Evidence of activated microglia in focal cortical dysplasia
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…
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
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].”
From MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response (2012) · cites this paper as [40]
Cited by
Sorted by citations
MicroRNA-146a: A Key Regulator of Astrocyte-Mediated Inflammatory Response
Iyer, A., Zurolo, E., Prabowo, A., Fluiter, K., Spliet, W. G. M., van Rijen, P. C., Gorter, J. A., & Aronica, E. (2012) · PLoS ONE · doi:10.1371/journal.pone.0044789 · Cited by 330 · see citing works
Self-citationSeizure-induced brain-borne inflammation sustains seizure recurrence and blood-brain barrier damage
Librizzi, L., Noè, F., Vezzani, A., de Curtis, M., & Ravizza, T. (2012) · Annals of Neurology · doi:10.1002/ana.23567 · Cited by 253 · see citing works
Noninvasive Molecular Imaging of Neuroinflammation
Jacobs, A. H., Tavitian, B., & the INMiND consortium (2012) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2012.53 · Cited by 245 · see citing works
Noninflammatory Changes of Microglia Are Sufficient to Cause Epilepsy
Zhao, X., Liao, Y., Morgan, S., Mathur, R., Feustel, P., Mazurkiewicz, J., Qian, J., Chang, J., Mathern, G. W., Adamo, M. A., et al. (2018) · Cell Reports · doi:10.1016/j.celrep.2018.02.004 · Cited by 190 · see citing works
Benson, M. J., Manzanero, S., & Borges, K. (2015) · Epilepsia · doi:10.1111/epi.12960 · Cited by 176 · see citing works
Boer, K., Crino, P. B., Gorter, J. A., Nellist, M., Jansen, F. E., Spliet, W. G. M., Van Rijen, P. C., Wittink, F. R. A., Breit, T. M., Troost, D., et al. (2010) · Brain Pathology · doi:10.1111/j.1750-3639.2009.00341.x · Cited by 148 · see citing works
Self-citationMicroglia: dismantling and rebuilding circuits after acute neurological injury
Ziebell, J. M., Adelson, P. D., & Lifshitz, J. (2015) · Metabolic Brain Disease · doi:10.1007/s11011-014-9539-y · Cited by 84 · see citing works
What are activated and reactive glia and what is their role in neurodegeneration?
Bennett, M. L., & Viaene, A. N. (2021) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.105172 · Cited by 77 · see citing works
Zimmer, T. S., Broekaart, D. W. M., Gruber, V.-E., van Vliet, E. A., Mühlebner, A., & Aronica, E. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.01028 · Cited by 48 · see citing works
Self-citationZhang, J., Argueta, D., Tong, X., Vinters, H. V., Mathern, G. W., & Cepeda, C. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1486315 · Cited by 3 · see citing works
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review