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We found that early to mid stage (Hoehn and Yahr 1�C3) non-demented PD patients have both reduced FA and increased MD across several regions of cerebral white matter. These areas include major white matter tracts in the frontal and parietal lobes. Although the changes in FA and MD had a similar spatial Romidepsin distribution, the dataset acquired with more gradient directions appeared to be more sensitive to reductions in FA, whilst the dataset acquired with more b values appeared to be more sensitive to increases in MD (although the direct comparison between the two datasets was not significant). Whilst TBSS identified these widespread alterations in PD white matter microstructure at an appropriately corrected statistical threshold, a voxel-based approach was successful only when a more liberal uncorrected threshold was used. With regards to the impact of white matter pathology on cognition, FA and MD in LMTK2 prefrontal white matter correlated with phonemic fluency, an index of executive function. Although previous region-of-interest diffusion studies of PD have shown reduced FA in specified subcortical structures and cerebral white matter tracts (Chan et al., 2007, Gattellaro et al., 2009, Modrego et al., 2011, Peran et al., 2010, Rolheiser et al., 2011?and?Vaillancourt et al., 2009), our results demonstrate more spatially extensive white matter pathology in PD than previously identified in these studies. We have replicated previous findings using whole-brain analysis methods (Hattori et al., 2012, Ibarretxe-Bilbao et al., 2010, Karagulle Kendi et al., 2008, Lee et al., 2010b, Zhan et al., 2012?and?Zhang et al., 2011), finding reduced FA in the gyrus rectus (olfactory tract), prefrontal white matter, and the corticospinal tract. Here, we also identified reductions in FA in prefrontal, parietal and temporal lobe white matter, throughout the length U0126 cost of the corpus callosum, and in the mid- and superior corticospinal tract. Increases in MD, similarly a marker of white matter pathology, were found in prefrontal, parietal and temporal white matter, the corpus callosum, in the mid- and superior corticospinal tract, and the internal and external capsules. Together, our results suggest that many regions of cerebral white matter are affected in PD, even in early to mid motor stage patients. It is difficult to make specific inferences as to the underlying axonal or myelin pathology related to changes in FA and MD using DTI alone. It has been suggested that changes in the first tensor eigenvalue, or axial diffusivity (AD), might be related to axonal pathology (such as reduced axonal density or calibre), whilst changes in the second and third tensor eigenvalues, or radial diffusivity (RD), might be related to myelin pathology (Song et al., 2002). We did indeed find increases in both the AD and RD at p?