• Journal of Physiology & Pathology in Korean Medicine
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• v.29 no.1
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• pp.39-45
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• 2015

This experiment was designed to investigate the effect of Added Chongmyung-tang (ACM) on Alzheimer's disease mouse model. Effects of ACM on learning behavior were investigated using the Morris water maze method. Expression levels of molecular factors related to Alzheimer's disease such as glial fibrillary acidic protein (GFAP), cluster of differentiation antigen 68 (CD68), and tau protein in the hippocampus of APP-SWE Tg2576 mice were analyzed by immunofluorescence staining method. ACM reduced escape latency in the Morris water maze test. ACM decreased the expression level of GFAP and tau protein in the hippocampus. These results suggest that ACM may be involved in regulating molecules that are known to play an important role in the pathogenesis of Alzheimer's disease.

• Journal of Physiology & Pathology in Korean Medicine
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• v.36 no.1
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• pp.11-17
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• 2022

In this study, we investigated the effects of Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng extracts (FRG) on cognitive function in scopolamine-induced memory-impaired mice. We measured the effects of G, R, and FRG on the improvement of memory and cognition via behavior analysis. In addition, we measured the acetylcholinesterase (AChE) activity in the hippocampus of each group of mice. The expression of β-amyloid, Tau, and BDNF in the brain tissues were observed through immunohistochemical staining. Ginseng Radix (G) and Fermented red-ginseng (FRG) have effectively improved cognitive function in the water maze test. Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) have improved the willingness of mice to explore the new environment, as confirmed by Y maze test. In addition, immunohistochemical staining revealed that Ginseng Radix (G) decreased the expression of β-amyloid and Tau in the hippocampus. In addition, fermented red-ginseng (FRG) increased the expression of BDNF. Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) have decreased the concentration of acetylcholinesterase in the hippocampus as compared with the control group of mice. In conclusion, Ginseng Radix (G), Rehmanniae Radix (R), and Fermented red-ginseng (FRG) are considered to have the potential for development as candidate drugs to control the progression of Alzheimer's disease (AD).

• Biomedical Science Letters
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• v.27 no.4
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• pp.208-215
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• 2021

The purpose of this study was to explain the pathology of Alzheimer's disease (AD) and to investigate the correlation between AD and microRNA. AD is the most common type of dementia, accounting for about 80% of all types of dementia, causing dysfunction in various daily activities such as memory loss, cognitive impairment, and behavioral impairment. The typical pathology of AD is explained by the accumulation of beta-amyloid peptide plaques and neurofibrillary tangles containing hyperphosphorylated tau protein. On the other hand, microRNA is small non-coding RNA 22~23 nucleotides in length that binds to the 3' untranslated region of messenger RNA to inhibit gene expression. Many reports explain that microRNAs found in circulating biofluids are abundant in the central nervous system, are involved in the pathogenic mechanism of AD, and act as important factors for early diagnosis and therapeutic agents of AD. Therefore, this paper aims to clarify the correlation between AD and microRNA. In this review, the basic mechanism of miRNAs is described, and the regulation of miRNAs in the pathological processes of AD are highlighted. Furthermore, we suggest that miRNA-based system in development of therapeutic and diagnostic agents of AD can be a promising tool.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.3
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• pp.633-642
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• 2003

A pain is the symptom which defends against noxious stimulus about a human body, it is known that if the periphery of perceptive nerve were stimulated by a physical or chemical factors, the stimulation is induced by transmission to pain center in the cerebral cortex according to pain conduction tract. The treatment of pain is to decrease a stimulus that causes a pain or block off a nerve transmitting a stimulus or puts on a way to calm down pain center, but It is for adjustment of a pain to be the most representative in acupuncture among various ways to cure a pain in Oriental medicine. However, the analgesic effect of an individual response to acupuncture stimulation shows marked individual variations, so these days genetic a few approach is attempted. On this the author determined that the responding group was appointed those whose tail flick latency (TFL) responding time delayed the minimum of 30 % comparing with basal reaction time. For those whose TFL time had shorter than 30 % was grouped as a non-responding group. And then the hypothalamus of each group was dissected and RNA was further purified. After synthesizing cDNA using oligo dT primer, products were finally applied to the PCR. The results were as follows; The ratio of responding group to non-responding group was 6:4. Ach T (acetylcholinesterase T subunit), BF-I (Brain factor-I), DBH (Dopamine β-hydroxylase) and PNM (Phosphotidylethanolamine N-Methyltransferase) were revealed significantly in the responding group. Cathepsin B and Tau were revealed significantly in the non-responding group. The PCR results show that Ach T, BF-I, DBH and PNM are expressed abundantly in the responding group, where as cathepsin B and tau are abundant in the non-responding group. These results suggest that the analgesic effect on acupuncture stimulation is related to regulation of neurotransmitter as well as neurodegeration of cerebrum.

