gms | German Medical Science

57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie (DGNN)

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie

12. - 15.09.2012, Erlangen

Banner: 57. Jahrestagung der Deutschen Gesellschaft für Neuropathologie und Neuroanatomie

Blood-brain barrier dysfunction and astroglial albumin storage in epilepsy-associated lesions

Meeting Abstract

  • presenting/speaker Ann Kristin Schmitz - University of Bonn, Institute of Neuropathology, Bonn, Germany
  • Anna Raabe - University of Bonn, Institute of Neuropathology, Bonn, Germany; University of Bonn Medical Center, Epileptology, Bonn, Germany
  • Alexander Grote - University of Bonn Medical Center, Neurosurgery, Bonn, Germany
  • Horst Urbach - University of Bonn Medical Center, Neuroradiology, Bonn, Germany
  • Alon Friedman - Zlotowski Center for Neuroscience, Dept. of Physiology and Neurosurgery, Beer-Sheeva, Israel
  • Marec von Lehe - University of Bonn Medical Center, Neurosurgery, Bonn, Germany
  • Albert Becker - University of Bonn, Institute of Neuropathology, Bonn, Germany
  • Pitt Niehusmann - University of Bonn, Institute of Neuropathology, Bonn, Germany

Deutsche Gesellschaft für Neuropathologie und Neuroanatomie. 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN). Erlangen, 12.-15.09.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. Doc12dgnnPP6.2

DOI: 10.3205/12dgnn113, URN: urn:nbn:de:0183-12dgnn1135

Veröffentlicht: 11. September 2012

© 2012 Schmitz et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Drug-refractory focal epilepsy is often associated with structural lesions or low grade glioneuronal tumors, e.g. focal cortical dysplasia (FCDIIb), cavernomas (CAs), ateriovenous malformations (AVMs) and gangliogliomas (GGs). However, too little is known with respect to mechanisms related to epileptogenicity. Recently, we could show astrocytic albumin accumulation within epilepsy-associated vascular lesions (CAs/AVMs) indicating an impairment of the blood-brain barrier (BBB). Considering the increasingly hypothesized TGF-beta receptor-mediated albumin uptake into astrocytes as an epileptogenic factor, we extended our analysis to the lesions/tumors mentioned above. Hence we examined hemosiderin deposits and astroglial albumin accumulation in tumor and adjacent preexisting brain tissue of GGs (WHO grade I, n=10; i.e., vascular component containing neoplastic chronic focal epilepsy group), focal cortical dysplasias (FCD IIb; n=10; i.e., non-vascular component containing non-neoplastic chronic focal epilepsy control group), diffuse astrocytoma WHO grade II (DA; n=5; i.e., non-vascular component containing neoplastic, non-epileptic control group) and renal cell carcinoma brain metastasis (RCCM; n=6; i.e. vascular component containing neoplastic acute seizure control group).

In GGs prussian-blue staining revealed strong hemosiderin deposits and fluorescent double-immunocytochemistry showed substantial albumin uptake exclusively in neoplastic astrocytes and not in reactive astrocytes of adjacent areas. Remarkably, we did not detect substantial astrocytic albumin uptake in/adjacent to FCD IIb, DA and RCCM. This mechanism obviously is only present in astroglial cells of (a) long-term epilepsy associated, (b) vascular component containing tumors. Our findings may indicate intratumoral BBB dysfunction and subsequent accumulation of albumin by neoplastic astroglia as a new putative epileptogenic mechanism for low-grade glioneuronal tumors providing novel antiepileptic therapy perspectives. Additional data addressing potential molecular mechanisms of BBB impairment will be presented.

Supported by DFG SFB TR3, BMBF NGFN, ESF “EuroEpinomics”, EKFS, BONFOR.