• Nutrition Research and Practice
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• 제13권1호
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• pp.64-69
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• 2019

BACKGROUND/OBJECTIVES: Alzheimer's disease is a neurodegenerative disease that induces symptoms such as a decrease in motor function and cognitive impairment. Increases in the aggregation and deposition of amyloid beta protein ($A{\beta}$) in the brain may be closely correlated with the development of Alzheimer's disease. In this study, the effects of an adzuki bean extract on the aggregation of $A{\beta}$ were examined; moreover, the anti-Alzheimer's activity of the adzuki extract was examined. MATERIALS/METHODS: First, we undertook thioflavin T (ThT) fluorescence analysis and transmission electron microscopy (TEM) to evaluate the effect of an adzuki bean extract on $A{\beta}_{42}$ aggregation. To evaluate the effects of the adzuki extract on the symptoms of Alzheimer's disease in vivo, $A{\beta}_{42}$-overexpressing Drosophila were used. In these flies, overexpression of $A{\beta}_{42}$ induced the formation of $A{\beta}_{42}$ aggregates in the brain, decreased motor function, and resulted in cognitive impairment. RESULTS: Based on the results obtained by ThT fluorescence assays and TEM, the adzuki bean extract inhibited the formation of $A{\beta}_{42}$ aggregates in a concentration-dependent manner. When $A{\beta}_{42}$-overexpressing flies were fed regular medium containing adzuki extract, the $A{\beta}_{42}$ level in the brain was significantly lower than that in the group fed regular medium only. Furthermore, suppression of the decrease in motor function, suppression of cognitive impairment, and improvement in lifespan were observed in $A{\beta}_{42}$-overexpressing flies fed regular medium with adzuki extract. CONCLUSIONS: The results reveal the delaying effects of an adzuki bean extract on the progression of Alzheimer's disease and provide useful information for identifying novel prevention treatments for Alzheimer's disease.

• 한국산학기술학회논문지
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• 제20권5호
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• pp.241-251
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• 2019

본 연구에서는 Alzheimer's disease(AD) 마우스 모델에서 미세전류의 적용을 통한 인지능력 개선 효과를 확인하였다. ICR 마우스에 amyloid beta($A{\beta}$)를 뇌 내 주입하여 인지능력 손상을 유도한 후, 4가지 파형의 미세전류를 각각 적용하여 손상된 인지능력에 미치는 미세전류의 영향을 검토하였다. AD 마우스의 공간 및 물체 인지능력을 확인하기 위해 행동실험을 실시한 결과, novel object recognition test와 Morris water maze test에서 $A{\beta}$로 인해 손상되었던 인지능력이 미세전류 적용군에서 유의적으로 개선됨을 확인하였으며, 지질과산화 반응으로 인한 malondialdehyde의 뇌 내 생성량 또한 감소하였다. 뇌 조직에서 AD 관련 단백질 발현을 측정한 결과, 특히 미세전류 Wave4 [STEP FORM 파형(0, 1.5, 3, 5V), 중첩Hz 적용] 적용군에서 $A{\beta}$ 생성 관련 단백질인 ${\beta}$-secretase, presenilin 1, presenilin 2의 발현이 감소하였고 신경영양인자인 brain-derived neurotrophic factor 단백질 발현이 증가하였다. 이 결과를 바탕으로 AD 마우스에서 미세전류를 이용한 손상된 인지능력에 대한 개선 효과를 확인하였으며, AD 예방 및 치료를 위한 비약물적인 방법으로서 적용할 수 있을 것으로 기대된다.

• Molecules and Cells
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• 제42권1호
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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.

• 동의생리병리학회지
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• 제18권1호
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• pp.254-259
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• 2004

Jeongshin-tang (JST) is a Korean herbal prescription, which has been successfully applied for the various neuronal diseases. However, it's effect remains unknown in experimental models. To investigate the biological effect of JST in Alzheimer's disease (AD) in vitro model, we analized the production of interleukin (IL)-6 and IL-8, and expression of cyclooxygenase (COX)-2 in IL-1β plus β-amyloid [25-35] fragment (A)-stimulated human astrocytoma cell line U373MG. JST alone had no effect on the cell viability. The production of IL-6 and IL-8 was significantly inhibited by pretreatment with JST (1mg/㎖) on IL-1β plus A-stimulated U373MG cells. Maximal inhibition rate of IL-6 and IL-8 production by JST was about 41.22% (P<0.01) and 34.45% (P<0.05), respectively. The expression level of COX-2 protein was up-regulated by IL-1β plus A but the increased level of COX-2 was inhibited by pretreatment with JST (1 mg/㎖). These data indicate that JST has a regulatory effect on cytokine production and COX-2 expression, which might explain it's beneficial effect in the treatment of AD.

