• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 춘계학술대회 논문집
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• pp.93-94
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• 2003

beta-Amyloid peptide is considered to be responsible for the formation of senile plagues that accumulate in the brains of patients with Alzheimers disease. There has been a paucity of evidence to support the involvement of reactive oxygen and/or nitrogen species (ROS and/or RNS) in beta-amyloid-induced neuronal cell death. (omitted)

• 생물정신의학
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• 제5권1호
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• pp.66-70
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• 1998

Apoptosis is a form of cell death in which the cells shrink and exhibit nuclear chromatin condensation and DNA fragmentation, and yet maintain membrane integrity. Many lines of evidence have shown that brain neurons are vulnerable to degeneration by apoptosis. Also it has been suggested that apoptosis is one of the mechanism contributing neuronal loss in Alzheimer's disease(AD), since the conditions in the disease($A{\beta}$ peptide, oxidative stress, low energy metabolism) are the inducers that activate apoptosis. Indeed some neurons in vulnerable regions of the AD brain show DNA damage, chromatin condensation, and apoptic bodies. Consistently, mutations in AD causative genes(Amyloid precursor protein, Presenilin-1 and Presenilin- 2) increase $A{\beta}$ $peptide_{1-42}(A{\beta}_{1-42})$ and sensitize neuronal cell to apoposis. However, several lines of evidence have shown that the location of neuronal loss and $A{\beta}$ peptide deposition is not correlated in AD brain and transgenic mice brain over-expressing $A{\beta}_{1-42}$. Taken together, these data may indicated that $A{\beta}$ peptide(and other causative factors of AD) can interact with other cellular insults or risk factors to exacerbate pathological mechansim of AD through apoptosis. Thus, this review discusses possible role and mechanism of apoptosis in AD.

• 센서학회지
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• 제21권5호
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• pp.339-344
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• 2012

This article describes a novel method for the detection of amyloid-${\beta}$($A{\beta}$) peptide that utilizes a photo-sensitive field-effect transistor (p-FET). According to a recent study, $A{\beta}$ protein has been known to play a central role in the pathogenesis of Alzheimer's disease (AD). Accordingly, we investigated the variation of photo current generated from p-FET with and without intracellular magnetic beads conjugated with $A{\beta}$ peptides, which are placed on the p-FET sensing areas. The decrease of photo current was observed due to the presence of the magnetic beads on the channel region. Moreover, a similar characteristic was shown when the Raw 264 cells take in magnetic beads treated with $A{\beta}$ peptide. This means that it is possible to simply detect a certain protein using magnetic beads and a p-FET device. Therefore, in this paper, we suggest that our method could detect tiny amounts of $A{\beta}$ for early diagnosis of AD using the p-FET devices.

• Nutrition Research and Practice
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• 제8권4호
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• pp.386-390
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• 2014

BACKGROUND: Acanthopanax divaricatus var. albeofructus (ADA) extract has been reported to have anti-oxidant, immunomodulatory, and anti-mutagenic activity. MATERIALS/METHODS: We investigated the effects of ADA extract on two mouse models of Alzheimer's disease (AD); intracerebroventricular injection of ${\beta}$-amyloid peptide ($A{\beta}$) and amyloid precursor protein/presenilin 1 (APP/PS1)-transgenic mice. RESULTS: Intra-gastric administration of ADA stem extract (0.25 g/kg, every 12 hrs started from one day prior to injection of $A{\beta}1$-42 until evaluation) effectively blocked $A{\beta}1$-42-induced impairment in passive avoidance performance, and $A{\beta}1$-42-induced increase in immunoreactivities of glial fibrillary acidic protein and interleukin (IL)-$1{\alpha}$ in the hippocampus. In addition, it alleviated the $A{\beta}1$-42-induced decrease in acetylcholine and increase in malondialdehyde levels in the cortex. In APP/PS1-transgenic mice, chronic oral administration of ADA stem extract (0.1 or 0.5 g/kg/day for six months from the age of six to 12 months) resulted in significantly enhanced performance of the novel-object recognition task, and reduced amyloid deposition and IL-$1{\beta}$ in the brain. CONCLUSIONS: The results of this study suggest that ADA stem extract may be useful for prevention and treatment of AD.

