• Journal of Veterinary Clinics
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• v.38 no.2
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• pp.89-93
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• 2021

2-Month-old, three related Perro de Presa Canario dogs were evaluated for similar neurological symptoms like circling, head pressing, depressed mental status, hypermetria, and vocalization. On magnetic resonance imaging (MRI) of the brain, there were large, bilaterally symmetrical lesions with involvement of thalamus, and brainstem that were T2- and FLAIR-hyperintense and T1-iso/hypointense. There was no inclusion of cerebellum. Single-voxel spectroscopy acquisition was located in the thalamus where abnormalities were found in MR images. The results of magnetic resonance spectroscopy (MRS) showed markedly decreased N-acetylaspartic acid value. Euthanasia was performed and lesions consistent with the canine spongy degeneration. Alteration in metabolites in the brain can be determined by MRS, which helps in diagnosing degeneration/leukodystrophy of the central nervous system in dogs.

• Annals of Clinical Neurophysiology
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• v.4 no.1
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• pp.21-27
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• 2002

Background : Spatial analysis of EEG is a phenomenal assessment and not so informative for phase space and dynamic aspect of EEG data. In contrast, nonlinear EEG analysis attempts to characterize the dynamics of neural networks in the brain. We have analyzed the features of EEG nonlinearly in subjects with white matter change on brain MRI and compared the results with cognitive function in each. Methods : Digital EEG data were taken for 30 seconds in 9 subjects with white matter degeneration and in 5 healthy normal controls without white matter change on MRI. Then we analyzed them nonlinearly to calculate the correlation dimension(D2) using the MATLAB software. The cognitive function was assessed by 3MS(modified mini-mental state examination). The severity of white matter change was assessed by Scheltens scale. Results : The mean D2 value of normal control was greater than that of white matter degeneration group. The D2s of some channels were correlative with 3MS and degree of white matter degeneration significantly. Conclusions : nonlinear analysis of EEG can be used as one of adjuvant functional studies for prediction of cognitive impairment in subjects with white matter degeneration and subcortical white matter change can be influential on cognitive function and correlation dimension of EEG.

• Herbal Formula Science
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• v.11 no.2
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• pp.95-110
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• 2003

Alzheimer's disease(AD) is a geriatric dementia that is widespread in old age. In the near future AD will be the biggest problem in public health service. Although a variety of oriental prescriptions in study Jeonmaedan 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 A${\beta}$ peptide devided from APP causes apoptotic neurotoxicity in AD brain. However, recent evidence suggests that CTl05(carboxy terminal 105 amino acid peptide fragment of APP) may be an important factor causing neurotoxicity in AD. In addition, AD is one of brain degeneration disease. So we studied on herbal medicine that have a relation of brain degeneration. In Oriental Medicine, Jeonmaedan has been used for disease in relation to brain degeneration. As the result of this study, in Jeonmaedan the apoptosis in the nervous system is inhibited, the repair against the degerneration of SK-N-SH cell lines by CT105 expression is promoted. So Jeonmaedan may be beneficial for the treatment of AD.

• Journal of Korean Neurosurgical Society
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• v.59 no.1
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• pp.1-5
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• 2016

Chronic subdural hematomas (CSHs) are generally regarded to be a traumatic lesion. It was regarded as a stroke in 17th century, an inflammatory disease in 19th century. From 20th century, it became a traumatic lesion. CSH frequently occur after a trauma, however, it cannot occur when there is no enough subdural space even after a severe head injury. CSH may occur without trauma, when there is sufficient subdural space. The author tried to investigate trends in the causation of CSH. By a review of literature, the author suggested a different view on the causation of CSH. CSH usually originated from either a subdural hygroma or an acute subdural hematoma. Development of CSH starts from the separation of the dural border cell (DBC) layer, which induces proliferation of DBCs with production of neomembrane. Capillaries will follow along the neomembrane. Hemorrhage would occur into the subdural fluid either by tearing of bridge veins or repeated microhemorrhage from the neomembrane. That is the mechanism of hematoma enlargement. Trauma or bleeding tendency may precipitate development of CSH, however, it cannot lead CSH, if there is no sufficient subdural space. The key determinant for development of CSH is a sufficient subdural space, in other words, brain atrophy. The most common and universal cause of brain atrophy is the aging. Modifying Virchow's description, CSH is sometimes traumatic, but most often caused by degeneration of the brain. Now, it is reasonable that degeneration of brain might play pivotal role in development of CSH in the aged persons.

• Molecules and Cells
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• v.45 no.11
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• pp.846-854
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• 2022

Neurons make long-distance connections via their axons, and the accuracy and stability of these connections are crucial for brain function. Research using various animal models showed that the molecular and cellular mechanisms underlying the assembly and maintenance of neuronal circuitry are highly conserved in vertebrates. Therefore, to gain a deeper understanding of brain development and maintenance, an efficient vertebrate model is required, where the axons of a defined neuronal cell type can be genetically manipulated and selectively visualized in vivo. Placental mammals pose an experimental challenge, as time-consuming breeding of genetically modified animals is required due to their in utero development. Xenopus laevis, the most commonly used amphibian model, offers comparative advantages, since their embryos ex utero during which embryological manipulations can be performed. However, the tetraploidy of the X. laevis genome makes them not ideal for genetic studies. Here, we use Xenopus tropicalis, a diploid amphibian species, to visualize axonal pathfinding and degeneration of a single central nervous system neuronal cell type, the retinal ganglion cell (RGC). First, we show that RGC axons follow the developmental trajectory previously described in X. laevis with a slightly different timeline. Second, we demonstrate that co-electroporation of DNA and/or oligonucleotides enables the visualization of gene function-altered RGC axons in an intact brain. Finally, using this method, we show that the axon-autonomous, Sarm1-dependent axon destruction program operates in X. tropicalis. Taken together, the present study demonstrates that the visual system of X. tropicalis is a highly efficient model to identify new molecular mechanisms underlying axon guidance and survival.

