• Clinical and Experimental Pediatrics
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• 제46권9호
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• pp.934-938
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• 2003

저자들은 신생아기에 경련을 보였던 환아에서 소변의 N-acetylaspartic acid의 정량검사를 통해 확진하였으며, 뇌자기공명 소견상 뇌백질의 퇴행성변화를 보였던 Canavan 병 1례를 경험하였기에 문헌 고찰과 함께 보고하는 바이다.

• 동의생리병리학회지
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• 제18권2호
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• pp.507-516
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• 2004

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the commom disease in public health service. Although a variety of oriental presciptions in study POD(Polygala tenuifolia extracted from dichlorometan) have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet fully elucidated. It has been widely believed that AP peptide divided from APP causes apoptotic neurotoxicity in AD brain. However, recent evidence suggests that CT105, carboxy terminal 105 aminoacids peptide fragment of APP, may be an important factor causing neurotoxicity in AD. SK-N-SH cells expressed with CT105 exhibited remarkable apoptotic cell damage. Based on morphological observations by phase contrast microscope and NO formation in the culture media, the CT105-induced cell death was significantly inhibited by POD. In addition, AD is one of brain degeneration disease. So We studied on herbal medicine that have a relation of brain degeneration. From old times, In Oriental Medicine, PO water extract has been used for disease in relation to brain degeneration. We were examined by ROS formation, neurite outgrowth assay and DPPH scravage assay. Additionally, we investigated the association between the CT105 and neurite degeneration caused by CT105-induced apoptotic response in neurone cells. We studied on the regeneratory and inhibitory effects of anti-Alzheimer disease in pCT105-induced neuroblastoma cell lines by POD. Findings from our experiments have shown that POD inhibits the synthesis or activities of CT105, which has neurotoxityies and apoptotic activities in cell line. In addition, treatment of POD(>50 ㎍/㎖ for 12 hours) partially prevented CT(105)-induced cytotoxicity in SK-N-SH cell lines, and were inhibited by the treatment with its. POD(>50 ㎍/㎖ for 12 hours) repaired CT105-induced neurite outgrowth when SK-N-SH cell lines was transfected with CT105. As the result of this study, In POD group, the apoptosis in the nervous system is inhibited, the repair against the degerneration of Neuroblastoma cells by CT105 expression is promoted. Decrease of memory induced by injection of scopolamin into rat was also attenuted by POD, based on passive avoidance test. Taken together, POD exhibited inhibition of CT105-induced apoptotic cell death. POD was found to reduce the activity of AchE and induced about the CA1 in rat hippocampus. Base on these findings, POD may be beneficial for the treatment of AD.

• 생물정신의학
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• 제30권1호
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• pp.1-6
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• 2023

Many psychiatric disorders are associated with brain functional dysfunctions and neuronal degeneration. According to the research so far, enhanced brain plasticity reduces neurodegeneration and recovers neuronal damage. Brain-derived neurotrophic factor (BDNF) is one of the most extensively studied neurotrophins in the mammalian brain that plays major roles in neuronal survival, development, growth, and maintenance of neurons in brain circuits related to emotion and cognitive function. Also, BDNF plays an important role in brain plasticity, influencing dendritic spines in the hippocampus neurogenesis. Changes in neurogenesis and dendritic density can improve psychiatric symptoms and cognitive functions. BDNF has potent effects on brain plasticity through biochemical mechanisms, cellular signal pathways, and epigenetic changes. There are pharmacological and non-pharmacological interventions to increase the expression of BDNF and enhance brain plasticity. Non-pharmacological interventions such as physical exercise, nutritional change, environmental enrichment, and neuromodulation have biological mechanisms that increase the expression of BDNF and brain plasticity. Non-pharmacological interventions are cost-effective and safe ways to improve psychiatric symptoms.

