• Proceedings of the Korean Society of Toxicology Conference
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• 2002.05a
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• pp.111-111
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• 2002

Many cases of early onset autosomal dominant inherited forms of Alzheimer's disease (AD) are caused by mutation in the genes encoding presenilin-2 (PS-2) on chromosome 1. It is characterized by amyloid deposition and associated with loss of neuron. However, molecular mechanisms underlying the role of PS-2 mutation in the pathogenic AD are not known.(omitted)

• Biomolecules & Therapeutics
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• v.14 no.2
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• pp.106-109
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• 2006

Neprilysin (Nep) is known to be important to degrade $A{\beta}$ derived from amyloid precursor protein (APP) by cleavage with $\beta-and\;\gamma$-secretases. In order to determine whether a correspondence between $A{\beta}-42/{\gamma}-secretase$ activity and Nep levels exists in postnatal aging of transgenic mice expressing either neuron-specific enolase (NSE)-controlled human mutant presenilin-2 (hPS2m) or APPsw alone, the levels of Nep expression and $A{\beta}-42/{\gamma}-secretase$ activity were examined age of 5, 12, and 20 months, respectively. The levels of Nep expression in both types of transgenic brains were decreased relative to those of control mice in a aging-related manner, while the level of $A{\beta}-42/{\gamma}-secretase$ activity was reversibly increased. Thus, changes in $A{\beta}-42$ may all reflect variation in amounts of Nep enzyme.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.109-109
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• 2002

• Archives of Pharmacal Research
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• v.29 no.10
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• pp.884-889
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• 2006

Mutation in the presenilin 2 (PS2mt) is known to be one of factors involved in the development of Alzheimer's disease (AD). It was recently revealed that an abnormality of lipid metabolism is a phenomenon occurring in AD. Therefore, the aim of this study was to investigate the potential relationship between the mutation of PS2 and alterations of the lipid profile within the brain. The results showed there increases in the levels of cholesterol, low density lipoprotein and triglyceride, but a decrease in the level of high density lipoprotein in brain tissues expressing mutant PS2. These findings indicated that PS2mt is involved in the abnormalities of the lipid profile, which could cause or result in the development of AD.

• Proceedings of the Korean Society of Applied Pharmacology
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• 2006.04a
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• pp.33-58
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• 2006

• Journal of the Korea Academia-Industrial cooperation Society
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• v.20 no.5
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• pp.241-251
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• 2019

In the present study, we investigated the effect of microcurrent against cognitive impairment in Alzheimer's disease (AD) mice model. The cognitive impairment was induced by intracerebroventricularly injection of amyloid beta ($A{\beta}$) to ICR mouse brain, and four kinds of micorocurrent wave were applied to AD mice. We observed the improved cognitive ability in microcurrent-applied AD mice through novel object recognition test and Morris water maze test, compared to $A{\beta}$-injected control group. The contents of malondialdehyde generated by $A{\beta}$ in the brain were also reduced by microcurrent application. These effects of microcurrent were related to the modulation of $A{\beta}$ producing and brain-derived neurotrophic factor (BDNF). Microcurrent down-regulated ${\beta}$-secretase, presenilin 1, and presenilin 2 which were related amyloidogenic pathway, and up-regulated human brain-derived neurotrophic factor in the mice brain, especially Wave4 group [STEP FORM wave form (0, 1.5, 3, 5V), wave superposition]. These results suggest that microcurrent application could provide help for improvement learning and memory ability, at least partly.

• The Korea Journal of Herbology
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• v.21 no.4
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• pp.123-131
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• 2006

Objectives : This research was investigated the effect of the Ginseng Radix plus Crataegi Fructus on the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. Methods : Observed a change of the injury of brain tissue and reduced the infarction area of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. Results : 1. The Gin-CF extract reduced the infarction area of hippocampus, and controlled the injury of brain tissue in the mice with Alzheimer's disease induced by ${\beta}A$. 2. The Gin-CF extract reduced the Tau protein, GFAP protein, and presenilin1/presenilin2 protein (immunohistochemistry) of hippocampus in the mice with Alzheimer's disease induced by ${\beta}A$. Conclusion : These results suggest that the Ginseng Radix plus Crataegi Fructus extract may be effective for the prevention and treatment of Alzheimer's disease. Investigation into the clinical use of the Ginseng Radix plus Crataegi Fructus extract for Alzheimer's disease is suggested for future research.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.149.1-149.1
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• 2002

• Journal of Life Science
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• v.20 no.3
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• pp.444-452
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• 2010

The purpose of this study was to investigate the effects of treadmill exercise on $A{\beta}$-42, cytochrome c, SOD-1, 2 and Sirt-3 protein expressions in brain cytosol and mitochondria in mutant (N141I) presenilin-2 transgenic mice with Alzheimer's disease (AD). The mice were divided into four groups (Non-Tg-sedentary, n=5; Non-Tg treadmill exercise, n=5; Tg-sedentary, n=5; Tg treadmill exercise, n=5). To evaluate the neuroprotective effect of treadmill exercise, Non-Tg and Tg mice were subjected to exercise training on a treadmill for 12 wk, after which their brain cytosol and mitochondria were evaluated to determine whether any changes in the cognitive performance, $A{\beta}$-42 protein, cytochrome c protein, anti-oxidant enzymes (SOD-1, SOD-2) and Sirt-3 protein had occurred. The results indicated that treadmill exercise resulted in amelioration in cognitive deficits of Tg mice. In addition, the expressions of mitochondrial $A{\beta}$-42 and cytosolic cytochrome c protein were decreased in the brains of Tg mice after treadmill exercise, whereas antioxidant enzymes, SOD-l and SOD-2 were significantly increased in response to treadmill exercise. Furthermore, treadmill exercise significantly increased the expression of Sirt-3 protein in Non-Tg and Tg mice. Taken together, these results suggest that treadmill exercise is a simple behavioral intervention which can sufficiently improve cognitive performance and inhibit $A{\beta}$-induced oxidative stress in AD.

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2003.05a
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• pp.73-74
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• 2003