• Korean Journal of Clinical Laboratory Science
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• v.47 no.1
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• pp.51-58
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• 2015

Ethanol has long been implicated in triggering apoptotic neurodegeneration. Alcohol also may indirectly harm the fetus by imparing the mother's physiology. We examined the effects of ethanol on immature brain of mice. Three-weeks-old female ICR strain mice daily intraperitoneally injected with ethanol at the concentration of 4 and 20% in saline for 0, 6, and 24 hours and 1 and 4 weeks. The mice were weighted and sacrificed, and the brains were ectomized for the present histological, immunohistochemical and TUNEL assays. Based on the histologic hematoxylin and eosin stain, immunohistochemical expression of glutamate receptor protein and neuronal cell adhesion molecule (NCAM) were evaluated. The cerebral cortex of the ethanol-treated group showed few typical symptoms of apoptosis such as chromosome condensation and disintegration of the cell bodies. TUNEL staining revealed DNA fragmentation in the 6 and 24 hours. This results demonstrated that acute ethanol administration causes neuronal cell death. I found that either glutamate receptor inhibition or activation could induce cerebellar degeneration as ethanol effect. Neuronal death also can be induced by excess activity of certain neurotransmitter, including glutamate. Neurons must establish cell-to-cell contact during growth and development in order to survive, migrate to their final destination, and develop appropriate connections with neighboring cell. Purkinje cell in cerebellar are especially vulnerable to the cell death and degeneration. After ethanol treatment in cerebellar, NCAM had decreased by 4 weeks. This result suggest that apoptosis seems to be involved in the slow elimination of neuron and cerebellar degeneration.

• Korean Journal of Food Science and Technology
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• v.27 no.6
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• pp.915-920
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• 1995

This study was performed to investigate the effect of aluminum compound on the aluminum contents and histological change in brain tissue of rats. Seventy five male Sprague-Dawley strains were divided into five groups consisting of the control, 250 ppm $AlCl_3$ group, 500 ppm $AlCl_3$ group, 250 ppm $Al_2(SO_4)_3$ group, 500 ppm $Al_2(SO_4)_3$ group and kept on the diet for 2 weeks. The weight gain was increased by administration of $AlCl_3$ but decreased by administration of $Al_2(SO_4)_3$ as compared to control group. The aluminum contents in brain tissue of each group; 250 ppm $AlCl_3$ group, 500 ppm $AlCl_3$ group, 250 ppm $Al_2(SO_4)_3$ group and 500 ppm $Al_2(SO_4)_3$ group were 64.63, 102.21, 132.64 and 180.41 ppm, respectively. Aluminum accumulation in brain tissue was higher with administration of $Al_2(SO_4)_3$ than with administration of $AlCl_3$. In $AlCl_3$ administration group, multiple small intracytoplasmic granules and microvacuole were seen in large pyramidal cells of cortex and granulovacuolar degeneration. In $Al_2(SO_4)_3$ administration group revealed pollagis pallor, cellular pyknosis, microcavitation resulted from edema in deeper cortical layers were observed. Blue-pigmentation which represents the accumulation of aluminum was noted In granulovacuolar degeneration site in $Al_2(SO_4)_3$ administration group.

• Proceedings of the Zoological Society Korea Conference
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• 1998.10b
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• pp.112-112
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• 1998

No Abstract, See Full Text

• The Korean Journal of Nuclear Medicine
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• v.37 no.1
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• pp.13-23
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• 2003

Neurodegenerative disorders cause a variety of dementia including Alzheimer disease, frontotemporal dementia, dementia with Lewy bodies, corticobasal degeneration, progressive supranuclear palsy, and Huntington's disease. PET scan is useful for early detection and differential diagnosis of these dementing disorders. Also, it provides valuable information about clinico-anatomical correlation, allowing better understanding of function of brain. Here we discuss recent achievements PET studies regarding these dementing disorders. Future progress in PET technology, new tracers, and image analysis will play an important role in further clarifying the disease pathophysiology and brain functions.

• Biomolecules & Therapeutics
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• v.31 no.4
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• pp.417-424
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• 2023

Parkinson's disease (PD) which has various pathological mechanisms, recently, it is attracting attention to the mechanism via microbiome-gut-brain axis. 6-Shogaol, a representative compound of ginger, have been known for improving PD phenotypes by reducing neuroinflammatory responses. In the present study, we investigated whether 6-shogaol and ginger attenuate degeneration induced by Proteus mirabilis (P. mirabilis) on the intestine and brain, simultaneously. C57BL/6J mice received P. mirabilis for 5 days. Ginger (300 mg/kg) and 6-shogaol (10 mg/kg) were treated by gavage feeding for 22 days including the period of P. mirabilis treatment. Results showed that 6-shogaol and ginger improved motor dysfunction and dopaminergic neuronal death induced by P. mirabilis treatment. In addition, they suppressed P. mirabilis-induced intestinal barrier disruption, pro-inflammatory signals such as toll-like receptor and TNF-α, and intestinal α-synuclein aggregation. Moreover, ginger and 6-shogaol significantly inhibited neuroinflammation and α-synuclein in the brain. Taken together, 6-shogaol and ginger have the potential to ameliorate PD-like motor behavior and degeneration of dopaminergic neurons induced by P. mirabilis in mice. Here, these findings are meaningful in that they provide the first experimental evidence that 6-shogaol might attenuate PD via regulating gut-brain axis.