Neuropathology : official journal of the Japanese Society of Neuropathology
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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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To characterize the cellular density and proliferative activity of GFAP-negative cells in pilocytic astrocytoma (PA), surgically excised tissues of PAs (n=37) and diffuse astrocytomas (DAs) (n=11) were examined morphologically and immunohistochemically using antibodies against GFAP, Olig2, Iba1 and Ki-67 (MIB-1). In PA, Olig2 immunoreactivity was significantly expressed in protoplasmic astrocytes in microcystic, loose areas and cells in oligodendroglioma-like areas. Iba1-positive, activated microglia/macrophages were also commonly observed in microcystic areas. ⋯ Conversely, the percentage of Olig2-positive, proliferating cells in total Olig2-positive cells (7.2+/-3.9%) was higher than that of Iba1-positive, proliferating cells in total Iba1-positive cells (0.9+/-0.6%). In conclusion, the present study found that PA consisted of numerous GFAP-negative cells, including Olig2-positive cells with high proliferation. Semiquantitative analysis of Olig2 immunohistochemistry in microcystic areas might therefore be useful for the differential diagnosis of PA and DA.
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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.