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

Oral presentation

Clinical and neuropathological evolution of the hydrocephalus developed by the mutant mouse hyh

Federico Bátiz¹ , Patricia Páez², Antonio J Jiménez², Sara Rodrìguez¹, José Manuel Pérez-Fígares² and Esteban M Rodríguez¹

¹  Instituto de Histología y Patología, Universidad Austral de Chile, Valdivia, Chile

²  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):S9doi:10.1186/1743-8454-2-S1-S9

Published:	30 December 2005

First paragraph (this article has no abstract)

The hyh (hydrocephalus with hop gait) mutant mice develop inherited hydrocephalus. A key feature in this mutant is that there is a foetal-onset ependymal denudation which precedes cerebral aqueduct obliteration and hydrocephalus [1]. Recently, a point mutation in alpha-SNAP protein has been identified as responsible of the hyh phenotype [2]. However, preliminary findings from our laboratory have suggested clinical and pathological heterogeneity in the expression of hydrocephalus, indicating that other (nongenetic?) factors may influence the degree of severity of this pathology. This is in accordance with findings in other hydrocephalic mutant strains [3,4]. The present investigation was designed to (a) study the clinical evolution of hydrocephalic mice in order to evaluate wether or not clinical heterogeneity does actually occur, (b) identify nongenetic factors (maternal age, multiparity) that may affect such an evolution, and (c) identify neuropathologic events underlying clinical heterogeneity.