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Chinese Journal of Pathology ; (12): 311-315, 2013.
Article in Chinese | WPRIM | ID: wpr-233463

ABSTRACT

<p><b>OBJECTIVE</b>To investigate whether mammalian target of rapamycin (mTOR) kinase was abnormally activated in maldeveloped balloon cells and dysmorphic neurons of focal cortical dysplasia (FCD) with refractory epilepsy.</p><p><b>METHODS</b>A total of 12 archival cases of FCD typeIIwith medically intractable epilepsy treated between 2008 and 2010 were retrieved. Perilesional brain tissue was used as control specimens (n = 8). The expression of phosphorylated p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was investigated by imunocytochemistry.</p><p><b>RESULTS</b>The expression of p-AKT (Ser473), p-mTOR (Ser2448) and p-P70S6K (Thr389) was found in meldeveloped balloon cells and dysmorphic neurons of FCD. A weak stain in a small amount of pyramid neurons was also found in the control group.</p><p><b>CONCLUSION</b>Abnormal activation of mTOR in maldeveloped balloon cells and dysmorphic neurons of FCD may be a key molecular mechanism underlying the histological changes and repeated seizures.</p>


Subject(s)
Adolescent , Adult , Child, Preschool , Female , Humans , Male , Young Adult , Brain Diseases , Metabolism , Pathology , Epilepsy , Metabolism , Pathology , Glial Fibrillary Acidic Protein , Metabolism , Immunohistochemistry , Malformations of Cortical Development , Metabolism , Pathology , Malformations of Cortical Development, Group I , Nestin , Metabolism , Neurons , Metabolism , Phosphorylation , Proto-Oncogene Proteins c-akt , Metabolism , Ribosomal Protein S6 Kinases, 70-kDa , Metabolism , TOR Serine-Threonine Kinases , Metabolism
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