• Journal of the Korean Society of Radiology
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• v.81 no.3
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• pp.488-500
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• 2020

Accumulating evidence suggests that Alzheimer's disease (AD) is not only caused by accumulation of abnormal proteins, including amyloid and tau, but is also closely associated with abnormalities in the microvascular environment including the blood-brain barrier (BBB), both of which lead to neuroinflammation and neurodegeneration. Application of in vivo magnetic resonance imaging (MRI) has recently increased to assess BBB permeability in AD and related diseases. Here, we provide a narrative review of BBB permeability-related pathology in Alzheimer dementia and recent MRI research on BBB permeability changes in AD and related diseases. Furthermore, we briefly introduce the measurement of BBB permeability using MRI and its methodological issues.

• BMB Reports
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• v.52 no.12
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• pp.679-688
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• 2019

The decrease of metabolism in the brain has been observed as the important lesions of Alzheimer's disease (AD) from the early stages of diagnosis. The cumulative evidence has reported that the failure of mitochondria, an organelle involved in diverse biological processes as well as energy production, maybe the cause or effect of the pathogenesis of AD. Both amyloid and tau pathologies have an impact upon mitochondria through physical interaction or indirect signaling pathways, resulting in the disruption of mitochondrial function and dynamics which can trigger AD. In addition, mitochondria are involved in different biological processes depending on the specific functions of each cell type in the brain. Thus, it is necessary to understand mitochondrial dysfunction as part of the pathological phenotypes of AD according to each cell type. In this review, we summarize that 1) the effects of AD pathology inducing mitochondrial dysfunction and 2) the contribution of mitochondrial dysfunction in each cell type to AD pathogenesis.

• Tuberculosis and Respiratory Diseases
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• v.47 no.3
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• pp.347-355
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• 1999

Background: Phospholipase C(PLC) plays a central role in cellular signal transduction and is important in cellular growth, differentiation and transformation. There are currently ten known mammalian isozymes of PLC reported to this date. Hydrolysis of phosphatidylinositol 4,5-bisphosphate($PIP_2$) by PLC produces two important second messengers, inositol 1,4,5-trisphosphate($IP_3$) and diacylglycerol. PLC-${\gamma}1$, previously, was known to be activated mainly through growth factor receptor tyrosine kinase. Other mechanisms of activating PLC-yl have been reported such as activation through tau protein in the presence of arachidonic acid in bovine brain and activation by $IP_3$, phosphatidic acid, etc. Very recently, another PLC-${\gamma}1$ activator protein such as tau has been found in bovine lung tissue, which now is considered to be AHNAK protein. But there has been no report concerning AHNAK and its associated disease to this date. In this study, we examined the expression of the PLC-${\gamma}1$ activator, AHNAK, in lung cancer specimens and their paired normal. Methods: From surgically resected human lung cancer tissues taken from twenty-eight patients and their paired normal counterparts, we evaluated expression level of AHNAK protein using immunoblot analysis of total tissue extract Immunohistochemical stain was performed with primary antibody against AHNAK protein. Results: Twenty-two among twenty-eight lung cancer tissues showed overexpression of AHNAK protein (eight of fourteen squamous cell lung cancers, all of fourteen adenocarcinomas). The resulting bands were multiple ranging from 70 to 200 kDa in molecular weight and each band was indistinct and formed a smear, reflecting mobility shift mainly due to proteolysis during extraction process. On immunohistochemistry, lung cancer tissues showed a very heavy, dense staining with anti-AHNAK protein antibody as compared to the surrounding normal lung tissue, coresponding well with the results of the western blot Conclusion: The overexpression of PLC-${\gamma}1$ activator protein, AHNAK in lung cancer may provide evidence that the AHNAK protein and PLC-${\gamma}1$ act in concerted manner in carcinogenesis.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.4
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• pp.299-310
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• 2020

