• Title/Summary/Keyword: Alzheimer's disease${\beta}$-amyloid

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Effects of Jujadokseo-hwan on Mice with Alzheimer's Disease Induced by $Amyloid-{\beta}$ (주자독서환(朱子讀書丸)의 아밀로이드베타로 유발된 생쥐 알츠하이머모델에 대한 효과)

  • Leem, Kang-Hyun;Ko, Heung;Kyung, Hyuk-Su
    • 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 $amyloid-{\beta}$.

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[ ${\beta}-Amyloid$ ] Imaging Probes (베타아밀로이드 영상용 프로브)

  • Jeong, Jae-Min
    • Nuclear Medicine and Molecular Imaging
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    • v.41 no.2
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    • pp.112-117
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    • 2007
  • Imaging distribution of ${\beta}-amyloid$ plaques in Alzheimer's disease is very important for early and accurate diagnosis. Early trial of the ${\beta}-amyloid$ plaques includes using radiolabeled peptides which can be only applied for peripheral ${\beta}-amyloid$ plaques due to limited penetration through the blood brain barrier (BBB). Congo red or Chrysamine G derivatives were labeled with Tc-99m for imaging ${\beta}-amyloid$ plaques of Alzheimer patient's brain without success due to problem with BBB penetration. Thioflavin T derivatives gave breakthrough for ${\beta}-amyloid$ imaging in vivo, and a benzothiazole derivative [C-11]6-OH-BTA-1 brought a great success. Many other benzothiazole, benzoxazole, benzofuran, imidazopyridine, and styrylbenzene derivatives have been labeled with F-18 and I-123 to improve the imaging quality. However, [C-11]6-OH-BTA-1 still remains as the best. However, short half-life of C-11 is a limitation of wide distribution of this agent. So, it is still required to develop an Tc-99m, F-18 or I-123 labeled agent for ${\beta}-amyloid$ imaging agent.

A Comparative Study of [F-18] Florbetaben (FBB) PET Imaging, Pathology, and Cognition between Normal and Alzheimer Transgenic Mice

  • Thapa, Ngeemasara;Jeong, Young-Jin;Kang, Hyeon;Choi, Go-Eun;Yoon, Hyun-Jin;Kang, Do-Young
    • Biomedical Science Letters
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    • v.25 no.1
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    • pp.7-14
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    • 2019
  • Alzheimer's disease (AD) is highly prevalent in dementia, with no specifically effective treatment having yet been discovered. Amyloid plaques are one of the key hallmarks of AD. Transgenic mouse models exhibiting Alzheimer's disease-like pathology have been widely used to study the pathophysiology of Alzheimer's disease. In this study, we showed an age-dependent correlation between cognitive function, pathological findings, and [F-18] Florbetaben (FBB) PET images. Nineteen transgenic mice (12 with AD, 7 with controls) were used for this study. We observed an increase in ${\beta}$-Amyloid deposition ($A{\beta}$) in brain tissue and [F-18] FBB amyloid PET imaging in the AD group. The [F-18] FBB data showed a mildly negative trend with cognitive function. Pathological findings were negatively correlated with cognitive functions. These finding suggests that amyloid beta deposition can be well-monitored with [F-18] FBB PET and a decline in cognitive function is related to the increase in amyloid plaque burden.

Inhibitory potency of Acetylcholinesterase and Amyloid beta(1-42) peptide aggregation to the Extracts of Enthusiasm Reducing herbals (청열약 추출물들의 아세틸콜린에스테라제 저해와 베타아밀로이드 펩티드 응집 억제 효능)

  • Kwon, Young-Ee
    • Korean Journal of Pharmacognosy
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    • v.38 no.4
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    • pp.308-311
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    • 2007
  • Inhibition of acetylcholinesterase and amyloid beta(1-42) peptide is good drug targets for Alzheimer's disease therapeutics. Among the twenty enthusiasm reducing herbals, the 70% methanol extracts (1 mg/ml) of Moutan Radicis Cortex and Forsythiae Fructus showed 91.5% and 85.3% about acethylcholinesterase inhibition, respectively. The extracts (1 mg/ml) of Coptidis Rhizoma and Paeoniae Radix Rubra showed more than 85% inhibition rate against amyloid beta (1-42) peptide aggregation. The neuroprotective effect of the extracts (1 mg/ml) of Moutan Radicis Cortex, Forsythiae Fructus and Paeoniae Radix Rubra showed 90.0%, 87.4% and 85.1% to compare with amyloid beta (1-42) peptide treated cells (IMR-32), respectively. Three herbs, Moutan Radicis Cortex, Forsythiae Fructus and Paeoniae Radix Rubra are promising candidates from natural products for development of Alzheimer's disease therapeutics.

Usefulness of 18F-Florbetaben in Alzheimer's Disease Diagnosis (알츠하이머병 진단에서 18F-Florbetaben의 유용성)

  • Lee, Hyo-Yeong;Im, In-Chul;Song, Min-jae;Shin, Seong-gyu
    • 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.