• Physical Therapy Rehabilitation Science
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• 제11권3호
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• pp.296-303
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• 2022

Objective: In general, macular degeneration, cataracts and glaucoma generally cause visual injury in clinical settings. This study aimed to examine the effects of low visual acuity simulations on hand manual dexterity function and brainwaves in healthy young adults. Design: Cross-sectional study design Methods: This study was an observational, cross-sectional study. Seventy healthy young adults participated in this study. To evaluate the effects of low visual acuity simulations on hand function and brain waves, this study involved four different visual conditions including (1) normal vision, (2) simulated cataracts, (3) simulated glaucoma, and (4) simulated macular degeneration. The hand function was measured to use the Minnesota manual dexterity test (MMDT), and the brainwaves was also measured to use the electroencephalography. Results: In hand function, placing and turning performance on the MMDT in the normal visual condition was significantly different than that in the cataract and macular degeneration conditions (p<0.05), and the placing performance was significantly differred in the normal condition than that in the simulated glaucoma. However, turning was not significantly different in the normal condition than that in the simulated glaucoma. The alpha, beta, and gamma waves did not significantly differ among the four visual conditions (p>0.05). Conclusions: The results suggest that limited visual information negatively affects the ability to perform tasks requiring arm-hand dexterity and eye-hand coordination. However, the effectiveness of low visual acuity on the brainwaves should be further studied for rehabilitative evidence of visual impairment.

• Journal of Korean Neurosurgical Society
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• 제65권5호
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• pp.680-687
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• 2022

Objective : The influence of moderate-to-severe traumatic brain injury (TBI) on acute pulmonary injury is well established, but the association between acute pulmonary injury and mild TBI has not been well studied. Here, we evaluated the histological changes and fluctuations in inflammatory markers in the lungs to determine whether an acute pulmonary inflammatory response occurred after mild TBI. Methods : Mouse models of mild TBI (n=24) were induced via open-head injuries using a stereotaxic impactor. The brain and lungs were examined 6, 24, and 72 hours after injury and compared to sham-operated controls (n=24). Fluoro-Jade B staining and Astra blue and hematoxylin staining were performed to assess cerebral neuronal degeneration and pulmonary histological architecture. Quantitative real-time polymerase chain reaction analysis was done to measure inflammatory cytokines. Results : Increased neuronal degeneration and the mRNA expression of interleukin (IL)-6, tumor necrosis factor (TNF)-α, IL-10, and transforming growth factor (TGF)-β were observed after mild TBI. The IL-6, TNF-α, and TGF-β levels in mice with mild TBI were significantly different compared to those of sham-operated mice 24 hours after injury, and this was more pronounced at 72 hours. Mild TBI induced acute pulmonary interstitial edema with cell infiltration and alveolar morphological changes. In particular, a significant infiltration of mast cells was observed. Among the inflammatory cytokines, TNF-α was significantly increased in the lungs at 6 hours, but there was no significant difference 24 and 72 hours after injury. Conclusion : Mild TBI induced acute pulmonary interstitial inflammation and alveolar structural changes, which are likely to worsen the patient's prognosis.

• 생물정신의학
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• 제2권2호
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• pp.157-168
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• 1995

The neuropsychiatric sequelae of traumatic brain unjury(TBI) are effects on complex aspect of behavior, cognition and emotional expression. They include psychiatric disorders such as depression, psychosis, personality change, dementia, and postconcussion syndrome. The damage is done not only to the cortex of the brain but also to subcortical and axial structures. The diffuse degeneration of cerebral white mailer is axonal damage that is caused by mechanical forces shearing the neuronal fiber at the moment of impact(diffuse axonal injury, DAI). The DAI and the changed receptor-agonist mechanism ore the most important mechanisms in genesis of neuropsychiatric sequalae by mild TBI. The most important instrument for diagnosis of neuropsychiatric sequalae of TBI is a physician or psychiatrist with experience and knowledge. The most effective therapeutic tool is a professional who understands the nature of the problem.

• 한국멀티미디어학회논문지
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• 제16권9호
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• pp.1018-1030
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• 2013

The corpus callosum is the largest connective structure in the brain, and its shape and size are correlated to sex, age, brain growth and degeneration, handedness, musical ability, and neurological diseases. Manually segmenting the corpus callosum from brain magnetic resonance (MR) image is time consuming, error prone, and operator dependent. In this paper, two semi-automatic segmentation methods are present: the active contour model-based approach and the active shape model-based approach. We tested these methods on an MR image of the human brain and found that the active contour approach had better segmentation accuracy but was slower than the active shape approach.