Alzheimer's disease (AD) is a multi-faceted neurodegenerative disease. Thus, current therapeutic strategies require multitarget-drug combinations to treat or prevent the disease. At the present time, single drugs have proven to be inadequate in terms of addressing the multifactorial pathology of AD, and multitarget-directed drug design has not been successful. Based on these points of views, it is judged that combinatorial drug therapies that target several pathogenic factors may offer more attractive therapeutic options. Thus, we explored that the combination therapy with lower doses of cilostazol and aripiprazole with add-on donepezil (CAD) might have potential in the pathogenesis of AD. In the present study, we found the superior efficacies of donepezil add-on with combinatorial mixture of cilostazol plus aripiprazole in modulation of expression of AD-relevant genes: Aβ accumulation, GSK-3β, P300, acetylated tau, phosphorylated-tau levels, and activation of α-secretase/ADAM 10 through SIRT1 activation in the N2a Swe cells expressing human APP Swedish mutation (N2a Swe cells). We also assessed that CAD synergistically raised acetylcholine release and choline acetyltransferase (CHAT) expression that were declined by increased β-amyloid level in the activated N2a Swe cells. Consequently, CAD treatment synergistically increased neurite elongation and improved cell viability through activations of PI3K, BDNF, β-catenin and α7-nicotinic cholinergic receptors in neuronal cells in the presence of Aβ_1-42. This work endorses the possibility for efficient treatment of AD by supporting the synergistic therapeutic potential of donepezil add-on therapy in combination with lower doses of cilostazol and aripiprazole.

• Research in Plant Disease
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• v.29 no.1
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• pp.64-71
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• 2023

In October 2021, soft rot disease seriously affected radish crop in Dangjin, Chungcheongnam-do, Korea. The infected radishes were stunted and turned dark green, with yellowish leaf foliage. A slimy, wet, and decayed pith region was observed in the infected roots. The bacterial strain KNUB-03-21 was isolated from infected roots. The biochemical and morphological characteristics of the isolate were similar to those of Pectobacterium brasiliense. Phylogenetic analysis based on the sequences of the 16S rRNA region and the concatenated DNA polymerase III subunit tau (dnaX), leucine-tRNA ligase (leuS), and recombinase subunit A (recA) genes confirmed that the isolate is a novel strain of P. brasiliense. Artificial inoculation of radish with P. brasiliense KNUB-03-21 resulted in soft rot symptoms similar to those observed in infected radish in the field; subsequently, P. brasiliense KNUB-03-21 was reisolated and reidentified. To our knowledge, this is the first report of P. brasiliense as a causal pathogen of radish soft rot in Korea.

• Dementia and Neurocognitive Disorders
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• v.17 no.4
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• pp.163-173
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• 2018

Background and Purpose: Behavioral variant frontotemporal dementia (bvFTD) is a subtype of frontotemporal dementia, which has clinical symptoms of progressive personality and behavioral changes with deterioration of social cognition and executive functions. The pathology of bvFTD is known to be tauopathy or TDP-43 equally. We analyzed the $^{18}F-THK5351$ positron emission tomography (PET) scans, which were recently developed tau PET, in patients with clinically-diagnosed bvFTD. Methods: Forty-eight participants, including participants with behavioral variant frontotemporal dementia (bvFTD, n=3), Alzheimer's disease (AD, n=21) and normal cognition (NC, n=24) who completed 3T magnetic resonance images, $^{18}F-THK5351$ PET scans, and detailed neuropsychological tests were included in the study. Voxel-wise statistical analysis and region of interest (ROI)-based analyses were performed to evaluate the retention of THK in bvFTD patients. Results: In the voxel-based and ROI-based analyses, patients with bvFTD showed greater THK retention in the prefrontal, medial frontal, orbitofrontal, anterior cingulate, insula, anterior inferior temporal and striatum regions compared to NC participants. Left-right asymmetry was noted in the bvFTD patients. A patient with extrapyramidal symptoms showed much greater THK retention in the brainstem. Conclusions: The distribution of THK retention in the bvFTD patients was mainly in the frontal, insula, anterior temporal, and striatum regions which are known to be the brain regions corresponding to the clinical symptoms of bvFTD. Our study suggests that $^{18}F-THK5351$ PET imaging could be a supportive tool for diagnosis of bvFTD.