• 제목/요약/키워드: amyloid ${\beta}$

검색결과 431건 처리시간 0.029초

자기 비드를 이용한 알츠하이머병 조기 진단 방법에 대한 연구 (Alzheimer Disease Diagnosis using Magnetic Bead)

  • 채철주;조정민;강재민;김관수;송기봉
    • 한국전기전자재료학회:학술대회논문집
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    • 한국전기전자재료학회 2010년도 하계학술대회 논문집
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    • pp.219-219
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    • 2010
  • In a past, the method in which it used the fluorescent material or it analyzes a gene was used in order to detect the Alzheimer's disease. However, in this paper, the magnetic bead is used in order to detect the Alzheimer's disease. The 'magnetic bead used in this paper is able to make the amyloid-beta and the selective binding known as cause of the Alzheimer's disease.

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알츠하이머 조기 진단을 위한 변형된 대식세포의 기초적 연구 (Primary Cellular Study of Phagocytosis for Alzheimer Disease Diagnosis)

  • 조정민;채철주;강재민;김관수;송기봉
    • 한국전기전자재료학회:학술대회논문집
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    • 한국전기전자재료학회 2010년도 하계학술대회 논문집
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    • pp.280-280
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    • 2010
  • Alzheimer disease is a progressive neurodegenerative disease of the aged, characterized by memory loss and dementia. For diagnosis of Alzheimer disease we have simply modified macrophage with amyloid beta bonded with different molecules. Modified Macrophage was observed with microscope for co-localization of amyloid beta molecule. For this experiment we used fluoroscene labeling substances. The macrophage was modified also with cell staining method. For cell staining method was used avidin-biotin reaction principles. All experiments were carried out on poly-L-lysine coated and sterilized glass substrates. In the presentation we will show the further investigations and applications with modified macrophage.

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PRESENILIN-2 MUTATION ALTERS NEURITE EXTENTION, APOPTOSIS AND TRANSCRIPTION FACTOR(NF-KB) ACTIVATION

  • Seong, Min Je;Song, Youn Sook;Shin, Im chul;Park, Cheol Beom;Oh, Ki Wan;Lee, Myung Koo;Kim, Young Ku;Hwang, Dae Hyun;Chung, Soo Youn
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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    • pp.109-109
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    • 2002
  • Alzheimer's disease (AD) is characterized by $\beta$-amyloid deposition and associated with loss of neuron cells in brain regions involved in learning and memory process. Many cases of early onset autosomal dominant inherited forms of AD are caused by mutation in the genes encoding presenilin-2 (PS-2).(omitted)

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Green Tea Catechin Causes an Weight Loss in Transgenic Mice Over-expressing Carboxyl Terminus of Amyloid Precusor Protein

  • Lim Hwa-J.;Kim Yong-K.;Sheen Yhun-Y.
    • Biomolecules & Therapeutics
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    • 제14권2호
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    • pp.96-101
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    • 2006
  • Amyloid$\beta(A{\beta})$ has been reported have an effect on the induction of oxidative stress that involves the functional and structural abnormalities in Alzheimer's disease. As a role of a radical scavenger, a green tea treatment was found have some inhibitory effect on the neurodegenerative process. The aim of this study was to determine if green tea catechin (GTC) reduces in transgenic model. To test this, transgenic mice carrying neuronspecific enolase (NSE) controlled C-terminus (105) of APP (APP-C105) were created and treated them with a low ana high dose of GTC for 6 months. Herein, we conclude that transgenic mice expressing NSE/APP-C105 were successfully created and the GTC-treated group exhibited significant reduction in body weight. Thus, GTC might be a good prevention of obesity or good treatment for AD patient.

수면과 알츠하이머 치매의 관계 (Relationship Between Sleep and Alzheimer's Dementia)

  • 이경환;김호찬
    • 수면정신생리
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    • 제29권1호
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    • pp.1-3
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    • 2022
  • Sleep is associated with Alzheimer's dementia. Many previous researches have shown that inadequate sleep is one of the risk factors that predict Alzheimer's dementia. The causal mechanism of this association is not clear. Slow wave sleep and REM sleep are critical stages in memory consolidation, and by sequential hypothesis both stages are important. Deposition of amyloid beta and tau, the main pathology of Alzheimer's dementia, are also associated with sleep. This review provides the association of sleep and Alzheimer's dementia, and future research is necessary to examine the specific mechanism of this association between sleep and Alzheimer's dementia, which may lead to an early intervention in sleep.

