Mcm2 labelling of balloon cells in focal cortical dysplasia

Balloon cells (BC) are the prominent and defining cellular component of type IIB Focal Cortical Dysplasia (FCD), a common cause of focal epilepsy in patients undergoing surgical treatment. BC are considered immature cells of uncommitted cellular differentiation having immunophenotypical characteristics of both neurones and glia. They are often located in the lower cortical layers and white matter underlying the dysplastic cortex, suggesting migratory arrest during development. We investigated the proliferative potential of BC in 15 cases of FCD from patients with a wide range of ages using immunohistochemistry for Mcm2 (mini chromosome maintenance protein) and Ki67. In the majority of cases, BC showed Mcm2 nuclear positivity. In addition, cells with intermediate neuronal‐glial characteristics were labelled whilst the dysmorphic or hypertrophic pyramidal neuronal components of FCD were not. Ki67 labelled only occasional BC. These findings support the view that BC cells represent a pool of less differentiated glial cells with proliferative capacity which may have potential for delayed neuronal differentiation. Furthermore, as Mcm2 specifically identifies BC populations, this marker may be of diagnostic value in the subtyping of FCD lesions in patients with epilepsy.

[1]  H. Vinters,et al.  An assessment of the proliferative potential of ‘balloon cells’ in focal cortical resections performed for childhood epilepsy , 1992, Neuropathology and applied neurobiology.

[2]  J. Trojanowski,et al.  Internexin, MAP1B, and nestin in cortical dysplasia as markers of developmental maturity , 1997, Acta Neuropathologica.

[3]  D. Geschwind,et al.  Dentate Granule Cell Neurogenesis Is Increased by Seizures and Contributes to Aberrant Network Reorganization in the Adult Rat Hippocampus , 1997, The Journal of Neuroscience.

[4]  H. Lüders,et al.  Histopathological Correlates of Epileptogenicity as Expressed by Electrocorticographic Spiking and Seizure Frequency , 1998, Epilepsia.

[5]  G. Mathern,et al.  Cerebral Cortical Dysplasia: Giant Neurons Show Potential for Increased Excitation and Axonal Plasticity , 1999, Developmental Neuroscience.

[6]  R. J. Seitz,et al.  Focal cortical dysplasia of the temporal lobe with late-onset partial epilepsy: serial quantitative MRI , 2000, Neuroradiology.

[7]  S. Sisodiya.  Surgery for malformations of cortical development causing epilepsy. , 2000, Brain : a journal of neurology.

[8]  G. Williams,et al.  Replicative Mcm2 protein as a novel proliferation marker in oligodendrogliomas and its relationship to Ki67 labelling index, histological grade and prognosis , 2001, Neuropathology and applied neurobiology.

[9]  A L Benabid,et al.  Cortical Dysplasia: Electroclinical, Imaging, and Neuropathologic Study of 13 Patients , 2001, Epilepsia.

[10]  G. Williams,et al.  DNA replication licensing and human cell proliferation. , 2001, Journal of cell science.

[11]  C. Elger,et al.  Focal cortical dysplasia of Taylor's balloon cell type: Mutational analysis of the TSC1 gene indicates a pathogenic relationship to tuberous sclerosis , 2002, Annals of neurology.

[12]  J. Blow,et al.  Geminin Becomes Activated as an Inhibitor of Cdt1/RLF-B Following Nuclear Import , 2002, Current Biology.

[13]  L Tassi,et al.  Focal cortical dysplasia: neuropathological subtypes, EEG, neuroimaging and surgical outcome. , 2002, Brain : a journal of neurology.

[14]  Horst Urbach,et al.  Focal Cortical Dysplasia of Taylor's Balloon Cell Type: A Clinicopathological Entity with Characteristic Neuroimaging and Histopathological Features, and Favorable Postsurgical Outcome , 2002, Epilepsia.

[15]  S. Weiss,et al.  Radial glial cells as neuronal precursors: The next generation? , 2002, Journal of neuroscience research.

[16]  P. Crino,et al.  Neurodevelopmental Disorders as a Cause of Seizures: Neuropathologic, Genetic, and Mechanistic Considerations , 2002, Brain pathology.

[17]  M. Mizuguchi,et al.  Doublecortin immunoreactivity in giant cells of tuberous sclerosis and focal cortical dysplasia , 2002, Acta Neuropathologica.

[18]  P. Crino,et al.  Single cell lineage analysis in human focal cortical dysplasia. , 2003, Cerebral cortex.

[19]  C. Cepeda,et al.  Morphological and electrophysiological characterization of abnormal cell types in pediatric cortical dysplasia , 2003, Journal of neuroscience research.

[20]  G. Klem,et al.  Epileptogenicity of Focal Malformations Due to Abnormal Cortical Development: Direct Electrocorticographic–Histopathologic Correlations , 2003, Epilepsia.

[21]  H. Otsubo,et al.  Malformations of cortical development with balloon cells , 2003, Neurology.

[22]  E. Aronica,et al.  mTOR cascade activation distinguishes tubers from focal cortical dysplasia , 2004, Annals of neurology.

[23]  A. Palmini,et al.  Terminology and classification of the cortical dysplasias , 2004, Neurology.

[24]  A. Maslov,et al.  Neural Stem Cell Detection, Characterization, and Age- Related Changes in the Subventricular Zone of Mice , 2022 .

[25]  A. Schulze-Bonhage,et al.  CD34-immunoreactive balloon cells in cortical malformations , 2004, Acta Neuropathologica.

[26]  A. Álvarez-Buylla,et al.  For the Long Run Maintaining Germinal Niches in the Adult Brain , 2004, Neuron.

[27]  K. Stoeber,et al.  DNA replication licensing in somatic and germ cells , 2004, Journal of Cell Science.