1. Defects in cell-cell junctions lead to neuroepithelial/ependymal denudation in the telencephalon of human hydrocephalic foetuses
- Author
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Wilfred F. A. den Dunnen, Antonio J. Jiménez, María Dolores Dominguez Pinos, Deborah A Sival, Esteban M. Rodríguez, Luis Federico Bátiz, Montserrat Guerra, and José Manuel Pérez-Fígares
- Subjects
congenital, hereditary, and neonatal diseases and abnormalities ,Pathology ,medicine.medical_specialty ,Cell junction ,lcsh:RC346-429 ,Pathogenesis ,Cellular and Molecular Neuroscience ,Developmental Neuroscience ,medicine ,lcsh:Neurology. Diseases of the nervous system ,reproductive and urinary physiology ,Spina bifida ,business.industry ,Cerebrum ,medicine.disease ,nervous system diseases ,Hydrocephalus ,Neuroepithelial cell ,medicine.anatomical_structure ,Neurology ,Poster Presentation ,embryonic structures ,Neuropathogenesis ,business ,Ependyma ,Neuroscience - Abstract
Background In human foetal hydrocephalus and spina bifida aperta (SBA), the pathogenesis of abnormal cortical development is poorly understood. Previous reports have shown that neuroepithelial/ependymal denudation is involved in the neuropathogenesis of human foetal hydrocephalus and SBA. Interestingly, loss of the neuroepithelium/ ependyma (denudation) at the Sylvian aqueduct is preceded by defective expression of adherent and gap junction proteins. In human foetal hydrocephalus, we aimed to investigate whether abnormal cortical development is similarly associated with intercellular ependymal defects at the telencephalic (sub)ventricular zones.
- Published
- 2010