• Title/Summary/Keyword: Amyloid

검색결과 626건 처리시간 0.029초

Phagocytic Roles of Glial Cells in Healthy and Diseased Brains

  • Jung, Yeon-Joo;Chung, Won-Suk
    • Biomolecules & Therapeutics
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    • 제26권4호
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    • pp.350-357
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    • 2018
  • Glial cells are receiving much attention since they have been recognized as important regulators of many aspects of brain function and disease. Recent evidence has revealed that two different glial cells, astrocytes and microglia, control synapse elimination under normal and pathological conditions via phagocytosis. Astrocytes use the MEGF10 and MERTK phagocytic pathways, and microglia use the classical complement pathway to recognize and eliminate unwanted synapses. Notably, glial phagocytosis also contributes to the clearance of disease-specific protein aggregates, such as ${\beta}$-amyloid, huntingtin, and ${\alpha}$-synuclein. Here we reivew recent findings showing that glial cells are active regulators in brain functions through phagocytosis and that changes in glial phagocytosis contribute to the pathogenesis of various neurodegenerative diseases. A better understanding of the cellular and molecular mechanisms of glial phagocytosis in healthy and diseased brains will greatly improve our current approach in treating these diseases.

Isolation of 6,6'-Bieckol from Grateloupia elliptica and its Antioxidative and Anti-Cholinesterase Activity

  • Lee, Bong Ho;Choi, Byoung Wook;Lee, Soo Young
    • Ocean and Polar Research
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    • 제39권1호
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    • pp.45-49
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    • 2017
  • During the search for anticholinesterase compounds from marine organisms, we were able to isolate 6,6'-bieckol from a red alga, Grateloupia elliptica. This compound showed moderate acetylcholinesterase (AChE) inhibitory activity in a micromole range ($IC_{50}$ $44.5{\mu}M$). However, for butyrylcholinesterase (BuChE), a new target for the treatment of Alzheimer's disease (AD), it showed particularly potent inhibitory activity ($IC_{50}$ $27.4{\mu}M$), which is more potent compared to AChE. It also inhibits BACE-1, a new target for reducing the generation of ${\beta}-amyloid$.

Isolated Tricuspid Regurgitation: Initial Manifestation of Cardiac Amyloidosis

  • Yoon, Dong Woog;Park, Byung-Jo;Kim, In Sook;Jeong, Dong Seop
    • Journal of Chest Surgery
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    • 제48권6호
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    • pp.422-425
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    • 2015
  • Amyloid deposits in the heart are not exceptional in systemic amyloidosis. The clinical manifestations of cardiac amyloidosis may include restrictive cardiomyopathy, characterized by progressive diastolic and eventually systolic biventricular dysfunction; arrhythmia; and conduction defects. To the best of our knowledge, no previous cases of isolated tricuspid regurgitation as the initial manifestation of cardiac amyloidosis have been reported. We describe a rare case of cardiac amyloidosis that initially presented with severe tricuspid regurgitation in a 42-year-old woman who was successfully treated with tricuspid valve replacement. Unusual surgical findings prompted additional evaluation that established a diagnosis of plasma cell myeloma.

인삼(人蔘), 목과(木瓜) 추출액이 Alzheimer성 치매의 병태(病態) 모델에 미치는 영향 (Effects of a Mixture Ginseng Radix, Chaenomelis Fructus on the Mice Model of Alzheimer's Disease)

  • 한신희;길기정
    • 대한본초학회지
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    • 제22권1호
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    • pp.41-48
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    • 2007
  • Objectives : This research was investigated the effect of the Ginseng Radix plus Chaenomelis Fructus on Alzheimer's disease. Methods : Specifically, the effects of the Ginseng Radix plus Chaenomelis Fructus extract on $IL-1{\beta}$, $TNF-{\alpha}$ of BV2 microglia cell line treated with lipopolysacchride. Results : The Ginseng Radix plus Chaenomclis Fructus 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 ${\beta}$ amyloid peptide. Conclusion: These results suggest that the Ginseng Radix plus Chaenomelis Fructus extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the Ginseng Radix plus Chaenomelis Fructus extract for Alzheimer's disease is suggested for future research.

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The Role of Autophagy in Systemic Metabolism and Human-Type Diabetes

  • Kim, Jinyoung;Lim, Yu-Mi;Lee, Myung-Shik
    • Molecules and Cells
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    • 제41권1호
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    • pp.11-17
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    • 2018
  • Autophagy is critical for the maintenance of organelle function and intracellular nutrient environment. Autophagy is also involved in systemic metabolic homeostasis, and its dysregulation can lead to or accelerate the development of metabolic disorders. While the role of autophagy in the global metabolism of model organisms has been investigated mostly using site-specific genetic knockout technology, the impact of dysregulated autophagy on systemic metabolism has been unclear. Here, we review recent papers showing the role of autophagy in systemic metabolism and in the development of metabolic disorders. Also included are data suggesting the role of autophagy in human-type diabetes, which are different in several key aspects from murine models of diabetes. The results shown here support the view that autophagy modulation could be a new modality for the treatment of metabolic syndrome associated with lipid overload and human-type diabetes.

