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1C) and WM (Fig. 1D). To our knowledge, this was the first study to investigate and observe patterns of cerebellar GM and WM atrophy in DLB and AD compared with healthy subjects of similar age using DARTEL-VBM. Two results emerged from this analysis. First, DLB had a pattern of cerebellar GM loss distinct but not significantly different from AD. Second, compared with findings in controls, WM cerebellar deficits were apparent in AD but not in DLB. GM matter loss has been previously reported across the continuum from mild cognitive impairment to AD (Thomann et al., 2008, Dos Santos et al., 2011, Spulber et al., 2012?and?Moller et al., 2013), and thus our findings are consistent with these. Since total GM volumes are proportional to total WM volumes in both AD and DLB (AD: r=0.55, PBGJ398 manufacturer that are likely to occur as a result of the significant cortical GM loss under this condition which could impact upon the widespread connectivity between the cortex and cerebellum. By similar argument, there was less cortical atrophy in DLB, and this may potentially explain the lack of cerebellar WM loss observed in DLB compared with controls. The pattern of GM loss in DLB compared with the pattern in controls Fluconazole primarily involved the posterior and lateral cerebellum, areas which have been associated with cognitive functions such as executive function and working memory ( Stoodley et al., 2010), and atrophy in these areas has also been implicated in psychopathology and thought disorder observed in schizophrenia ( Schmahmann, 1991?and?Andreasen et al., 1998) as well as with cerebellar ��dysmetria of thought�� ( Schmahmann, 1991); the latter is a concept that implies that in addition to the canonical motor function of the cerebellum to regulate force, rhythm, timing and accuracy of movement, the cerebellum also performs an analogous regulatory role for higher cognitive and mental functions ( Schmahmann, 1998). In the present study, we did not observe any associations between the severity of volumetric change (GM or WM) and a wide range of clinical variables including cognitive and neuropsychiatric measures in either DLB or AD. It could be that the observed cerebellar structural changes are epiphenomena which are not central to the clinical selleckchem phenotypes seen in either disease state or that cerebellar atrophy, in itself, is not necessarily relevant to cognitive and neuropsychiatric symptoms in DLB/AD, but more a representation of the broader neurodegenerative disease process. However, alterations in functional state of the cerebellum rather than structure may be more salient to cognitive and psychiatric symptomatology in DLB; for example, there is a reported association between cerebellar hypermetabolism in DLB and visual hallucinations (Miyazawa et al., 2010).