• KSBB Journal
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• 제28권4호
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• pp.230-237
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• 2013

Amyloid ${\beta}$ peptide (A${\beta}$) still best known as a molecule to cause Alzheimer's disease (AD). AD is characterized by the accumulation and deposition of A${\beta}$ within the brain, leading to neuronal cell loss and perturbation of synaptic function by causing free radical formation, inflammation and apoptosis. We investigated the inflammatory action of A${\beta}$ on two types of brain cells, neuronal cells (SH-SY5Y) and neuroglia cells (C6), and its mechanism. We measured the production of NO-iNOS, TNF-${\alpha}$, and ICAM-1 using RT-PCR and Western blot analysis less than the concentration of cytotoxic effects (> 70% survivability). A${\beta}$ had no effect on the production of NO and TNF-${\alpha}$, but significantly increases of iNOS and ICAM-1. Based on this, we suggest that the inflammatory effect of A${\beta}$ results from the action of ICAM-1 in neuronal cells, rather than the release of inflammatory mediators such as NO and TNF-${\alpha}$ in neuroglia cells. In addition, we confirmed whether p53 was related to the action of A${\beta}$ by using SH-SY5Y ($p53^{-/-}$) dominant cells. Neither the expression of p53 nor the cytotoxicity of SH-SY5Y ($p53^{-/-}$) cells were directly affected by A${\beta}$. However, ICAM-1 was not expressed in SH-SY5Y ($p53^{-/-}$) cells. This means that p53- independent pathway exists in the expression of ICAM-1 by A${\beta}$ while p53 plays a role as an on-and-off switch.

• Preventive Nutrition and Food Science
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• 제16권1호
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• pp.18-23
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• 2011

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by neuronal loss and extracellular senile plaques containing $\beta$-amyloid peptide (A$\beta$). The deposition of the A$\beta$ peptide following proteolytic processing of amyloid precursor protein (APP) by $\beta$-secretase (BACE1) and $\gamma$-secretase is a critical feature in the progression of AD. Among the plant extracts tested, the ethanol extract of Petasites japonicus leaves showed novel protective effect on B103 neuroblastoma cells against neurotoxicity induced by A$\beta$, as well as a strong suppressive effect on BACE1 activity. Ethanol extracts of P. japonicus leaves were sequentially extracted with methylene chloride, ethyl acetate and butanol and evaluated for potential to inhibit BACE1, as well as to suppress A$\beta$-induced neurotoxicity. Exposure to A$\beta$ significantly reduced cell viability and increased apoptotic cell death. However, pretreatment with ethyl acetate fraction of P. japonicus leaves prior to A$\beta$ (50 ${\mu}M$) significantly increased cell viability (p<0.01). In parallel, cell apoptosis triggered by A$\beta$ was also dramatically inhibited by ethyl acetate fraction of P. japonicus leaves. Moreover, the ethyl acetate fraction suppressed caspase-3 activity to the basal level at 30 ppm. Taken together, these results demonstrated that P. japonicus leaves appear to be a useful source for the inhibition and/or prevention of AD by suppression of BACE1 activity and attenuation of A$\beta$ induced neurocytotoxicity.

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-2
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• pp.141.2-142
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• 2003

beta-Amyloid (A$\beta$) peptide is the major component of senile plaques and considered to have a causal role in the development and progression of Alzheimer's disease. There has been compelling evidence supporting that $A\beta$-induced cytotoxicity is mediated through oxidative and/or nitrosative stress. Recently, considerable attention has been focused on dietary manipulation of oxidative and/or nitrosative damage. L-Egrothioneine (EGT) is a low-molecular weight naturally occurring thiol compound of dietary origin which exists in milimolar concentrations in the brain, liver, kindney, erythrocytes, ocular tissues and in seminal fluids of mammals. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.204.1-204.1
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• 2003

Azheimer's Disease (AD) known as senile dementia accounts for 50％ of all dementia cases and is in growing status as population goes up. Generally. AD is a progressive neurodegenerative disease and includes much of senile plaque in cerebral hippocampus and cortex in patient's brain. For decades. AD theory is explained by amyloid cascade hypothesis. In process of the hypothesis, amyloid hypothesis forms fibrillar form beta-amyloid peptide (A${\beta}$ peptide) and extraordinarily accumulates in brain tissue, and lastly senile plaque is formed, which pathologically affect the brain. (omitted)

• 한국식품저장유통학회지
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• 제14권4호
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• pp.425-430
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• 2007

Amyloid ${\beta}-peptide$에 의해 유도되는 세포사멸을 보호하는 물질을 검색하기 위하여 250여 식물 재료 및 식품성분으로부터 스크리닝한 결과 가장 효과가 있는 시금치 추출물을 이용하여 뇌신경세포사멸(neuronal cell death)을 어느 정도 보호할 수 있는지를 알아보았다. 시금치 추출물이 항산화 활성과 acetylcholinesterase 활성에 대한 저해효과는 시금치 추출물 처리농도가 높을수록 유의적으로 높게 나타났다. 과산화수소와 amyloid ${\beta}-peptide$에 의해 유도된 SH-SY5Y 세포주의 세포사멸에 대한 시금치추출액의 억제효과를 살펴본 결과, 과산화수소에 의한 세포사멸에 대하여 시금치 추출물은 억제효과를 나타내었으나, amyloid ${\beta}-peptide$의 경우는 세포사멸억제효과를 나타내지 않았다.

• 한국독성학회:학술대회논문집
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• 한국독성학회 2003년도 추계학술대회
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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)