• Journal of Korean Biological Nursing Science
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• v.22 no.4
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• pp.223-231
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• 2020

Purpose: The purpose of this study was to investigate the effects of taro extract on brain resilience in in vitro Parkinson's disease model induced by 6-hydroxydopamine (6-OHDA). Methods: To induce a neuroinflammatory reaction and the in vitro Parkinson's disease model, SH-SY5Y cells were stimulated with lipopolysaccharide (LPS) and 6-OHDA, respectively. After that, cells were treated with at various concentrations (1, 5, and 10 mg/mL) of taro extract. Then nitric oxide (NO) production, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, synaptophysin (SYP) and growth associated protein (GAP)-43 messenger ribonucleic acid (mRNA) expression level were measured. Results: Taro extract significantly suppressed LPS-induced NO production. Meanwhile, iNOS and IL-6 mRNA expression decreased in a dose-dependent manner. In addition, taro increased the mRNA expression of SYP and GAP-43 mRNA. Conclusion: These findings indicate that taro played an important role in brain resilience by inhibiting neuronal cell death and promoting neurite outgrowth, synaptogenesis, and neural plasticity. The results of this study suggest that taro may contribute to the prevention of neurodegenerative disease and become a new and safe therapeutic strategy for Parkinson's disease.

• Journal of Genetic Medicine
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• v.10 no.2
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• pp.88-93
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• 2013

Alexander disease (ALXD) is a rare demyelinating disease of the white matter of the brain that is caused by a mutation in the glial fibrillary acidic protein (GFAP) gene. The overexpression of GFAP in astrocytes induces a failure in the developmental growth of the myelin sheath. The neurodegenerative destruction of the myelin sheath of the white matter is accompanied by an accumulation of abnormal deposits of Rosenthal fibers in astrocytes, which is the hallmark of ALXD. The disease can be divided into four groups based on the onset age of the patients: neonatal, infantile, juvenile, or adult. Early-onset disease is more severe, progresses rapidly, and results in a shorter life span than late-onset cases. Magnetic resonance imaging and genetic tests are mostly used for diagnostic purposes. Pathological tests of brain tissue for Rosenthal fibers are definitive diagnostic methods. Therapeutic strategies are being investigated. Ceftriaxone, which is an enhancer of glial glutamate transporter (GLT-1) expression, is currently in clinical trials for the treatment of patients with ALXD. To date, there are no clinically available treatments. The cause, pathology, pathophysiology, inheritance, clinical features, diagnosis, and treatment of ALXD will be reviewed comprehensively.

• Journal of Ginseng Research
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• v.31 no.1
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• pp.51-53
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• 2007

Ginseng shows protective and trophic effects in neurodegenerative diseases in experimental models, and showed cognitive improvement in normal population. To investigate the efficacy of ginseng in patients with Alzheimer's disease, patients, who met NINDS-ADRDA criteria for AD were studied Subjects were randomly assigned to ginseng group and control group, and ginseng group was treated with Korean white ginseng powder (4.5 g/day) for 12 weeks. Efficacy variables included changes in mini-mental status exam (MMSE) and cognitive subscales of Alzheimer's disease assessment scale (ADAS-cog) at 4 weeks and 12 weeks. Baseline MMSE and ADAS scores showed no difference between the two groups. Results showed that ginseng improved ADAS-cog compared to the control group at 12 weeks (p<0.05). MMSE was also increased by ginseng treatment compared to the control at 12 weeks (p<0.01). This study suggests the symptomatic efficacy of ginseng in patients with Alzheimer's disease.

• Nuclear Medicine and Molecular Imaging
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• v.41 no.2
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• pp.102-111
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• 2007

Dementia is a major burden for many countries including South Korea, where life expectancy is continuously growing and the proportion of aged people is rapidly growing. Neurodegenerative disorders, such as, Alzheimer disease, dementia with Lewy bodies, frontotemporal dementia, Parkinson disease, progressive supranuclear palsy, corticobasal degeneration, Huntington disease, can cause dementia, and cerebrovascular disease also can cause dementia. Depression or hypothyroidism also can cause cognitive deficits, but they are reversible by management of underlying cause unlike the forementioned dementias. Therefore these are called pseudodementia. We are entering an era of dementia care that will be based upon the identification of potentially modifiable risk factors and early disease markers, and the application of new drugs postpone progression of dementias or target specific proteins that cause dementia. Efficient pharmacologic treatment of dementia needs not only to distinguish underlying causes of dementia but also to be installed as soon as possible. Therefore, differential diagnosis and early diagnosis of dementia are utmost importance. F-18 FDG PET is useful for clarifying dementing diseases and is also useful for early detection of the diseases. Purpose of this article is to review the current value of FDG PET for dementing diseases including differential diagnosis of dementia and prediction of evolving dementia.

• 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 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 Korean Nuclear Society Conference
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• 2005.05a
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• pp.938-939
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• 2005

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.142.1-142.1
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• 2003

Excessive accumulation of beta-amyloid (A$\beta$) peptides is one of the leading hypotheses to explain neurodegenerative processes in Alzheimer's disease (AD). It has been suggested that $A\beta$ toxicity is associated with increases in reactive oxygen species. whose overproduction may in turn initiate neurotoxic events. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.216.1-216.1
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• 2003

Neuronal apoptosis may contribute to the pathological neuronal loss in certain disease states such as neurodegenerative diseases. Staurosporine (ST), a nonselective protein kinase inhibitor, has been shown to induce apoptosis in a variety of cells including nerve cell lines. In this study, we investigated the neuroprotective effect of sauchinone, which is a unique lignan from Sauchinone Chinensis, on ST-induced apoptosis in C6 rat glioma cells. (omitted)

• 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)