• Journal of Life Science
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• v.34 no.1
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• pp.37-47
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• 2024

FUN14 domain-containing protein 1 (FUNDC1), an outer mitochondrial membrane protein, contributes to removal of damaged mitochondria through mitophagy. In this study, to elucidate the role of the FUNDC1 in the amyloid beta peptide (A_β)-induced neuropathy, changes in the degree of mitochondrial dysfunction and cell injury caused by A_β treatment were examined in the HT-22 neuronal cells in which the FUNDC1 expression was transiently silenced or overexpressed. We found that A_β treatment causes a time-dependent decrease of the FUNDC1 expression. In the A_β-treated cells, there were a drop in MTT reduction ability, depletion of cellular ATP, disruption of mitochondrial membrane potential, stimulation of cellular ROS production, and increased mitochondrial Ca²⁺ load. Activation of caspase-3 and induction of apoptotic cell death were also observed. Transient silencing of the FUNDC1 expression by transfection with the FUNDC1 small interfering RNA per se caused mitochondrial dysfunction and apoptotic cell death like the effect of A_β treatment. Conversely, in cells in which the FUNDC1 was transiently overexpressed by FUNDC1-Myc transfection, overexpression itself had no effect on the mitochondrial functional integrity and cell survival but showed a significant prevention effect against mitochondrial and cell injury caused by A_β treatment. Overall, these results suggest that the FUNDC1 is importantly involved in the A_β-induced mitochondrial dysfunction and cell injury in the HT-22 neuronal cells.

• Journal of the Korean Applied Science and Technology
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• v.41 no.1
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• pp.58-68
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• 2024

The purpose of this study was to investigate the effects of treadmill exercise treadmill exercise (TE) and environmental enrichment (EE) interventions on cognitive function, muscle function, and the expression of tight junction proteins in an Alzheimer's disease (AD) animal model. To create the AD animal model, aluminum chloride (AlCl₃) was administered for 90 days (40mg/kg/day), while simultaneously exposing the animals to TE (10-12m/min, 40-60min/day) or EE. The results showed that cognitive impairment and muscle dysfunction induced by AlCl₃ administration were alleviated by TE and EE. Furthermore, TE and EE reduced the increased expression of β-amyloid(Aβ), alpha-synuclein, and tumor necrosis factor-α (TNF-α) proteins observed in AD pathology. Additionally, TE and EE significantly increased the expression of decreased adhesive adjacent proteins (Occludin, Claudin-5, and ZO-1) induced by AlCl₃ administration. Lastly, correlation analysis between Aβ protein and tight junction proteins showed negative correlations (Occludin: r=-0.853, p=0.001; Claudin-5: r=-0.352, p=0.915; ZO-1: r=-0.424, p=0.0390). In conclusion, TE or EE interventions are considered effective exercise methods that partially alleviate pathological features of AD, improving cognitive and muscle function.

• Bulletin of the Korean Chemical Society
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• v.32 no.5
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• pp.1751-1753
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• 2011

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.203.2-204
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• 2003

As medicinal knowledge developed. population system has been migrating into the aged society. These aged society evokes the social problem of senile diseases. One of these. Alzheimer's Disease (AD) has been an issue. and its causative. ${\beta}$-amyloid(A${\beta}$) has also been a key target in drug development. In AD, microglial cell affects neuron cells in any way of positive and negative. (omitted)

• Bulletin of the Korean Chemical Society
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• v.32 no.2
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• pp.731-734
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• 2011

• Proceedings of the Korean Society of Crop Science Conference
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• 2006.04a
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• pp.556-557
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• 2006

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.10a
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• pp.115-115
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• 2001

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 Alzheimers disease (AD). Inflammatory as well as oxidative tissue damage has been associated with 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 Ginseng society Conference
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• 1998.05a
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• pp.39-39
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• 1998

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.151.1-151.1
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• 2003

Polyunsaturated fatty acids (PUFAs) play many important physiological roles on cellular process through the regulations of intracellular signaling. Recent clinical studies suggest that PUFAs such as n-3 fatty acids (docosahexaenoic acid, 22:6 and a-lnolenic acid, 18:3) may reduce the risk of incident Alzheimer's disease (AD). And also the reports regarding the decrease of n-3 fatty acids in AD brain support the correlation between PUFAs and AD. AD is a neurodegenerative disorder with pathological hallmarks of amyloid plaques and neurofibrillary tangles. (omitted)

• Korean Circulation Journal
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• v.54 no.4
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• pp.221-222
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• 2024