Neuropathology : official journal of the Japanese Society of Neuropathology
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Estrogen is neuroprotective against status epilepticus (SE)-induced hippocampal damage in female animals. In male animals, estrogen is converted from testosterone via aromatization the activity of which is upregulated by brain damage. However, it is controversial whether estrogen is neuroprotective or neuroinvasive against male hippocampal damage after SE. ⋯ On the other hand, reactive astrocytes, which newly appeared after SE and formed gliosis at CA1, were confirmed to express both ERs in the nucleus, cytoplasm, and process. There were no differences in immunoreactivity between antibodies. Our results indicate that endogenous estrogen affects the pyramidal cells through ERalpha and beta under normal circumstances in adult male rats, whereas the targets of estrogen shift to the reactive astrocytes through ERalpha and beta after SE.
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Case Reports
Chordoid glioma of the third ventricle: a report of two cases, one with ultrastructural findings.
Chordoid glioma, which generally occurs in adults, is a rare CNS tumor arising in the anterior part of the third ventricle. We report two cases of chordoid glioma of the third ventricle in a 42-year-old woman and a 51-year-old man, respectively. Both tumors showed essentially the same histological and immunohistochemical features; the tumors were composed of cords and nests of epithelioid, GFAP-immunoreactive cells in a mucinous stroma with lymphoplasmacytic infiltrates at the tumor periphery. ⋯ Of interest was that small blood vessels with fenestrated endothelial cells were present in the stroma. In the brain, the presence of fenestrated endothelial cells is a feature of the circumventricular organs (except the subcommissural organ), among which the organum vasculosum of the lamina terminalis is located in the anterior part of the third ventricular floor that is lined by specialized ependymal cells known as tanycytes. These findings further strengthen the hypothesis that chordoid glioma may represent a peculiar clinicopathological subtype of ependymoma (chordoid ependymoma) originating from the lamina terminalis area.
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The pathogenesis of acquired immunodeficiency syndrome dementia complex (ADC) is still poorly understood. Many studies suggest that proinflammatory cytokines such as IL-1beta and TNF-alpha released by microglia/macrophages or astrocytes play a role in CNS injury. A microscopic finding of a microglial nodule with multinucleated giant cells (MNGCs) is a histopathologic hallmark of ADC and named HIV encephalitis. ⋯ SIVenv and TNF-alpha was demonstrated in a few perivascular macrophages. These findings indicate that virus-infected microglia/macrophages do not always express IL-1beta and TNF-alpha, which suggests an indirect role of HIV-1-infected cells in cytokine-mediated pathogenesis of ADC. Our macaque model for human ADC may be useful for better understanding of its pathogenesis.
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Case Reports
Congenital anaplastic astrocytoma differentiated into pilocytic astrocytoma: an autopsy case.
We report an autopsy case of congenital astrocytoma and its histopathological changes during 5 years of the patient's development from birth to death. At birth, a right exophthalmic tumor was observed, and MRI revealed that the tumor occupied the right orbital space and had also affected the suprasellar diencephalic structures. The right orbital tumor, which was enucleated at 2 months of age, was a highly cellular tumor with moderate pleomorphism resembling anaplastic astrocytoma. ⋯ Immunohistochemical examination confirmed that all three phases of the tumors showed an astrocytic lineage, and the Ki-67 labeling index decreased rapidly after 2 months of age. We believe that this congenital anaplastic astrocytoma differentiated into a pilocytic astrocytoma during the 5 years of the patient's development. The transformation of the congenital astrocytoma from anaplastic to pilocytic forms can be attributed to the nature of the tumor, namely postmitotic neoplastic cells are characterized by their ability to undergo self-differentiation, along with the organotropism of the developing brain.
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Emerging evidence suggests the involvement of programmed cell death and inflammation in amyotrophic lateral sclerosis (ALS). To assess molecular pathological effects of the anti-inflammatory peroxisome proliferator-activated receptor-gamma (PPARgamma) agonist pioglitazone in ALS, we verified changes in the population of neurons, astrocytes, and microglia in the ventral horns of spinal cord lumbar segments from the pioglitazone-treated and non-treated groups of mice carrying a transgene for G93A mutant human superoxide dismutase-1 (SOD1) (ALS mice) and non-transgenic littermates (control mice), performed immunohistochemical and immunoblot analyses of PPARgamma, active form of phosphorylated p38 mitogen-activated protein kinase (p-p38) and inhibitor of nuclear factor-kappaB (NF-kappaB)-alpha (IkappaBalpha) in the spinal cords, and compared the results between the different groups. ⋯ Immunoblot analysis showed that pioglitazone treatment resulted in no significant change in nuclear PPARgamma-immunoreactive density, a significant decrease in cytosolic p-p38-immunoreactive density, and a significant increase in cytosolic IkappaBalpha-immunoreactive density. Our results suggest that pioglitazone protects motor neurons against p38-mediated neuronal death and NF-kappaB-mediated glial inflammation via a PPARgamma-independent mechanism.