As in the human disease, CAG repeat lengths appear to be associated with disease onset and severity. However, mice with extreme repeat lengths in this model present with a disease having a delayed phenotype. This delay in the onset and reduction in the severity of symptoms, in parallel with neurodegenerative changes, provides a model with the potential to elucidate more of the underlying pathogenesis. In addition to the R6/2 model, a number of other models have been made that were aimed at recapitulating better the genetics of HD. These include full length knock-in models, a yeast artificial chromosome model, and a bacterial artificial chromosome model. Historically, magnetic resonance imaging findings for individual patients were diagnostic only in later stages of HD, for example where caudate atrophy contributed to the characteristically large ventricles seen. More recently, analytical methodologies, such as tensor-based morphometry, have been used to show progressive structural changes in presymptomatic HD patients. Neuroimaging studies based on voxel-based morphometry are also used widely to investigate developing pathology in humans and assess prospective treatments. These automated methods for characterising structural differences or changes in the living brain have also been used in mouse models to show that many pathological features are shared between the mouse models and humans with the disease. Here we describe a large dataset of MR images of mice used in models of HD that includes transgenic R6/2 lines of various CAG expansion lengths, yeast artificial chromosome and wildtype mice. In addition, we include the MRI data sets from a colony of complexin 1 knockout mice that showed subtle morphological abnormalities detectable with MRI that reflect behavioural abnormalities seen in the mice. The most common alternative approach to automated analysis involves ignoring the images once they have been registered to a common atlas and instead performing statistical tests on the registration parameters. Retaining some image intensity information in the form of GM maps allows greater scope for chemical changes that are not associated with volume changes to be observed. Using measures of shape change to compare brains, such as the Jacobian determinant of transformation fields, will reveal only microstructural changes when these cause the registration model to geometrically warp the brain to ��correct�� the differences in signal as a geometric change rather than one in chemical environment. This is particularly relevant here, as we have shown that not only are there size differences in key brain regions of the R6/2 mouse, but also signal intensity changes. We are releasing these datasets to the neuroscience community to facilitate research into structural differences seen in mice and to provide common datasets that can be used for advancing methodological techniques of automated assessment of structural phenotypes. We are also releasing online the structural data, segmented GM and WM tissue maps for each brain, as well as population-average templates that can be used for VBM investigations. We are making our extensive collection of high-resolution MR images of R6/2, YAC128, Cplx1 KO and WT mice publically available to download in permanence for use for any purpose. This will be an invaluable resource for the neuroscience and neuroimaging communities to improve our understanding of the pathogenesis in HD via study of its morphological phenotype.
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