• Annals of Clinical Neurophysiology
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• v.23 no.1
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• pp.65-67
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• 2021

• Applied Chemistry for Engineering
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• v.32 no.1
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• pp.1-9
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• 2021

Alzheimer's disease (AD), an irreversible degenerative disorder, is associated with accumulation and aggregation of amyloid-β peptides, hyperphosphorylated tau proteins, and high level of metal ions in the brain. Up to date, there is no effective therapeutic agent to stop the progress of the disease and thus early and accurate diagnosis of AD has gained increasing attention in recent years. Among several diagnostic methods, an optical imaging using fluorescent probes is one of the most promising tools to visualize AD biomarkers. In this review, we will introduce fluorescent probes that can be applied to in vivo brain imaging of AD models and also their structure. It is expected that the present review will provide useful information to many scientists in the related research fields.

• Biomolecules & Therapeutics
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• v.28 no.2
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• pp.145-151
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• 2020

Alzheimer's disease (AD) is a devastating neurodegenerative disease and a major cause of dementia in elderly individuals worldwide. Increased deposition of insoluble amyloid β (Aβ) fibrils in the brain is thought be a key neuropathological hallmark of AD. Many recent studies show that natural products such as polyphenolic flavonoids inhibit the formation of insoluble Aβ fibrils and/or destabilize β-sheet-rich Aβ fibrils to form non-cytotoxic aggregates. In the present study, we explored the structure-activity relationship of naturally-occurring biflavonoids on Aβ amyloidogenesis utilizing an in vitro thioflavin T assay with Aβ1-42 peptide which is prone to aggregate more rapidly to fibrils than Aβ1-40 peptide. Among the biflavonoids we tested, we found amentoflavone revealed the most potent effects on inhibiting Aβ1-42 fibrillization (IC₅₀: 0.26 µM), as well as on disassembling preformed Aβ1-42 fibrils (EC₅₀: 0.59 µM). Our structure-activity relationship study suggests that the hydroxyl groups of biflavonoid compounds play an essential role in their molecular interaction with the dynamic process of Aβ1-42 fibrillization. Our atomic force microscopic imaging analysis demonstrates that amentoflavone directly disrupts the fibrillar structure of preformed Aβ1-42 fibrils, resulting in conversion of those fibrils to amorphous Aβ1-42 aggregates. These results indicate that amentoflavone affords the most potent anti-amyloidogenic effects on both inhibition of Aβ1-42 fibrillization and disaggregation of preformed mature Aβ1-42 fibrils.

• The Korean Journal of Physiology and Pharmacology
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• v.22 no.6
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• pp.689-696
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• 2018

Increasing evidence implicates changes in $[Ca^{2+}]_i$ and oxidative stress as causative factors in amyloid beta ($A{\beta}$)-induced neuronal cell death. Cyanidin-3-glucoside (C3G), a component of anthocyanin, has been reported to protect against glutamate-induced neuronal cell death by inhibiting $Ca^{2+}$ and $Zn^{2+}$ signaling. The present study aimed to determine whether C3G exerts a protective effect against $A{\beta}_{25-35}$-induced neuronal cell death in cultured rat hippocampal neurons from embryonic day 17 fetal Sprague-Dawley rats using MTT assay for cell survival, and caspase-3 assay and digital imaging methods for $Ca^{2+}$, $Zn^{2+}$, MMP and ROS. Treatment with $A{\beta}_{25-35}$ ($20{\mu}M$) for 48 h induced neuronal cell death in cultured rat pure hippocampal neurons. Treatment with C3G for 48 h significantly increased cell survival. Pretreatment with C3G for 30 min significantly inhibited $A{\beta}_{25-35}$-induced $[Zn^{2+}]_i$ increases as well as $[Ca^{2+}]_i$ increases in the cultured rat hippocampal neurons. C3G also significantly inhibited $A{\beta}_{25-35}$-induced mitochondrial depolarization. C3G also blocked the $A{\beta}_{25-35}$-induced formation of ROS. In addition, C3G significantly inhibited the $A{\beta}_{25-35}$-induced activation of caspase-3. These results suggest that cyanidin-3-glucoside protects against amyloid ${\beta}$-induced neuronal cell death by reducing multiple apoptotic signals.

