• The Journal of Internal Korean Medicine
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• v.27 no.1
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• pp.253-264
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• 2006

Object: This research investigated effects of Jujadokseo-hwan on mice with Alzheimer's Disease induced by $amyloid-{\beta}$. According to Dongyibogam, Jujadokseo-hwan can cure amnesia. Amyloid-B is believed to induce oxidative stress and inflammation in the brain, postulated to play important roles in the pathogenesis of Alzheimer's disease. In this way $Amyloid-{\beta}$ induces Alzheimer's Disease. Methods : In order to make an efficient prescription and cope with dementia, learning and memory functions of mice were tested on passive avoidance test and V-maze task. $NF-{\kappa}B$ were measured from protein derived from the brain. RT-PCR was done for !gene analysis. Primers were protein kinase Band $NGF-{\alpha}$. Results : 1. Jujadokseo-hwan was effective for memory capacity on passive avoidance test. but noneffective for spatial memory capacity and locomotor activity on Y -maze task. 2. The measurement of $NF-{\kappa}B$ showed upward tendancies and the result of RT-PCR showed up-regulation when given Jujadokseo-hwan by mouth. Conclusion: Results suggest that Jujadokseo-hwan is effective on mice with Alzheimer's Disease induced by $amyloid-{\beta}$.

• Journal of Ginseng Research
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• v.31 no.1
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• pp.51-53
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• 2007

Ginseng shows protective and trophic effects in neurodegenerative diseases in experimental models, and showed cognitive improvement in normal population. To investigate the efficacy of ginseng in patients with Alzheimer's disease, patients, who met NINDS-ADRDA criteria for AD were studied Subjects were randomly assigned to ginseng group and control group, and ginseng group was treated with Korean white ginseng powder (4.5 g/day) for 12 weeks. Efficacy variables included changes in mini-mental status exam (MMSE) and cognitive subscales of Alzheimer's disease assessment scale (ADAS-cog) at 4 weeks and 12 weeks. Baseline MMSE and ADAS scores showed no difference between the two groups. Results showed that ginseng improved ADAS-cog compared to the control group at 12 weeks (p<0.05). MMSE was also increased by ginseng treatment compared to the control at 12 weeks (p<0.01). This study suggests the symptomatic efficacy of ginseng in patients with Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
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• v.17 no.2
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• pp.91-122
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• 2006

Objective : This research investigates the effect of the Jangwon-Dan,(JWD) on Alzheimer's disease. Method : The effects of the JWN extract on (1) $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) amyloid precursor proteins(APP), acetylcholinesterase(AChE), and glial fibrillary acidic protein(GFAP) mRNA, the AChE activity and the APP production of PC-12 cell treated with CT-105; (3) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, $IL-1{\beta}$ mRNA, and $TNF-{\alpha}$ mRNA, (5) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. Result : 1. The JWN extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in THP-1 cells treated with LPS. 2. The JWN extract suppressed the expression of APP, AChE, and GFAP mRNA in PC-12 cells treated with CT-105. 3. The JWN extract suppressed the AChE activity, and the production of APP significantly in PC-12 cells treated with CT-105. 4. For the JWN extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 5. The JWN extract suppressed the over-expression of $IL-1{\beta}$ protein, $TNF-{\alpha}$ protein, MDA, $IL-1{\beta}$ mRNA, $TNF-{\alpha}$ mRNA, and CD68/GFAP, in the mice with Alzheimer's disease induced by ${\beta}A$. 6. The JWN extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusion : These results suggest that the JWN extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the JWN extract for Alzheimer's disease is suggested for future research.

• Journal of Oriental Neuropsychiatry
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• v.17 no.1
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• pp.37-57
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• 2006

Objective : This research investigates the effect of the CMT and MCMT on Alzheimer‘s disease. Methods : The effects of the CMT and MCMT extract on (1) amyloid precursor proteins(APP), acetylcholinesterase(AChE) mRNA of PC-12 cells treated with CT-105; (2) the AChE activity and the APP production of PC-12 cell treated with CT-105; (3) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, GFAP, CD68 abd CD11b; (5) the infarction area of the hippocampus in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. Results : 1. The CMT and MCMT extract suppressed the expression of APP, AChE, and mRNA in PC-12 cells treated with CT-105. 2. The CMT and MCMT extract suppressed the AChE activity, and the production of APP significantly in PC-12 cells treated with CT-105. 3. For the CMT and MCMT extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 4. The CMT and MCMT extract suppressed the over-expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, GFAP, CD68 abd CD11bCD68/GFAP, in the mice with Alzheimer's disease induced by ${\beta}A$. 5. The CMT and MCMT extract reduced the infarction area of hippocampus with Alzheimer's disease induced by ${\beta}A$ 6. The MCMT showed more excellent effects than CMT in the every experiments except PC-12 cells. Conclusions : These results suggest that the CMT and MCMT extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the CMT and MCMT extract for Alzheimer's disease is suggested for future research.