Vaccinium uliginosum L. Improves Amyloid β Protein-Induced Learning and Memory Impairment in Alzheimer's Disease in Mice

  • Choi, Yoon-Hee;Kwon, Hyuck-Se;Shin, Se-Gye;Chung, Cha-Kwon
    • Preventive Nutrition and Food Science
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    • v.19 no.4
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    • pp.343-347
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    • 2014
  • The present study investigated the effects of Vaccinium uliginosum L. (bilberry) on the learning and memory impairments induced by amyloid-${\beta}$ protein ($A{\beta}P$) 1-42. ICR Swiss mice were divided into 4 groups: the control ($A{\beta}40$-1A), control with 5% bilberry group ($A{\beta}40$-1B), amyloid ${\beta}$ protein 1-42 treated group ($A{\beta}1$-42A), and $A{\beta}1$-42 with 5% bilberry group ($A{\beta}1$-42B). The control was treated with amyloid ${\beta}$-protein 40-1 for placebo effect, and Alzheimer's disease (AD) group was treated with amyloid ${\beta}$-protein 1-42. Amyloid ${\beta}$-protein 1-42 was intracerebroventricular (ICV) micro injected into the hippocampus in 35% acetonitrile and 0.1% trifluoroacetic acid. Although bilberry added groups tended to decrease the finding time of hidden platform, no statistical significance was found. On the other hand, escape latencies of $A{\beta}P$ injected mice were extended compared to that of $A{\beta}40$-1. In the Probe test, bilberry added $A{\beta}1$-42B group showed a significant (P<0.05) increase of probe crossing frequency compared to $A{\beta}1$-42A. Administration of amyloid protein ($A{\beta}1$-42) decreased working memory compared to $A{\beta}40$-1 control group. In passive avoidance test, bilberry significantly (P<0.05) increased the time of staying in the lighted area compared to AD control. The results suggest that bilberry may help to improve memory and learning capability in chemically induced Alzheimer's disease in experimental animal models.

The Effects of Daejo-hwan(DJR) on the Alzheimer's Disease Model Induced by ${\beta}$-amyloid. (대조환(大造丸) 추출물이 ${\beta}$-amyloid로 유도된 Alzheimer's disease 병태(病態)모델에 미치는 영향)

  • Lee, Ji-In;Chung, Dae-Kyoo
    • Journal of Oriental Neuropsychiatry
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    • v.18 no.3
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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.

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Amyloid pore-channel hypothesis: effect of ethanol on aggregation state using frog oocytes for an Alzheimer's disease study

  • Parodi, Jorge;Ormeno, David;Paz, Lenin D. Ochoa-de la
    • BMB Reports
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    • v.48 no.1
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    • pp.13-18
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    • 2015
  • Alzheimer's disease severely compromises cognitive function. One of the mechanisms to explain the pathology of Alzheimer's disease has been the hypotheses of amyloid-pore/channel formation by complex $A{\beta}$-aggregates. Clinical studies suggested the moderate alcohol consumption can reduces probability developing neurodegenerative pathologies. A recent report explored the ability of ethanol to disrupt the generation of complex $A{\beta}$ in vitro and reduce the toxicity in two cell lines. Molecular dynamics simulations were applied to understand how ethanol blocks the aggregation of amyloid. On the other hand, the in silico modeling showed ethanol effect over the dynamics assembling for complex $A{\beta}$-aggregates mediated by break the hydrosaline bridges between Asp 23 and Lys 28, was are key element for amyloid dimerization. The amyloid pore/ channel hypothesis has been explored only in neuronal models, however recently experiments suggested the frog oocytes such an excellent model to explore the mechanism of the amyloid pore/channel hypothesis. So, the used of frog oocytes to explored the mechanism of amyloid aggregates is new, mainly for amyloid/pore hypothesis. Therefore, this experimental model is a powerful tool to explore the mechanism implicates in the Alzheimer's disease pathology and also suggests a model to prevent the Alzheimer's disease pathology.

Thiolated Protein A-functionalized Bimetallic Surface Plasmon Resonance Chip for Enhanced Determination of Amyloid Beta 42

  • Kim, Hyung Jin;Kim, Chang-Duk;Sohn, Young-Soo
    • Applied Chemistry for Engineering
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    • v.30 no.3
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    • pp.379-383
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    • 2019
  • The capability of detecting amyloid beta 42 ($A{\beta}42$), a biomarker of Alzheimer's disease, using a thiolated protein A-functionalized bimetallic surface plasmon resonance (SPR) chip was investigated. An optimized configuration of a bimetallic chip containing gold and silver was obtained through calculations in the intensity measurement mode. The surface of the SPR bimetallic chip was functionalized with thiolated protein A for the immobilization of $A{\beta}42$ antibody. The response of the thiolated protein A-functionalized bimetallic chip to $A{\beta}42$ in the concentration range of 50 to 1,000 pg/mL was linear. Compared to protein A without thiolation, the thiolated protein A resulted in greater sensitivity. Therefore, the thiolated protein A-functionalized bimetallic SPR chip can be used to detect very low concentrations of the biomarker for Alzheimer's disease.

Non-Fibrillar $\beta$-Amyloid Exerts Toxic Effect on Neuronal Cells

  • Kim, Hyeon-Jin;Hong, Seong-Tshool
    • Animal cells and systems
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    • v.5 no.2
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    • pp.139-143
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    • 2001
  • Alzheimer's disease is the most common form of dementia and no cure is known so far. Extensive genetic works and in vitro experiments combined with clinical observations link amyloid $\beta$--protein (A$\beta$-) to the pathogenesis of Alzheimer's disease (AD). It was hypothesized that $A\beta$- becomes toxic when it adopts a fibrillar conformation. Recently, non-fibrillar form of $A\beta$- was observed and the potential role in the pathogenesis of AD became an interesting subject. In this study, the cytotoxicity of non-fibrillar $A\beta$- and fibrillar $A\beta$- was compared on oxidative stress, membrane damage, or nucleosome break down. Non-fibrillar $A\beta$- was not toxic in peripheral nervous system-derived cells but significantly toxic in central nervous system-derived cells while fibrillar $A\beta$- was non-selectively toxic in both cell culture. The neurotoxicity of non-fibrillar $A\beta$- was reproduced in semi-in vivo culture of mouse brain slice. In conclusion, non-fibrillar $A\beta$- could be more relevant to the selective neurodegeneration in Alzheimer's brains than fibrillar $A\beta$- and further research needs to be done for identification of the cause of AD.

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