Cited by 154

Evidence of activated microglia in focal cortical dysplasia

Boer, K., Spliet, W.G.M., van Rijen, P.C., Redeker, S., Troost, D., Aronica, E.·2006·Journal of Neuroimmunology

Abstract

Focal cortical dysplasia (FCD), which is caused by malformations of cortical development, is known to be a major cause of intractable epilepsy. Cortical laminar disorganization and the presence of abnormal neuronal and astroglial cell types are histological characteristics of FCD. Though, little information is known about the microglia/macrophage cell system in FCD and its possible contribution to the high epileptogenesis of this disorder. In the present study, the distribution of cells of the microglia/macrophage lineage was studied in 20 specimens of FCD (type II) by immunocytochemistry for CD68 and human HLA-DR. A significant number of microglial cells and macrophages were observed within the dysplastic cortex. The mean number of CD68- and HLA-DR-positive cells was significantly higher in FCD specimens than in normal-appearing control cortex obtained at autopsy. HLA-DR-positive cells, which represent activated microglia, were localized around blood vessels and also clustered around dysplastic neuronal cells. The density of these activated HLA-DR-positive microglial cells correlated with the duration of epilepsy, as well as with the frequency of seizures prior to surgical resection. CD68-positive macrophages were mainly located around vessels and the number of these cells did not correlate with seizure frequency, neither with the duration of symptoms prior to surgical resection. In conclusion, our findings demonstrate a specific and persistent increase in the numerical dens…

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Crossref · 10.1016/j.jneuroim.2006.01.002

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  • Gangliogliomas and focal cortical dysplasia type IIb are characterized by prominent activation of various inflammatory pathways, including the TIR signaling pathway.

    “GG and FCD type IIb represent a major cause of drug-resistant epilepsy [23], [25] and are characterized by a prominent activation of various inflammatory pathways, including the TIR signaling pathway [9], [40]–[43].”

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Authors
Boer, K., Spliet, W. G. M., van Rijen, P. C., Redeker, S., Troost, D., & Aronica, E.
Venue
Journal of Neuroimmunology
Publisher
Elsevier BV
Published
2006-04
Volume
173
Issue
1-2
Pages
188-195
ISSN
0165-5728
Cited by
154
References
0
Language
en

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