• The Journal of Korean Medicine
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• v.28 no.2 s.70
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• pp.137-154
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• 2007

Objective : This experiment was designed to investigate the effect of the GYZB hot water extract & ultra-fine powder on the Alzheimer's disease model induced by amyloid ${\beta}$ protein (${\beta}A$). Method : We measured the effects of the GYZB hot water extract on expression of $IL-1{\beta}$, IL-6 mRNA and production of IL-6, $TNF-{\alpha}$ in the BV2 microglial cell line treated with lipopolysaccharide (LPS). The effects of the GYZB hot water extract & ultra-fine powder on (1) the behavior, (2) expression of $IL-1{\beta}$ and $TNF-{\alpha}$, (3) glucose in serum, (4) the infarction area of the hippocampus, and brain tissue injury in mice induced with Alzheimer's diseased by ${\beta}A$ were investigated. Results : The GYZB hot water extract suppressed the expression of $IL-1{\beta}$ and IL-6 mRNA and significantly suppressed the production of IL-6 and $TNF-{\alpha}$ in the BV2 microglial cell line treated with LPS. The GYZB hot water extract & ultra-fine powder showed a significant inhibitory effect on the memory deficit of the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency and distance movement-through latency. The GYZB ultra-fine powder significantly suppressed the expression of $IL-1{\beta}$ and $TNF-{\alpha}$ protein, and the GYZB hot water extract significantly suppressed the expression of $TNF-{\alpha}$ protein in the microglial cell of mice with Alzheimer's disease induced by ${\beta}A$. The GYZB hot water extract & ultra-fine powder reduced the infarction area of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusions : These results suggest that GYZB hot water extract & ultra-fine powder may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of GYZB for Alzheimer's disease is suggested for future research.

• Journal of Oriental Neuropsychiatry
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• v.18 no.2
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• pp.101-132
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• 2007

Objective : This research investigates the effect of the NogYongDaeBoTang,(NYDBT) on Alzheimer's disease. Method : The effects of the NYDBT extract on (1) $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) acetylcholinesterase(AChE), amyloid precursor proteins(APP), and glial fibrillary acidic protein(GFAP) mRNA the AChE activity and the APP production of PC-12 cell treated with CT-105; (3) the behavior; (4) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, $IL-1{\beta}$ mRNA, and $TNF-{\alpha}$ mRNA; (5) the infarction area of the hippocampus, and brain tissue injury in Alzheimer‘s diseased mice induced with ${\beta}A$ were investigated. Results : 1. The NYDBT extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in BV2 microglia cell line treated with LPS. 2. The NYDBT extract suppressed the expression of $IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ protein production in BV2 microglia cell line treated with LPS. 3. For the NYDBT extract group a significant inhibitory effect on the memory deficit was shown for the mice with Alzheimer's disease induced by $A{\beta}$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 4. The NYDBT extract suppressed the over-expression of $IL-1{\beta}$ protein, $TNF-{\alpha}$ protein, MDA, and CD68/CD11b, in the mice with Alzheimer's disease induced by $A{\beta}$. 5. The NYDBT extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by $A{\beta}$. 6. The NYDBT extract reduced the Tau protein, GFAP protein, and presenilin1/2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by $A{\beta}$. Conclusions : These results suggest that the NYDBT extract may be effective for the prevention and treatment of Alzheimer's disease.

• Journal of Oriental Neuropsychiatry
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• v.16 no.1
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• pp.97-117
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• 2005

