• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.13 no.2
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• pp.152-164
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• 2000

1. We experienced one case with facial palsy and paralytic strabismus, which improved under the treatment of Acupuncture, Infrared, Electroacupuncture and Massage. 2. The prognostic factor of facial palsy was affected by On Set and neurodegeneration (such as synkinesis, contraction, spasm and crocodile tear). 3. In facial palsy, Myoneural Excitability Test by Electroacupuncture, which will need the objective clinical standard, was available for the evaluation of therapeutic effect and prognosis.

• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.691-691
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• 2002

In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.

• Journal of Microbiology and Biotechnology
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• v.12 no.4
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• pp.692-694
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• 2002

In the course of our screening for neuroprotective agents, a new compound (1) was isolated together with a known compound, caruilignan C (2), from the fruiting body of Daldinia concentrica. Their structures were determined on the basis of various spectral studies. Both compounds exhibited neuroprotective effect against iron-induced neurodegeneration in a primary culture of mouse cortical neurons.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.67-68
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• 2003

Cerebral ischemia, the most prevalent form of clinical stroke, is a medical problem of the first magnitude. Substantial efforts are being made to develop drugs which will protect the brain from the neurodegeneration that follows ischemic stroke. However, no medical treatment is currently approved for the treatment of stroke to reduce brain infarction or neurological disability beyond tissue plasminogen activator. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.123.2-123.2
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• 2003

The cellular mechanisms by which excess exposure to the excitatory neurotransmitter glutamate can produce neuronal injury are unknown. In this study, we found that glutamate induced cell death at IC (50) of 100 microM on the cultured human SH-SY5Y neuroblastoma cells. It has been hypothesized that glutamate excitotoxicity is related with the elevation of calcium (Ca) levels. To determine the dependence of glutamate neurotoxicity on Ca environment, extracellular (EDTA) and intracellular (BAPTA/AM) chelator were used. (omitted)

• BMB Reports
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• v.43 no.11
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• pp.756-760
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• 2010

Recent studies have reported that delayed-rectifier Kv channels regulate apoptosis in the nervous system. Herein, we investigated changes in the expression of the delayed-rectifier Kv channels Kv1.2, Kv2.1, and Kv3.1 after acute spinal cord injury (SCI) in rats. We performed RT-PCR analysis and found an increase in the level of Kv2.1 mRNA after SCI but no significant changes in the levels of Kv1.2 and Kv3.1 mRNA. Western blot analysis revealed that Kv2.1 protein levels rapidly decreased and then dramatically increased from 1 day, whereas Kv3.1b protein levels gradually and sharply decreased at 5 days. Kv1.2 protein levels did not change significantly. In addition, Kv2.1 clusters were disrupted in the plasma membranes of motor neurons after SCI. Interestingly, the expressional changes and translocation of Kv2.1 were consistent with the apoptotic changes on day 1. Therefore, these results suggest that Kv2.1 channels probably contribute to neuronal cell responses to SCI.

• Journal of the Korean Society of Tobacco Science
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• v.27 no.2
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• pp.212-218
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• 2005

Cigarette smoking has been known to have a few beneficial effects on some neuronal diseases such as Alzheimer's disease(AD), Parkinson's disease(PD) and prion disease by scrapie agent shows many similar properties with AD. In this respect, we investigated what biological effects are exerted by cigarette smoke exposure(CSE) in the brain of mouse infected by 87V scrapie. The scrapie agent was inoculated through stereotaxic microinjection of the homogenates of the scrapie agent infected brain into the intracerebral system in the 1M mice. The inoculation into mice typically exhibits neurochemical, physiological and histopathological characteristics of prion disease: loss of neurotransmitters and induction of astrocytosis and vacuolation in brain as well as reduction of spatial movement and loss of body weight. CSE led to alleviated the loss of body weight and also improved spatial movement of the infected mice. Most interestingly, CSE attenuated astrocytosis and vacuolation caused by scrapie infection in the brain. In addition, decreased levels of dopamine in striatal and hypothalamic regions as well as serotonin level in hippocampus caused by scrapie infection were also attenuated by exposure to cigarette smoke. These findings suggest that cigarette smoke, by its inhibition of astrocytosis and vacuolation followed by its restoration of levels of some neurotransmitters, may partly contribute to suppression in the progress of neurodegeneration caused by scrapie infection.

