For example, a simple extraction of total volumes from the GM maps presented here has shown how wholebrain GM volume shows different age trajectories for the R6/2 lines, adding to mounting evidence of different mechanisms underlying pathology in mice with ��super-expanded�� CAG expansions. Reconstructed cortical thickness maps are an example of how versatile the images can be and how they are amenable to a wide range of different analytical treatments with high power due to the large number of subjects available. We have shown that the values of cortical thickness obtained by our algorithms are in good agreement with manual measurements, and that both measures correspond well with those that would obtained by images prepared histologically. Since all of the data are now freely available, it is possible for other users to try alternative algorithms for cortical thickness measurement. The range of HD models AbMole Diatrizoic acid included in the library show a range of CAG repeat lengths. There is a growing body of data from behavioural and gene expression studies suggesting that mice carrying extremely long CAG repeat lengths show a delayed onset of phenotype. The explanation for this delay in onset remains unclear, since the mice still die prematurely of a neurological disease. One possibility is that the protein carrying the very long polyglutamine products of superlong CAG repeatcontaining gene fragments cannot enter the nucleus, and therefore cannot form the pathological inclusions that are characteristic pathology of mice with shorter repeats. Although there is no direct AbMole Metyrapone clinical analogue of extremely long somatic CAG repeats in patients, nevertheless very expanded CAG repeats are found in human post mortem brain, due to somatic instability. Interestingly, the mice with superlong CAG repeats show a more human-like brain pathology from those with shorter CAG repeats. The significance of these findings remains to be established, but it is hoped that identified differences in htt accumulation and their relationship to onset and progression of illness will suggest appropriate pathways for therapeutic agents and interventions. The data presented here show that the delays seen in phenotype for longer repeat include changes in the morphological phenotype as seen by MRI. Since one of the major goals of animal models of HD is to study the early pathology and potential interventions, the demonstration of changes in MRI phenotype is important particularly as MRI findings are increasingly used to monitor disease onset in patients. Large datasets better capture background variability and allow more subtle effects to be characterized. It is our intention to add files to the library as we continue to acquire more images from mice with different CAG expansions so that the various patterns of disease seen can be studied in depth. In addition, we plan to add our in vivo acquisitions to extend this resource. There is no comparable library of publically-available mouse brain datasets available and we hope that our publication will encourage other investigators to make their data available to provide new opportunities for insight into neurodegenerative disease. We are committed to open-source software and free access to data and in addition to the online database we will share the algorithms used in this manuscript with other users on request.