イケダ アサコ
  池田 麻子
   所属   医学部 医学科(附属足立医療センター)
   職種   非常勤講師
論文種別 原著
言語種別 英語
査読の有無 査読あり
表題 Abnormal maturation and differentiation of neocortical neurons in epileptogenic cortical malformation: unique distribution of layer-specific marker cells of focal cortical dysplasia and hemimegalencephaly.
掲載誌名 正式名:Brain research
略  称:Brain Res
ISSNコード:18726240/00068993
掲載区分国外
巻・号・頁 1470,pp.89-97
著者・共著者 Arai Asako, Saito Takashi, Hanai Sae, Sukigara Sayuri, Nabatame Shin, Otsuki Taisuke, Nakagawa Eiji, Takahashi Akio, Kaneko Yuu, Kaido Takanobu, Saito Yuko, Sugai Kenji, Sasaki Masayuki, Goto Yu-Ichi, Itoh Masayuki
担当区分 筆頭著者
発行年月 2012/08
概要 Focal cortical dysplasia (FCD) and hemimegalencephaly (HME) are major causes of intractable epilepsy in children. The probable pathogenesis of FCD and HMG is the abnormal migration and differentiation of neurons. The aim of the present study was to clarify the abnormal cytoarchitecture, based on neuronal immaturation. Tissue samples were obtained from 16 FCD and seven HME patients, aged between 2 months and 12 years, who had been diagnosed as typical FCD and HME, following surgical treatment for intractable epilepsy. Paraffin-embedded sections were stained with the antibodies of three layer-markers that are usually present only during the fetal period, namely SATB2 (expressed in the upper layer of the normal fetal neocortex), FOXP1 (expressed in the 5th layer), and TBR1 (expressed in the 6th layer). In FCD, SATB2-positive (+) cells located in the middle and deep regions of FCD Ia and Ib, but only in the superficial region of FCD IIa and IIb. FOXP1+ cells diffusely located in the neocortex, especially the upper layer of FCD IIa and IIb. TBR1+ cells mainly located in the middle and deep regions, and also white matter. In FCD IIb, TBR1+ cells were in the superficial region. In HME, SATB2+ and FOXP1+ cells were found diffusely. TBR1+ cells were in the middle and deep regions. On the basis of continued expression of fetal cortical layer-specific markers in FCD and HME brains, the abnormal neocortical formation in both is likely to be the result of disrupted neuronal migration and dysmaturation. The expression pattern is different between FCD and HME.
DOI 10.1016/j.brainres.2012.06.009
PMID 22759905