[ $A_1$ ] Receptor-mediated Protection against Amyloid Beta-induced Injury in Human Neuroglioma Cells

  • Cho, Yong-Woon;Jung, Hyun-Ju;Kim, Yong-Keun;Woo, Jae-Suk
    • The Korean Journal of Physiology and Pharmacology
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    • 제11권2호
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    • pp.37-43
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    • 2007
  • Adenosine has been reported to provide cytoprotection in the central nervous systems as well as myocardium by activating cell surface adenosine receptors. However, the exact target and mechanism of its action still remain controversial. The present study was performed to examine whether adenosine has a protective effect against $A{\beta}$-induced injury in neuroglial cells. The astrocyte-derived human neuroglioma cell line, A172 cells, and $A{\beta}_{25{\sim}35}$ were employed to produce an experimental $A{\beta}$-induced glial cell injury model. Adenosine significantly prevented $A{\beta}$-induced apoptotic cell death. Studies using various nucleotide receptor agonists and antagonists suggested that the protection was mediated by $A_1$ receptors. Adenosine attenuated $A{\beta}$-induced impairment in mitochondrial functional integrity as estimated by cellular ATP level and MTT reduction ability. In addition, adenosine prevented $A{\beta}$-induced mitochondrial permeability transition, release of cytochrome c into cytosol and subsequent activation of caspase-9. The protective effect of adenosine disappeared when cells were pretreated with 5-hydroxydecanoate, a selective blocker of the mitochondrial ATP-sensitive $K^+$ channel. In conclusion, therefore we suggest that adenosine exerts protective effect against $A{\beta}$-induced cell death of A172 cells, and that the underlying mechanism of the protection may be attributed to preservation of mitochonarial functional integrity through opening of the mitochondrial ATP-sensitive $K^+$ channels.

Engelhardtia chrysolepis의 라디칼 소거능 및 신경세포의 산화 스트레스 보호효과 (Radical Scavenging Effect and Neuroprotective Activity from Oxidative Stress of Engelhardtia chrysolepis Leaf)

  • 김은정;이아영;최수연;서혜린;이영아;조은주
    • 생약학회지
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    • 제47권3호
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    • pp.251-257
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    • 2016
  • In this study, the radical scavenging activity and protective effect of ethanol extract from leaf of Engelhardtia chrysolepis HANCE (ECE) against oxidative stress were investigated under in vitro and cellular system. ECE showed strong radical scavenging activities in 1,1-diphenyl-2-picrylhydrazyl, hydroxyl(${\cdot}OH$) and nitric oxide(NO) radical as a concentration-dependent manner. Particularly, strong scavenging activity against the ${\cdot}OH$ and NO radical were observed with the $IC_{50}$ value of $1.30{\mu}g/ml$ and $12.61{\mu}g/ml$, respectively. Furthermore, the cellular oxidative stress was induced by amyloid beta($A{\beta}_{25-35}$) in C6 glial cells. The treatment of $A{\beta}_{25-35}$ to C6 glial cells generated high levels of reactive oxygen species(ROS) and declined cell viability. However, production of ROS was decreased by the treatment of ECE. In addition, the cell viability was significantly increased at each concentration(10, 25, $50{\mu}g/ml$) as dose-dependent manner. The Alzheimer's disease-related protein expressions in $A{\beta}_{25-35}$-treated C6 glial cells were analyzed. The ECE treatment inhibited expression of amyloid precursor protein(APP), C-terminal fragment-${\beta}(CTF-{\beta})$, ${\beta}$-site APP cleaving enzyme(BACE), phosphorylated tau(p-tau) proteins in C6 glial cells induced by $A{\beta}_{25-35}$. The present study indicated that ECE has strong radical scavenging activity and neuroprotective effect through attenuating oxidative stress.

알쯔하이머 치매의 동물모형 (Animal Models of Alzheimer's Dementia)

  • 우성일
    • 생물정신의학
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    • 제6권2호
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    • pp.149-152
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    • 1999
  • Transgenic mice models of Alzheimer's disease were produced by overexpressing APP(amyloid precursor protein) mutant and presenilin mutant genes using the promotors that induced neuronal expression. The neuropathologies, electrophysiological changes and behavioral changes that were demonstrated in these transgenic mice models were amyloid changes, gliotic changes, A-beta increases, deficit in LTP(long-term potentiation) and behavioral changes. Some or all of the above changes were found in each transgenic mice model. These models generally showed amyloid neuropathology but they usually lacked the neurofibrillary tangles. So, they can be regarded as partial models of Alzheimer's disease. The development of them is undoubtedly the great progress toward future research.

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