• Journal of Ginseng Research
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• 제41권4호
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• pp.566-571
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• 2017

Background: A number of reports have described the protective effects of ginsenoside Rg1 (Rg1) in Alzheimer's disease (AD). However, the protective mechanisms of Rg1 in AD remain elusive. Methods: To investigate the potential mechanisms of Rg1 in ${\beta}$-amyloid peptide-treated SH-SY5Y cells, a comparative proteomic analysis was performed using stable isotope labeling with amino acids in cell culture combined with nano-LC-MS/MS. Results: We identified a total of 1,149 proteins in three independent experiments. Forty-nine proteins were significantly altered by Rg1 after exposure of the cells to ${\beta}$-amyloid peptides. The protein interaction network analysis showed that these altered proteins were clustered in ribosomal proteins, mitochondria, the actin cytoskeleton, and splicing proteins. Among these proteins, mitochondrial proteins containing HSD17B10, AARS2, TOMM40, VDAC1, COX5A, and NDUFA4 were associated with mitochondrial dysfunction in the pathogenesis of AD. Conclusion: Our results suggest that mitochondrial proteins may be related to the protective mechanisms of Rg1 in AD.

• 동의신경정신과학회지
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• 제19권1호
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• pp.29-42
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• 2008

Objectives : This study was performed to examine the effect of Sinchim on enhancing of memory in rat with water maze. Methods : Experimental animals(white rat) were classfied into normal, control, and aroma sample group. Then, they were injected .{\beta}-amyloid into control and aroma sample group rat's brain about $5{\mu}l$ to injure its brain. After rat smelt Sinchim about 12days, I did water maze test and anatomized its hippocampus. Sections were cut coronally at 30 ${\mu}m$.(XI00) Results: 1. In acquisition test of water maze learning, .{\beta}-amyloid injured group took more time than normal group to reach the escape platform noticeably and through the session of trial, Sinchim aroma sample group shortened time than .l3-amyloid injured group after 6 days. 2. In the acetyltransferase(AchE) immunostained method, it was shown that Sinchim aroma sample recovered tbe syntbesis of ChAT(Choloneacetyltransferase). Conclusion: Smelling Sinchim would be useful for enhancing of memory.

• Bulletin of the Korean Chemical Society
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• 제28권7호
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• pp.1231-1234
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• 2007

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 2007년도 추계 학술대회
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• pp.70-70
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• 2007

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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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)

• 동의신경정신과학회지
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• 제18권3호
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• pp.55-82
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• 2007

Ohjective: This research investigates the effect of the DJR on Alzheimer's disease. Method: 1.The effects of the DJR extract on IL.-$1{\beta}$, IL-6, TNF-${\alpha}$, cox-2, and NOS-II mRNA of BV2 microglia cell line treated with LPS; 2. the behavior: 3. the infarction area of the hippocampus, and brain tissue injury in Alzheimer's diseased mice induced with ${\beta}$A were investigated. Result: 1. The DJR extract suppressed the expression of IL-$1{\beta}$, IL-6 and TNF-${\alpha}$ mRNA in BV2 microglia cell line treated with LPS. 2. The DJR 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 DJR 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 Moms water maze experiment, which measured stop-through latency, and distance movement-through latency. 4. The DJR extract suppressed the over-expression of IL-$1{\beta}$ protein, TNF-${\alpha}$ protein and CD68/CD11b, in the mice with Alzheimer's disease induced by ${\beta}$A 5. The DJR 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. 6. The DJR extract reduced the tau protein, GFAP protein, and presenilin1/2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by ${\beta}$A. Conclusion: These results suggest that the DJR extract may he effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the DJR extract for Alzheimer's disease of suggested for future research.