• Transactions of the Korean Society of Mechanical Engineers A
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• v.41 no.7
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• pp.621-627
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• 2017

The understanding of the mechanical properties of amyloid fibers, which induce various neurodegenerative diseases, is directly related to the amyloid growth mechanism. Diverse studies have been performed on amyloid fibers from the viewpoint of disease epidemiology. Recently, attempts have been made to use amyloid fibers as new materials because of their notable mechanical properties and self-aggregation abilities. In this study, the mechanical properties of transthyretin (TTR105-115), which induces cardiovascular disease, were evaluated using a molecular dynamics (MD) simulation. In particular, the effect of the end-terminal capping on the structural stability of TTR105-115 was evaluated. The mechanical behavior and properties of TTR105-115 were measured by steered molecular dynamics (SMD). We clarified the factors affecting the mechanical properties of these materials and suggested the possibility of utilizing them as nature inspired materials.

• Biomedical Science Letters
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• v.24 no.4
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• pp.418-425
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• 2018

Amyloid brain positron emission tomography (PET) images are visually and subjectively analyzed by the physician with a lot of time and effort to determine the ${\beta}$-Amyloid ($A{\beta}$) deposition. We designed a convolutional neural network (CNN) model that predicts the $A{\beta}$-positive and $A{\beta}$-negative status. We performed 18F-florbetaben (FBB) brain PET on controls and patients (n=176) with mild cognitive impairment and Alzheimer's Disease (AD). We classified brain PET images visually as per the on the brain amyloid plaque load score. We designed the visual geometry group (VGG16) model for the visual assessment of slice-based samples. To evaluate only the gray matter and not the white matter, gray matter masking (GMM) was applied to the slice-based standard samples. All the performance metrics were higher with GMM than without GMM (accuracy 92.39 vs. 89.60, sensitivity 87.93 vs. 85.76, and specificity 98.94 vs. 95.32). For the patient-based standard, all the performance metrics were almost the same (accuracy 89.78 vs. 89.21), lower (sensitivity 93.97 vs. 99.14), and higher (specificity 81.67 vs. 70.00). The area under curve with the VGG16 model that observed the gray matter region only was slightly higher than the model that observed the whole brain for both slice-based and patient-based decision processes. Amyloid brain PET images can be appropriately analyzed using the CNN model for predicting the $A{\beta}$-positive and $A{\beta}$-negative status.

• The Journal of Korean Physical Therapy
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• v.33 no.3
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• pp.136-141
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• 2021

Purpose: Dementia is a disease in which cognitive function declines, leading to deterioration of body functions and activities of daily living. The purpose of this study is to explore the effects of dual-task training, including cognitive tasks, on cognitive and body function and β-amyloid levels in Alzheimer's dementia patients. Methods: 34 inpatients diagnosed with Alzheimer's dementia at a nursing hospital located in South Korea. The patients were randomly divided into a dual-task group (n=16) and a single-task group (n=18). Each group was trained for 30 minutes three times a week for eight weeks. The MMSE-K was used to measure the patients' cognitive function. To assess the patients' static balance ability, their LOS was measured using BioRescue. while dynamic balance was measured using the BBS. The 10MWT were conducted to evaluate the patients' walking ability. Blood analysis was performed to measure levels of β-amyloid. Results: Both groups exhibited statistically significant improvements in gait function after the training (p<0.05). The dual-task group exhibited statistically significant differences in cognitive function, static and dynamic balance function, and β-amyloid levels after training (p<0.05). A significant difference was observed between the two groups (p<0.05). Conclusion: Dual-task training were found to be effective in improving cognitive and bodily functioning and reducing β-amyloid levels in Alzheimer's dementia patients. Thus, this may be suggested as an effective exercise method for the treatment and early prevention of Alzheimer's dementia.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.11a
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• pp.191-191
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• 2002

• Bulletin of the Korean Chemical Society
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• v.35 no.11
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• pp.3369-3372
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• 2014

• Bulletin of the Korean Chemical Society
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• v.30 no.6
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• pp.1237-1238
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• 2009

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.94-94
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• 2002

• Bulletin of the Korean Chemical Society
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• v.29 no.12
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• pp.2331-2336
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• 2008

• Journal of the Korean Applied Science and Technology
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• v.37 no.3
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• pp.409-417
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• 2020

The purpose of this study was to investigate the effects of different types of exercise training on ẞ-Amyloid, Brain-Derived Nerurotrophic Factor(BDNF) and cognitive function in mice with Diabetes Mellitus Group(DM.G). 24 male C57BL/6 mice were randomly assigned to the control (C.G. n = 6) and Diabetes Mellitus Group(DM.G. n = 18) groups. After the Diabetes Mellitus induction period, the DM group was subdivided into DM.G. + sedentary (DM.G., n = 6), DM.G. + endurance exercise (A.G, n = 6), and DM.G. + resistance exercise (R.G., n = 6). The A.G. and R.G performed treadmill and ladder climbing exercises 5 times per week for 8 weeks, respectively. After 8 weeks the results are as follows: ẞ-Amyloid showed higher levels of DM.G. than in A.G., R.G., and C.G., but was not statistically significant(p>.05). BDNF was significantly lower in DM.G. than in C.G., A.G., and R.G.(p <0.05). The Y-maze task performance for cognitive function was significantly lower in DM.G. than in C.G., A.G., and R.G.(p <0.05). These results predict that diabetes can negatively affect ẞ-Amyloid, BDNF and cognitive function. It can also be predicted that low-intensity exercise can positively improve ẞ-Amyloid, BDNF and cognitive function regardless of the type of exercise.

• BMB Reports
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• v.42 no.9
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• pp.541-551
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• 2009

Amyloidogenesis defines a condition in which a soluble and innocuous protein turns to insoluble protein aggregates known as amyloid fibrils. This protein suprastructure derived via chemically specific molecular self-assembly process has been commonly observed in various neurodegenerative disorders such as Alzheimer's, Parkinson's, and Prion diseases. Although the major culprit for the cellular degeneration in the diseases remains unsettled, amyloidogenesis is considered to be etiologically involved. Recent recognition of fibrillar polymorphism observed mostly from in vitro amyloidogeneses may indicate that multiple mechanisms for the amyloid fibril formation would be operated. Nucleation-dependent fibrillation is the prevalent model for assessing the self-assembly process. Following thermodynamically unfavorable seed formation, monomeric polypeptides bind to the seeds by exerting structural adjustments to the template, which leads to accelerated amyloid fibril formation. In this review, we propose another in vitro model of amyloidogenesis named double-concerted fibrillation. Here, two consecutive assembly processes of monomers and subsequent oligomeric species are responsible for the amyloid fibril formation of $\alpha$-synuclein, a pathological component of Parkinson's disease, following structural rearrangement within the oligomers which then act as a growing unit for the fibrillation.