Log on/register
BioMed Central home | Journals A-Z | Feedback | Support | My details
 

This article is part of the supplement: 49th Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida .

Open AccessOral presentation

An alteration of the subcommissural organ (SCO) leads to aqueductal stenosis and hydrocephalus

Karin Vío1, Carolina Wagner1, Sara Rodrìguez1, Federico Bátiz1, Antonio J Jiménez2, José Manuel Pérez-Fígares2 and Esteban M Rodríguez1 email

Instituto de Histología y Patología, Universidad Austral de Chile, Valdivia, Chile

Departamento de Biología Celular, Universidad de Málaga, España

author email corresponding author email

from 49th Annual Meeting of the Society for Research into Hydrocephalus and Spina Bifida
Barcelona, Spain. 29 June – 2 July 2005

Cerebrospinal Fluid Research 2005, 2(Suppl 1):S8doi:10.1186/1743-8454-2-S1-S8

Published: 30 December 2005

First paragraph (this article has no abstract)

In all species developing congenital hydrocephalus in which the SCO has been investigated, changes in the SCO- Reissner fibre (RF) complex have been reported. However, the question whether these changes precede hydrocephalus, or are a consequence of it, has not been fully clarified. We have reported that in the rat, the maternal transfer of antibodies against RF-glycoproteins to the foetuses and to the pups prevents RF formation and leads to aqueductal stenosis and hydrocephalus [1]. This finding gave support to the early hypothesis of Overholser et al. [2] who had proposed that a maldevelopment of the SCO may result in hydrocephalus. We have now designed new experimental protocols to further test this hypothesis.


© 1999-2010 BioMed Central Ltd unless otherwise stated. Part of Springer Science+Business Media.