- Neurofilament Protein Subtype Expression in Neuronal Migration Disorders.
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Hyun Sik Oh, Yoo Duk Choi, Hyun Joong Kim, Kyung Hwa Lee, Myoung Kyu Kim, Young Jong Woo, Jae Hyu Kim, Min Cheol Lee
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Korean J Pathol. 2003;37(6):413-420.
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 Abstract
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- BACKGROUND
Neuronal migration disorder (NMD) is one of the causes of medically intractable epilepsy. As neurosurgical treatments for medically intractable epilepsy have expanded recently, precise histopathologic diagnosis is required.
Histopathologic grading of NMD is important due to its association with neocortical development and expectation of prognosis. Many studies revealed abnormalities of neuronal cytoskeletal protein in abnormal neuronal cells of NMD.
METHODS
We performed immunohistochemical staining for neurofilament protein (NF) subtypes, one of the neuronal cytoskeletal proteins, and investigated the staining pattern of specific cells in each grade of NMD.
RESULTS
NF-L was more intensely labeled in perikarya, dendrites, and axons of normal or small sized dysplastic neurons, cytomegalic neurons, and balloon cells than of normal-looking neurons. Furthermore, positive reaction was more intense in high-grade lesion. NF-H and NF-M were mainly positive in the axons of gray and white matter and weakly positive in a few cytomegalic neurons and some balloon cells.
CONCLUSION
NF-L is a better marker than NF-H and NF-M for the detection of normal or small sized dysplastic neurons, cytomegalic neurons, and balloon cells and for grading of NMD.
- Expression of Major Gangliosides in Normal and Alzheimer Disease Brain.
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Min Cheol Lee, Young Jong Woo, Seung U Kim, Tadashi Tai
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Korean J Pathol. 2002;36(6):400-405.
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Abstract
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- BACKGROUND
GM1 ganglioside-bound amyloid beta-protein (GM1/A) has been reported to be involved with senile plaque formation in Alzheimer disease.
METHODS
To investigate the binding of major gangliosides on senile plaques and neurofibrillary tangles of Alzheimer disease-specific pathology, we developed four monoclonal antibodies -- GM1, GD1a, GD1b, and GT1b -- employing the hydridoma technique, and applied them for immunohistochemical staining at the frontotemporal neocortex and hippocampus of Alzheimer disease brains and age-matched control brains.
RESULTS
Moderate immunopositivity for GM1 and GD1a was noted on the senile plaques and neurofibrillary tangles.
Mild immunopositivity for GD1b and GT1b on neurofibrillary tangles was noted. Strong GD1b immunopositivity was observed on a few neurons and neurites. Strong immunopositivity for GT1b, and moderate immunopositivity for GM1 and GD1a were noted on reactive astrocytes.
CONCLUSIONS
These observations suggest that GM1 and GD1a may be involved in the formation of senile plaques as well as neurofibrillary tangles in Alzheimer disease brains.
- Cytoskeletal Changes in Cortical Dysplasia.
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Min Young Lee, Jae Hun Chung, Young Jong Woo, Hyoung Ihl Kim, Min Cheol Lee
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Korean J Pathol. 2000;34(4):300-309.
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Abstract
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- Cortical dysplasia is a cause of intractable epilepsy and a candidate for surgical resection to control epileptic attacks. The neuronal cytomegaly and balloon cell change are the diagnostic hallmarks of cortical dysplasia. Little research has been performed about the normal-sized dysplastic neuron which has complex arborizing dendrites and lacks in its polarity. The aim of this study was to define the histopathologic characteristics of the neurons in cortical dysplasia.
Twelve cases of cortical dysplasia who underwent partial lobectomy for intractable seizures were selected and immunohistochemical staining for NF-M/H, MAP2, tau, and ubiquitin was performed.
The perikarya and dendrite of dysplastic neurons were more intensely labeled with antibodies for the high and medium molecular weight neurofilament proteins (NF-M/H) than normal neurons.
Immunoreactivity with the MAP2 antibody expressed mainly within the somatodendritic regions was present in the dysplastic or normal neurons without any significant difference in intensity.
The complex arborizing dendrites of dysplastic neurons were easily identified due to pronounced immunoreactivity within the somatodendritic regions.
Immunoreactivity with the primary antibody against tau and ubiquitin was present in the normal-looking neurons as well as the dysplastic neurons. This study suggests that the dysplastic neurons in cortical dysplasia are accompanied by changes of cytoskeletal neurofilaments, and the immunohistochemical stains for NF-M/H, MAP2, tau, and ubiquigin are useful to detect them.
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