• Journal of the Korean Society of Radiology
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• v.84 no.5
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• pp.1140-1145
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• 2023

Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels. It is a rare disease that mainly occurs in the elderly and is characterized by rapidly progressive dementia, headache, seizures, and focal neurologic deficits. CAA-RI can demonstrate characteristic brain MRI findings and can be reversed by steroids or other immunosuppressive therapies. Here, we report a case of CAA-RI, which was initially misdiagnosed as a subacute infarction but was diagnosed while reviewing follow-up brain MRI images, and spontaneous remission was achieved.

• Journal of Korea Multimedia Society
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• v.24 no.4
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• pp.519-527
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• 2021

Alzheimer's disease is one of the challenges to tackle in the coming aging era and is attempting to diagnose and predict through various biomarkers. While the application of various deep learning-based technologies as powerful imaging technologies has recently expanded across the medical industry, empirical design is not easy because there are various deep earning neural networks architecture and categorical hyperparameters that rely on problems and data to solve. In this paper, we show the possibility of optimizing a deep learning neural network structure and hyperparameters for Alzheimer's disease classification in amyloid brain images in a representative deep earning neural networks architecture using genetic algorithms. It was observed that the optimal deep learning neural network structure and hyperparameter were chosen as the values of the experiment were converging.

• Investigative Magnetic Resonance Imaging
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• v.15 no.1
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• pp.1-10
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• 2011

Pigmented villonodular synovitis, synovial chondromatosis, long-standing rheumatoid arthritis, hemophilic arthropathy, chronic tophaceous gout, amyloid arthropathy, tuberculous arthritis, and hemangioma are the synovial diseases showing low signal intensity on T2-weighted image. Synovial deposition of hemosiderin, urate, and amyloid and fibrosis or caseous necrosis of hypertrophied synovium are known as the pathologic causes of T2 signal intensity. Because of the low incidence of the synovial lesions showing T2 low signal intensity, recognition of these diseases would be helpful for the exact diagnosis.

• Journal of the Korean neurological association
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• v.36 no.4
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• pp.314-317
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• 2018

Focal subarachnoid hemorrhage occasionally presents as transient focal neurologic episodes mimicking transient ischemic attack (TIA). Unless properly diagnosed, it may aggravate cerebral hemorrhage by administering antithrombotic agents. Therefore, clinicians need to be aware that such focal subarachnoid hemorrhage sometimes cannot be detected on noncontrast computed tomography and blood-sensitive magnetic resonance imaging can detect even a small amount of hemorrhage. We describe an 85-year-old woman with focal subarachnoid hemorrhage and possible cerebral amyloid angiopathy who presented transient left arm weakness recurrently, which mimicked TIA.

• Journal of the Korean Society of Radiology
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• v.82 no.2
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• pp.429-434
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• 2021

Amyloidosis is a multisystemic disease characterized by the accumulation of abnormal proteins in extracellular spaces in various organs, with frequent involvement of the myocardium. We report a case of a patient who had cardiac amyloidosis with a trend of reduction in native T1 and T2 values and extracellular volume fraction on serial cardiac magnetic resonance imaging after chemotherapy and stem cell transplantation. The native T1 value and the extracellular volume fraction are closely associated with tissue amyloid burden in amyloidosis patients. This case demonstrated that cardiac magnetic resonance imaging may be used as a non-invasive and quantitative biomarker in the treatment monitoring of amyloidosis.

• Investigative Magnetic Resonance Imaging
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• v.24 no.2
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• pp.85-89
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• 2020

Amyloidosis is an all-inclusive disease of deposition of amyloid proteins in the extracellular spaces, which in localized or systemic form cause tissue damage and dysfunction. Herein, we report a case of small bowel involvement of systemic amyloidosis presenting with multiple polypoid wall thickening mimicking small bowel polyposis syndrome in an age 75 male. Interestingly, polypoid wall thickening and amyloidoma showed hypointensity on T2-weighted images. To our knowledge, there has been no literature describing MRI findings of poylpoid wall thickening and amyloidoma. Although the underlying mechanisms are unclear and need validation, hypointensity on T2-weighted images could be valuable in diagnosing small bowel involvement of amyloidosis in patients presenting with poylpoid wall thickening and amyloidoma.