• Journal of Physiology & Pathology in Korean Medicine
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• v.20 no.1
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• pp.138-148
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• 2006

This research investigated the effect of the CMT and SCMT on Alzheimer's disease. The effects of the CMT and SCMT extract on expression of proinflammatory cytokine(IL-$1{\beta}$, IL-6, TNF-$\alpha$) in the THP-1 cell; amyloid precursor proteins(APP), acetylcholinesterase(AChE) mRNA of PC-12 cells treated with CT105; the AChE activity and the APP production of PC-12 cell lysate treated with CT105 were investigated. The CMT and SCMT extract suppressed overexpression of IL-$1{\beta}$, IL-6, TNF-$\alpha$ in the THP-1 cell treated dy LPS; the expression of APP, AChE mRNA in PC-12 cells treated with CT105; the AChE activity and the production of APP in PC-12 cell Iysate treated with CT105 significantly. This study suggest that CMT and SCMT may be effective for the prevention and treatment of Alzheimer's disease.

• 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.

• Journal of Multimedia Information System
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• v.8 no.4
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• pp.233-242
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• 2021

Various anatomical MRI imaging biomarkers for Alzheimer's Disease (AD) identification have been recognized so far. Cortical and subcortical volume, hippocampal, amygdala volume, and genetics patterns have been utilized successfully to diagnose AD patients from healthy. These fundamental sMRI bio-measures have been utilized frequently and independently. The entire possibility of anatomical MRI imaging measures for AD diagnosis might thus still to analyze fully. Thus, in this paper, we merge different structural MRI imaging biomarkers to intensify diagnostic classification and analysis of Alzheimer's. For 54 clinically pronounce Alzheimer's patients, 58 cognitively healthy controls, and 99 Mild Cognitive Impairment (MCI); we calculated 1. Cortical and subcortical features, 2. The hippocampal subfield, amygdala nuclei volume using Freesurfer (6.0.0) and 3. Genetics (APoE ε4) biomarkers were obtained from the ADNI database. These three measures were first applied separately and then combined to predict the AD. After feature combination, we utilize the sequential feature selection [SFS (wrapper)] method to select the top-ranked features vectors and feed them into the Multi-Kernel SVM for classification. This diagnostic classification algorithm yields 94.33% of accuracy, 95.40% of sensitivity, 96.50% of specificity with 94.30% of AUC for AD/HC; for AD/MCI propose method obtained 85.58% of accuracy, 95.73% of sensitivity, and 87.30% of specificity along with 91.48% of AUC. Similarly, for HC/MCI, we obtained 89.77% of accuracy, 96.15% of sensitivity, and 87.35% of specificity with 92.55% of AUC. We also presented the performance comparison of the proposed method with KNN classifiers.

• BMB Reports
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• v.55 no.12
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• pp.621-626
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• 2022

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease characterized by the degeneration of motor neurons in the spinal cord. Main symptoms are manifested as weakness, muscle loss, and muscle atrophy. Some studies have reported that alterations in sphingolipid metabolism may be intimately related to neurodegenerative diseases, including ALS. Acid sphingomyelinase (ASM), a sphingolipid-metabolizing enzyme, is considered an important mediator of neurodegenerative diseases. Herein, we show that ASM activity increases in samples from patients with ALS and in a mouse model. Moreover, genetic inhibition of ASM improves motor function impairment and spinal neuronal loss in an ALS mouse model. Therefore, these results suggest the role of ASM as a potentially effective target and ASM inhibition may be a possible therapeutic approach for ALS.

• Journal of Integrative Natural Science
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• v.16 no.2
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• pp.61-67
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• 2023

Human body ages differently due to environmental, genetic and pathological factors. DNA methylation patterns also differs depending on various factors such as aging and several other diseases. The aging clock model, which uses these differences to predict age, analyzes DNA methylation patterns, recognizes age-specific patterns, predicts age, and grasps the speed and degree of aging. Aging occurs in everyone and causes various problems such as deterioration of physical ability and complications. Alzheimer's disease is a disease associated with aging and the most common brain degenerative disease. This disease causes various cognitive functions disabilities such as dementia and impaired judgment to motor functions, making daily life impossible. It has been reported that the incidence and progression of this disease increase with aging, and that increased phosphorylation of Aβ and tau proteins, which are overexpressed in this disease and accelerates epigenetic aging. It has also been reported that DNA methylation is significantly increased in the hippocampus and entorhinal cortex of Alzheimer's disease patients. Therefore, we calculated the biological age using the Epi clock, a pan-tissue aging clock model, and confirmed that the epigenetic age of patients suffering from Alzheimer's disease is lower than their actual age. Also, it was confirmed to slow down aging.

• Korean Journal of Biological Psychiatry
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• v.22 no.2
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• pp.40-46
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• 2015

Neuroglial cells are fundamental for brain homeostasis and defense to intrinsic or extrinsic changes. Loss of their function and over-reactivity to stimuli contribute to the aging of brain. Alzheimer's disease (AD) could be caused by more dramatic response in neuroglia associated with various chemokines and cytokines. Neuroglia of the AD brain shares some phenotypes with aging neuroglia. In addition, neuroglial activation and neuroinflammation are commonly showed in neurodegeneration. Thus neuroglia would be a promising target for therapeutics of AD.

• Korean Journal of Biological Psychiatry
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• v.6 no.2
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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.

• Proceedings of the Korean Institute of Electrical and Electronic Material Engineers Conference
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• 2010.06a
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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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.2
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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.

• Speech Sciences
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• v.15 no.2
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• pp.111-118
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• 2008

We identified the characteristic impairmants of linguistic semantic memory in patients with prodromal Alzheimer's disease(AD) and mild AD. To elucidate the earliest changes of semantic language function in subjects with AD, performances on confrontation naming test and verbal fluency task were compared among patients with AD patients (n=20), mild AD patients (n=27) and healthy elderly controls (n=20). Tasks in this study included the confrontation naming test of Test of Lexical Processing in Aphasia(TLPA/Japanese) and one-minute verbal fluency task (semantic/ phonetic categories). The results were as follows: 1) Performances of the prodromal AD group showed the comparable to those of the control group on the confrontation naming test, 2) In the semantic/phonetic verbal fluency tasks, the performances of the control group were better than those of the prodromal AD and mild AD groups, but no significant differences were shown between the prodromal AD and the mild AD group.