• Journal of the Korean Society of Tobacco Science
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• v.31 no.1
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• pp.29-38
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• 2009

Although prion diseases, a group of fatal neurodegenerative diseases of human and animals, are presumed to be caused by several mechanisms including abnormal change of prion protein, oxidative stress is still believed to play a central role in development of the diseases. Cigarette smoking has a few beneficial effects on neuronal diseases such as Alzheimer's disease and Parkinson's disease despite of many detrimental effects. In this study, we investigated how chronic cigarette smoking could exert such beneficial effect against oxidative damage. For this study, homogenates of 87V scrapie-infected brain was inoculated on intracerebral system of IM mice through stereotaxic microinjection and biochemical properties concerning with oxidative stress were examined. The scrapie infection decreased the activity of mitochondrial Mn-containing superoxide dismutase by 50% of the control, meanwhile the effects on other antioxidant enzymes including Cu or Zn-containing superoxide dismutase were not significant. Additionally, the infection elevated superoxide level as well as monoamine oxide-B (MAO-B) in the infected brain. Interestingly, many of the detrimental effects were improved in partial or significantly by long-term cigarette smoke exposure (CSE). CSE not only completely prevented the generation of mitochondrial superoxide but also significantly (p<0.05) decreased the elevated mitochondrial MAO-B activity in the infected brain. Concomitantly, CSE prevented subsequent protein oxidation and lipid peroxidation caused by scrapie infection; however, it did not affect the activities of antioxidant enzymes. These results suggest that chronic exposure of cigarette smoke contribute to in part preventing the progress of neurodegeneration caused by scrapie infection.

• Molecules and Cells
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• v.37 no.11
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• pp.767-776
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• 2014

Alzheimer's disease (AD) is clinically characterized with progressive memory loss and cognitive decline. Synaptic dysfunction is an early pathological feature that occurs prior to neurodegeneration and memory dysfunction. Mounting evidence suggests that aggregation of amyloid-${\alpha}$ ($A{\alpha}$) and hyperphosphorylated tau leads to synaptic deficits and neurodegeneration, thereby to memory loss. Among the established genetic risk factors for AD, the ${\varepsilon}4$ allele of apolipoprotein E (APOE) is the strongest genetic risk factor. We and others previously demonstrated that apoE regulates $A{\alpha}$ aggregation and clearance in an isoform-dependent manner. While the effect of apoE on $A{\alpha}$ may explain how apoE isoforms differentially affect AD pathogenesis, there are also other underexplored pathogenic mechanisms. They include differential effects of apoE on cerebral energy metabolism, neuroinflammation, neurovascular function, neurogenesis, and synaptic plasticity. ApoE is a major carrier of cholesterols that are required for neuronal activity and injury repair in the brain. Although there are a few conflicting findings and the underlying mechanism is still unclear, several lines of studies demonstrated that apoE4 leads to synaptic deficits and impairment in long-term potentiation, memory and cognition. In this review, we summarize current understanding of apoE function in the brain, with a particular emphasis on its role in synaptic plasticity and the underlying cellular and molecular mechanisms, involving low-density lipoprotein receptor-related protein 1 (LRP1), syndecan, and LRP8/ApoER2.

• Molecules and Cells
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• v.41 no.7
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• pp.646-652
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• 2018

Neurodegeneration can result in memory loss in the central nervous system (CNS) and impairment of taste and smell in the peripheral nervous system (PNS). The neurodegeneration seen in Parkinson's disease (PD) is characterized by functional loss of dopaminergic neurons. Recent studies have also found a role for dopaminergic neurons in regulating taste memory rewards in insects. To investigate how taste memories and sugar sensitivity can be affected in PD, we utilized the $DJ-1{\beta}$ mutant fruit fly, $DJ-1{\beta}^{ex54}$, as a PD model. We performed binary choice feeding assays, electrophysiology and taste-mediated memory tests to explore the function of the $DJ-1{\beta}$ gene in terms of sugar sensitivity as well as associative taste memory. We found that PD flies exhibited an impaired ability to discriminate sucrose across a range of sugar concentrations, with normal responses at only very high concentrations of sugar. They also showed an impairment in associative taste memory. We highlight that the taste impairment and memory defect in $DJ-1{\beta}^{ex54}$ can be recovered by the expression of wild-type $DJ-1{\beta}$ gene in the dopaminergic neurons. We also emphasized the role of dopaminergic neurons in restoring taste memory function. This impaired memory property of $DJ-1{\beta}^{ex54}$ flies also allows them to be used as a model system for finding supplementary dietary foods that can improve memory function. Here we provide evidence that the associative taste memory of both control and $DJ-1{\beta}^{ex54}$ flies can be enhanced with dietary supplementation of the medicinal plant, omija.