This research investigates the effect of the Chaenomelis fructus(CMF) on Alzheimer's disease. Specifically, the effects of the CMF extract on (1) >$IL-1{\beta}$, IL-6, and $TNF-{\alpha}$ mRNA of PC-12 cells treated with LPS; (2) amyloid precursor proteins(APP), acetylcholinesterase(AChE), and glial fibrillary acidic protein(GFAP) mRNA of PC-12 cells treated with CT-105; (3) the AChE activity and the APP production of PC-12 cell treated with CT-105; (4) the behavior of AD mice with ${\beta}A$; (5) expression of $IL-1{\beta}$, $TNF-{\alpha}$, MDA, $IL-1{\beta}$ mRNA, $TNF-{\alpha}$ mRNA, and ROS; (6) the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}A$ were investigated. The results were summarized as follows; 1. The CMF extract suppressed the expression of $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNA in THP-1 cells treated with LPS. 2. The CMF extract suppressed the expression of APP, AChE, and GFAP mRNA in PC-12 cells treated with CT-105. 3. The CMF extract suppressed the AChE activity, and the production of APP significantly in PC-12 cells treated with CT-105. 4. A significant inhibitory effect on the memory deficit was shown on the CMF extract group of the mice with Alzheimer's disease induced by ${\beta}A$ in the Morris water maze experiment, which measured stop-through latency, and distance movement-through latency. 5. The CMF extract suppressed the over-expression of $IL-1{\beta}$ protein, $TNF-{\alpha}$ protein, MDA, $IL-1{\beta}$ protein, mRNA, $TNF-{\alpha}$ mRNA, CD68/GFAP, and ROS in the mice with Alzheimer's disease induced by ${\beta}A$. 6. The CMF extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer’s disease induced by ${\beta}A$. These results suggest that the CMF extract may be effective for the treatment of Alzheimer’s disease. Investigation into the clinical use of the CMF extract for Alzheimer's disease is suggested for future research.

• Journal of the Korean Society of Radiology
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• v.10 no.5
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• pp.307-312
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• 2016

Alzheimer's disease is the most common degenerative brain diseases that causes dementia. ${\beta}$-amyloid neuritic plaque density that accumulates in the brain is difficult to perform daily living, such as memory loss, language ability deterioration. It is used to estimate ${\beta}$-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's disease and other causes of cognitive impairment. Using the $^{18}F$-Florbetaben with high sensitivity and specificity for the ${\beta}$-amyloid neuritic plaque density to evaluate the usefulness for the early diagnosis of Alzheimer's disease. In $^{18}F$-FDG Brain imaging shows no specific findings. And it appeared on the MR-Brain imaging without atrophy of the hippocampus. However, the intake of ${\beta}$-amyloid neuritic plaque density in $^{18}F$-Florbetaben informs that it is the progress of Alzheimer's disease. Therefore, $^{18}F$-Florobetaben is very useful for early diagnosis of Alzheimer's disease.

• Korean Journal of Plant Resources
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• v.20 no.4
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• pp.325-330
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• 2007

This study was conducted to investigate the effect of the mixed extract of P. ginseng C.A. Mey. and C. sinensis K. (Gin-CHF) on the infarction area of hippocampus in the mice with Alzheimer's disease induced by ${\beta}-amyloid({\beta}A)$. The Gin-CHF extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. The Gin-CHF extract reduced the Tau protein, GFAP protein, and presenilin1/presenilin2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. These results suggest that the Gin-CHF extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the Gin-CHF extract for Alzheimer's disease is suggested for further research.

• Journal of Dental Anesthesia and Pain Medicine
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• v.17 no.4
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• pp.271-280
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• 2017

Background: The number of patients with Alzheimer's disease is growing worldwide, and the proportion of patients requiring dental treatment under general anesthesia increases with increasing severity of the disease. However, outpatient anesthesia management for these patients involves great risks, as most patients with Alzheimer's disease are old and may show reduced cardiopulmonary functions and have cognitive disorders. Methods: This study retrospectively investigated 43 patients with Alzheimer's disease who received outpatient anesthesia for dental treatment between 2012-2017. Pre-anesthesia patient evaluation, dental treatment details, anesthetics dose, blood pressure, duration and procedure of anesthesia, and post-recovery management were analyzed and compared between patients who underwent general anesthesia or intravenous sedation. Results: Mean age of patients was about 70 years; mean duration of Alzheimer's disease since diagnosis was 6.3 years. Severity was assessed using the global deterioration scale; 62.8% of patients were in level ${\geq}6$. Mean duration of anesthesia was 178 minutes for general anesthesia and 85 minutes for intravenous sedation. Mean recovery time was 65 minutes. Eleven patients underwent intravenous sedation using propofol, and 22/32 cases involved total intravenous anesthesia using propofol and remifentanil. Anesthesia was maintained with desflurane for other patients. While maintaining anesthesia, inotropic and atropine were used for eight and four patients, respectively. No patient developed postoperative delirium. All patients were discharged without complications. Conclusion: With appropriate anesthetic management, outpatient anesthesia was successfully performed without complications for dental treatment for patients with severe Alzheimer's disease.