Huntington’s disease (HD) is a neurodegenerative disorder that affects motor and cognitive abilities. In this study, we present the outcome of a longitudinal multi-shell DWI investigation of the zQ175 HD mouse model using the diffusion tensor, diffusion kurtosis, and fixel-based analysis. This study reveals microstructural deficits at an early stage of the disease that mainly affect the diffusion tensor in corpus callosum and kurtosis in caudate putamen and grey matter, while fiber cross-section is reduced in major fiber bundles. At a late stage, many white matter fiber bundles show deficits that are indicative of differential myelination and potential axonal pathology.
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