Ines Blockx1, Marleen Verhoye1,2, Geert De Groof1, Johan Van Audekerke1, Kerstin Raber3, Dirk Poot2, Jan Sijbers2, Stephan von Horsten3, Annemie Van der Linden1
1Bio-Imaging Lab, University of Antwerp, Antwerp, Belgium; 2Vision Lab, University of Antwerp, Antwerp, Belgium; 3Experimental Therapy, Friedrich-Alexander University, Erlangen, Germany
The transgenic rat model for Huntingtons Disease (HD) resembles the late-onset form, exhibiting a behavioral phenotype with emotional disturbance, motor deficits, and cognitive decline. We used Diffusion Kurtosis Imaging (DKI) to study very young (P15-P30) HD rats and controls. In white matter of P30 HD pups we observed a significantly decreased fractional anisotropy and increased axial kurtosis as compared to controls. In grey matter of P30 HD pups axial kurtosis was significantly increased as well as Mean Kurtosis. The DKI changes we detected in HD pups, suggests that neurodegenerative processes of HD also involves neurodevelopment defects already detectable at P30.