• BMB Reports
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• v.44 no.11
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• pp.730-734
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• 2011

Amyloid ${\beta}$-peptide ($A{\beta}$-peptide)-induced oxidative stress is thought to be a critical component of the pathophysiology of Alzheimer's disease (AD). New chalcone derivatives, the Chana series, were recently synthesized from the retrochalcones of licorice. In this study, we investigated the protective effects of the Chana series against neurodegenerative changes in vitro and in vivo. Among the Chana series, Chana 30 showed the highest free radical scavenging activity (90.7%) in the 1,1-diphenyl-2- picrylhydrazyl assay. Chana 30 also protected against $A{\beta}$-induced neural cell injury in vitro. Furthermore, Chana 30 reduced the learning and memory deficits of $A{\beta}_{1-42}$-peptide injected mice. Taken together, these results suggest that Chana 30 may be a promising candidate as a potent therapeutic agent against neurodegenerative diseases.

• 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.

• BMB Reports
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• v.43 no.6
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• pp.413-418
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• 2010

Beta-Amyloid ($A{\beta}$)-induced neuroinflammation is one of the key events in the development of neurodegenerative disease. We previously reported that KHG21834, a benzothiazole derivative, attenuates $A{\beta}$-induced degeneration of cortical and mesencephalic neurons in vitro. In the present work, we show that KHG21834 reduces $A{\beta}$-mediated neuroinflammation in brain. In vivo intracerebroventricular infusion of KHG21834 leads to decreases in the numbers of activated astrocytes and microglia and level of proinflammatory cytokines such as interleukin-$1{\beta}$ and tumor necrosis factor-$\alpha$ induced by $A{\beta}$ in the hippocampus. This suppression of neuroinflammation is associated with decreased neuron loss, restoration of synaptic dysfunction biomarkers in the hippocampus to control level, and diminished amyloid deposition. These results may suggest the potential therapeutic efficacy of KHG21834 for the treatment of $A{\beta}$-mediated neuroinflammation.

• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.94-94
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• 2002

Oxidative stress induced by reactive oxygen and/or nitrogen species has been considered as a major cause of cellular injuries in a variety of neurodegenerative disorders including Alzheimer's disease (AD). Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of AD, and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD.(omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.327.2-327.2
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• 2002

Inflammatory as well as oxidative tissue damage has been associated with pathophysiology of Alzheimer's disease (AD), and nonsteroidal anti-inflammatory drugs have been shown to retard the progress of AD. In this study, we have investigated the molecular mechanisms underlying oxidative and inflammatory cell death induced by beta-amyloid (Abeta), a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD, in cultured PC12 cells. (omitted)

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.11
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• pp.115-120
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• 2019

This study was undertaken to determine the correlation between β-amyloid, serum lipid levels, and cognitive function in the elderly with mild Alzheimer's dementia. The study was conducted in December 2018, enrolling 45 elderly people with mild Alzheimer's disease. Blood analysis measured the β-amyloid and serum lipid levels, and cognitive function was measured using MMSE-K. The correlation between β-amyloid, serum lipid levels and cognitive function was determined using Pearson's correlation analysis. A significantly negative correlation was observed between the β-amyloid level and cognitive function (p<0.05). Furthermore, serum lipid levels and cognitive function also revealed a significantly negative correlation between TC and LDL levels (p<0.05). These results indicate that increasing levels of β-amyloid, TC, and LDL augments a negative correlation that decreases the cognitive function, signifying that management of pathologic factors related to dementia is important for the prevention and improvement of cognitive function in dementia patients.