1,8-cineole protected human lipoproteins from modification by oxidation and glycation and exhibited serum lipid-lowering and anti-inflammatory activity in zebrafish

  • Cho, Kyung-Hyun
    • BMB Reports
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    • 제45권10호
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    • pp.565-570
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    • 2012
  • We recently reported that a water extract of laurel or turmeric, 1,8-cineole enriched fractions, showed hypolipidemic activity in the zebrafish model. Therefore, the present study investigated the cineole's anti-oxidant and anti-inflammatory activities in lipoprotein metabolism in vitro and in vivo. Cineole had inhibitory effects on cupric ion-mediated oxidation of lipoproteins in general, while simultaneously enhancing ferric ion removal ability in high-density lipoprotein (HDL). Hypercholesterolemia was induced in zebrafish using cholesterol-feeding treatment, 4% cholesterol, for 3 weeks. After feeding with or without the addition of cineole, the results revealed that cineole possessed lipid-lowering and anti-inflammatory activities in hypercholesterolemic zebrafish. In addition, serum amyloid A and interleukin-6 levels were lowered and lipid accumulation was decreased in the liver. Conclusively, 1,8-cineole was found to have anti-oxidant activities in lipoprotein metabolism both in vitro and in vivo with simultaneous reduction of lipid accumulation in the liver of zebrafish.

삼령백출산(蔘笭白朮散)이 Alzheimer's Disease 동물모델의 Astrocyte 활성화 및 Apoptosis에 미치는 영향 (Effect of Samryungbaikchul-san on Astrocyte Activation and Apoptosis in Mouse Model of Alzheimer Disease)

  • 이상룡
    • 동의생리병리학회지
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    • 제23권2호
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    • pp.374-380
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    • 2009
  • Samryungbaikchul-san(SRBCS) has been used in oriental medicine for the treatments of gastrointestinal and neurological disorders. Here, potential protective function of SRBCS was investigated in neural tissues in Alzheimer's disease(AD) mouse model. In primary cultured cells from the spinal cord of newborn rats, treatment of ${\beta}$-amyloid peptide elevated cell counts positive to glial fibrillary acidic protein(GFAP) or caspase 3 immunoreactivity, but the co-treatment of SRBCS reduced positive cell counts. In vivo administration of scopolamine, an inhibitor of muscarinic receptor, resulted in increases in the number of glial fibrillary acidic protein(GFAP) and caspase 3-positive cells in hippocampal subfields, which was then decreased by the treatment of SRBCS or acetylcholinesterase inhibitor galathamine. The present data suggest that SRBCS may play a protective role in damaged neural tissues caused by scopolamine treatments in mice.

Presenilin-2 mutation perturbs ryanodine receptor-mediated calcium homeostasis, caspase-3 activation and increases vulnerability of PC12 cells

  • Hwang, In-Young;Shin, Im-Chul;Hwang, Dae-Youn;Kim, Young-Kyu;Yang, Ki-Hwa;Ha, Tae-Yeol;Hong, Jin-Tae
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2003년도 춘계학술대회 논문집
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    • pp.73-74
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    • 2003
  • Familial form of Alzheimer's disease (FAD) is caused by mutations in presenilin-1 and presenilin-2 (PS2). PS1 and PS2 mutation are known to similar effects on the production of amyloid $\beta$ peptide (A$\beta$) and cause of cell death in the Alzheimer's brain. The importance of the alternation of calcium homeostasis in the neuronal cell death by PS1 mutation in a variety of experimental system has been demonstrated. (omitted)

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INCREASE OF INTRACELLULAR $CA^{2+}$ AND CYTOTOXICITY INDUCED BY NEURO-TOXICANTS IN PC12 CELLS CARRYING MUTANT PRESENILIN-2

  • Shin, Im-Chul;Hwang, In-Young;Song, Youn-Sook;Park, Cheol-Beom;Oh, Ki-Wan;Lee, Myung-Koo;Kim, Young-Kyu;Hong, Jin-Tae
    • 한국독성학회:학술대회논문집
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    • 한국독성학회 2002년도 Current Trends in Toxicological Sciences
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    • pp.111-111
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    • 2002
  • Many cases of early onset autosomal dominant inherited forms of Alzheimer's disease (AD) are caused by mutation in the genes encoding presenilin-2 (PS-2) on chromosome 1. It is characterized by amyloid deposition and associated with loss of neuron. However, molecular mechanisms underlying the role of PS-2 mutation in the pathogenic AD are not known.(omitted)

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