This is a unique and natural model which provides the opportunity to study pathophysiological change in immature and chronically-traumatized brain tissue without any artificial induction. Cannot be completely prevented by postnatal shunt treatment. This suggests that, advances in shunt technology alone, will not be sufficient to normalize neurological outcome for hydrocephalic children and that additional therapies are needed for clinical treatment to be improved and optimized. Our goals are to understand the mechanisms which lead to permanent neurological damage in infantile hydrocephalus. This in turn would lead to the potential for additional therapy besides surgical treatment which would improve the long-term outcome for patients.
Some possibilities are antioxidant therapy, growth factors, transient gene therapy etc.
The goals of this project are to determine the progression and extent of periventricular fiber tract damage and to examine neuronal death and NOS expression in the forebrain grey matter at different stages of the disease process. The genetics basis for hydrocephalus in the H-Tx strain is not known. For this project we are performing genome scanning with the eventual aim of identifying the gene responsible for this neurological abnormality and linkage analysis. We are investigating novel methods for in vivo quantification of pathophysiological changes in hydrocephalic brain tissue and the effects of shunt treatment. Measurements of water compartmentation and diffusion will be used to investigate how the brain tissue adapts to the influx of fluid from the expanded ventricles.