• Journal of Chitin and Chitosan
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• v.23 no.4
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• pp.220-227
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• 2018

Amyloid plaque is a product of aggregation of ${\beta}$-amyloid peptide ($A{\beta}$) and is an important factor in the pathogenesis of Alzheimer's Disease (AD). $A{\beta}$ is a major component of amyloid plaque and vascular deposits in the AD brain. The enzyme ${\beta}$-secretase is required for the production of $A{\beta}$; thus, prevention of the formation of $A{\beta}$ through the inhibition of ${\beta}$-secretase is a major focus in the study of the treatment of AD. In this study, we investigated ${\beta}$-secretase inhibitory activity of an Arctoscopus japonicus peptide. An Alcalase hydrolysate had the highest ${\beta}$-secretase inhibitory activity. A ${\beta}$-secretase inhibitory activity peptide was separated using ion exchange column chromatography (carboxy-methyl: CM, quaternary methyl ammonium: QMA) and reverse phase high performance liquid chromatography (RP-HPLC) on a C18 column. The $IC_{50}$ value of the purified peptide was $248.2{\pm}1.73{\mu}g/mL$. The ${\beta}$-secretase inhibitory peptide was identified as a six amino acid residue of Gly-Pro-Val-Gly-Ala-Pro (MW: 497.27 Da). In cell viability experiments, the final purified fraction, the carboxy-methyl ion exchange column fraction (CM-F1) showed no significant cytotoxic effect in SH-SY5Y cells at concentrations below $100{\mu}g/mL$ in 24 h. The results of this study suggest that peptides separated from Arctoscopus japonicus may be beneficial as ${\beta}$-secretase inhibitor compounds in functional foods.

• Journal of Oriental Neuropsychiatry
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• v.16 no.1
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• pp.67-80
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• 2005

This experiment was designed to investigate the effect of Rheum palmatum(RHP) on the Alzheimer's disease. The effects of RHP extract on amyloid precursor proteins(APP), acetylcholinesterase(AChE), glial fibrillary acidic protein(GFAP) mRNA of PC-12 cell treated by $A{\beta}\;and\;IL-1{\beta},\;IL-6,\;TNF-{\alpha}$ mRNA of THP-1 cell treated by LPS and AChE activity of PC-12 cell lysate treated by $A {\beta}$and behavior of memory deficit rats induced by scopolamine and mice glucose, uric acid, AChE activity of memory deficit rats induced by scopolamine were investigated, respectively. The results were summarized as follows ; 1. RHP extract suppressed APP, AChE, GFAP mRNA in PC-12 cell treated by $A{\beta} $. 2. RHP extract suppressed $IL-1{\beta} $, IL-6 $TNF-{\alpha}$ mRNA in THP-1 cell treated by LPS. 3. RHP extract suppressed AChE activity in cell lysate of PC-12 cell treated by $A{\beta}$. 4. HP extract increased glucose, decreased uric acid and AChE significantly in the serum of the memory deficit rats induced by scopolamine. 5. RHP extract group showed significantly inhibitory effect on the memory deficit of mice induced by scopolamine in the experiment of Morris water maze. According to the above results, it is suggested that RHP extract might be usefully applied for prevention and treatment of Alzheimer’s disease and memory deficit symptom.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.139-140
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• 2003

Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of Alzheimer's disease (AD), and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD. In the present study, we investigated the effect of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on inflammatory cell death induced by beta-amyloid, a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.(omitted)

• Proceedings of the KIEE Conference
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• 2015.07a
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• pp.1223-1224
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• 2015

Recently, Alzheimer's Disease (AD) is one of the biggest threats to healthy society. Current medical AD diagnosis depends on interviews and the molecular neuroimaging. There is no cure for the disease, which worsens as it progresses, and eventually leads to death. Amyloid ${\beta}$ and Tau-meditated neuronal injury and dysfunction are candidates of biomarker for AD diagnosis using blood. For highly sensitive and selective biosensor platform, interdigitated microelectrodes (IMEs) sensor was prepared with micro fabrication process and Amyloid ${\beta}$ antibody. Amyloid ${\beta}$ concentration of 1, 10, 100, and 1000 pg/mL was injected in reaction chamber with IME sensors, impedance and conductance of IMEs changed respectively. These results show our newly proposed IMEs sensor can be usefully utilized for AD early diagnosis.