• 한국동물학회지
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• 제33권1호
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• pp.28-34
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• 1990

배추흰나비에서 좌측 촉각을 제거한지 1일 또는 2일후 뇌의 좌측배엽을 전자현미경으로 관찰하여 촉각으 촉각지각신경세포가 배엽에 종지하는지를 조사하였다. 촉각지각신경세포는 촉각제거로 받은 큰 손상으로 말미암아 배엽에서는 그 축색종말에 전자밀도가 낮거나, 중등도이거나 또는 높은 퇴행성변화를 나타내었다. 그러므로 뇌로 뻗은 촉각지각신경세포중 일부는 촉각 바로 뒤에 있는 배엽에 종지한다고 결론되었다.

• 대한한의학회지
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• 제28권2호통권70호
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• pp.213-223
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• 2007

Objective : Alzheimer's disease (AD) is a geriatric dementia that is widespread in old age. With an aging populace, AD is a looming problem in public health service. Alzheimer's disease is characterized by specific neuronal degeneration in certain areas of the brain. Mutations and abnormal expression of several genes are associated with ${\beta}-amyloid$ deposits and Alzheimer's disease; among them APP, PS1, and PS2, SOD, free radical, ROS. Methods:We studied herbal medicines that have a relationship to brain degeneration. From pre-modern times, although a variety of oriental prescriptions of Aster tataricus have been traditionally utilized for the treatment of AD, their pharmacological effects and action mechanisms have not yet been fully elucidated. Result : Based on morphological observations by phase-contrast microscope, TUNEL assay and MTT in the culture media, $H_20_2-induced$ cell death was significantly inhibited by Aticus. We examined by ROS formation, catalase activity and GSH activity. We studied the protective effect and inhibitory effects of neurotoxicity in $H_20_2-induced$ PC-12 cells by Aticus. Findings from our experiments show that Aticus inhibits apoptosis, which has neurotoxicities and cell damage in PC-12 cells. In addition, treatment with Aticus ($>25{\mu}g/ml$ for 6hrs) partially prevented $H_20_2-induced$ cytotoxicity in PC-12 cells, and induced a protective effect. Conclusion : As the result of this study, in the Aticus group, the apoptosis in the nervous system was inhibited, protected against the degeneration of PC-12 cells by $H_20_2$. Taken together, Aticus exhibited inhibition of $H_20_2-induced$ apoptotic cell death. Aticus was found to induce protective effect on GSH and catalase in PC-12 cells. Based on these findings, Aticus may be beneficial for the treatment of AD.

• 고려인삼학회:학술대회논문집
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• 고려인삼학회 1998년도 Advances in Ginseng Research - Proceedings of the 7th International Symposium on Ginseng -
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• pp.21-30
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• 1998

Ginseng root has been considered to prevent neuronal degeneration associated with brain ischemia, but experimental proof in support of this speculation is limited. Moreover, few studies have compared the neuroprotective actions of ginseng ingredients with those of peptide growth factors and cytokines isf vivo. Using a gerbil forebrain ischemia model, we demonstrated that the oral administration of red ginseng powder before an ischemic insult prevents delayed neuronal death in the hippocampal CAI field and that a neuroprotective molecule within red ginseng powder is ginsenoside Rbl. The neurotrophic effect of ginsenoside Rbl, when examined in the gerbil ischemia model and in neuronal cultures was as potent as or more potent than the effects of epidermal growth factor, ciliary neurotrophic factor, erythropoietin, prosaposin, interleukin-6 and interleukin-3. Besides the protection of hippocampal CAI neurons against brain ischemia/repercussion injuries, ginsenoside Rbl was shown to prevent place navigation disability, cortical infarction and secondary thalamic degeneration in stroke-prone spontaneous hypertensive rats with permanent occlusion of the unilateral middle cerebral artery distal to the striate branches. These findings may validate the empirical use of ginseng root for the treatment of cerebrovascular diseases