% and 18.7%, respectively), whereas these lifespan in high exercise group resulted in an unexpectedly decreased (13.5% and 12.1%, respectively) compared with control group. Body fat levels in 4 and 8 months of age were significantly decreased 43% to 51% in middle exercise group, whereas were remarkably deceased to 57% in high exercise group compared with control group. It is believed that extended median and maximum lifespan may be effected by calory restriction through the exercise training. Acetylcholine (ACh) levels were significantly increased 6.7% and 8.5% in middle and high exercise groups, and also choline acetyltransfease (ChAT) activities were significantly increased 10.3% and 11.9% in middle and high exercise groups. Conclusion: These results suggest that proper and regular exercises such as middle group ($\dot{V}O_2max$ 50%) may play an effective role in attenuating an oxygen radicals and may play an important role in improving a learning and memory impairments of senile dementia.

• Journal of Ginseng Research
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• v.34 no.4
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• pp.327-335
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• 2010

We reported previously that the administration of Korean red ginseng water extract (KRG-WE) protected the guinea pig testis against damage induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (a potent endocrine disruptor). We also found that crude saponin from ginseng was the active ingredient responsible for this protection. Here, we examined the biological role of KRG-WE in an animal model of age-induced dysfunction of spermatogenesis. Twenty-four male Sprague-Dawley (six 2-month-old and eighteen 12-month-old) rats were used. The young and old control groups received only vehicle. The ginseng saponin (GS)- and KRG-WE-treated groups received GS (40 mg/kg body weight/day) and KRG-WE (200 mg/kg body weight/day), respectively, for 4 months. The number of cells, Sertoli cell index, Johnsen's score, and sex hormone levels decreased significantly with age. However, the administration of KRG-WE and GS markedly improved the number of germ cells, seminiferous tubular size, and Johnsen's score in the old rats. Ginseng produced a distinct testicular histological improvement in old rats. KRG-WE and GS elevated testosterone levels, while attenuating the aberrant increase in follicle stimulating hormone and luteinizing hormone levels. Sperm kinematics evaluated by a computer-assisted sperm analyzer demonstrated improvement in the percentage of motile sperm, progressive sperm motility, and curvilinear velocity associated with sperm quality, supporting the beneficial role of red ginseng in senile spermatogenesis. Overall, the total water extract had a more potent effect than the corresponding saponin fraction. In conclusion, Korean red ginseng rejuvenated age-induced testicular dysfunction. Additionally, the total water extract was more potent than the corresponding saponin fraction.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.14 no.2
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• pp.207-223
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• 2001

The Wonyenaejang is equivalent to the (senile)cataract in western medicine. The word cataract is used to describe the natural lens that has turned cloudy. As the natural lens of the eye becomes cloudy, it does not allow light to pass through it. Cataracts usually start as a slight cloudiness that progressively grows more opaque. As the cataract becomes more mature(increasingly opaque and dense), the retina receives less and less light. The light that does reach the retina becomes increasingly blurred and distorted. This causes gradual impairment of vision. If left untreated, cataracts can cause needless blindness. Although there are many kinds of cataracts, a senile cataract is the most common one. We chose the oriental medicine textbooks and the oriental medicine journals that were dealing with the symptoms, etiology, and internal/external treatments. The results were as follows : 1. The main causes of this disease are weak liver and kidney, burning up of the wind and heat in the liver and gall, weak spleen and stomach. 2. As the internal treatment of the Cataract, Geegukjihwangtang is mostly prescribed. 3. As the external treatment of the Cataract, (l) In the field of medicine for external application is commonly prescribed (2) In the field of drug action, frequently used treatments are as follows. emission of the evil, alleviation of fever, removal of lump of blood, and the medicine for external applications. (3) In the field of four Qi, cold medicine is commonly prescribed. (4) In the field of five tastes, bitter/hot/sweet mdicine are commonly prescribed. (5) In the field of toxicity, non-togic medicine is commonly prescribed. (6) In the field of channel distribution, most of the medicine belong to liver channel.

• Molecules and Cells
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• v.42 no.1
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• pp.36-44
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• 2019

Alzheimer's disease (AD) is the most frequent age-related human neurological disorder. The characteristics of AD include senile plaques, neurofibrillary tangles, and loss of synapses and neurons in the brain. ${\beta}-Amyloid$ ($A{\beta}$) peptide is the predominant proteinaceous component of senile plaques. The amyloid hypothesis states that $A{\beta}$ initiates the cascade of events that result in AD. Amyloid precursor protein (APP) processing plays an important role in $A{\beta}$ production, which initiates synaptic and neuronal damage. ${\delta}-Catenin$ is known to be bound to presenilin-1 (PS-1), which is the main component of the ${\gamma}-secretase$ complex that regulates APP cleavage. Because PS-1 interacts with both APP and ${\delta}-catenin$, it is worth studying their interactive mechanism and/or effects on each other. Our immunoprecipitation data showed that there was no physical association between ${\delta}-catenin$ and APP. However, we observed that ${\delta}-catenin$ could reduce the binding between PS-1 and APP, thus decreasing the PS-1 mediated APP processing activity. Furthermore, ${\delta}-catenin$ reduced PS-1-mediated stabilization of APP. The results suggest that ${\delta}-catenin$ can influence the APP processing and its level by interacting with PS-1, which may eventually play a protective role in the degeneration of an Alzheimer's disease patient.