Table 1.
Demographic summary including cognitive features for Alzheimer’s disease patients and for a group of elderly controls.
Figure 1.
Depiction of average cognitive profiles for all subject cohorts assessed in this study.
Table 2.
Cognitive profile evolution of a group of early-stage Alzheimer’s disease patients that was followed-up for a period of 12 months.
Figure 2.
Depiction of the semi-automated callosal subdivision into splenium, truncus and genu (top), and their intersection with the mean FA skeleton inferred from N = 69 subjects–N = 43 Alzheimer’s disease patients and N = 26 matched controls (bottom).
Figure 3.
Cross-sectional study of very mild Alzheimer’s disease.
TBSS results for the very mild Alzheimer’s disease group compared to controls. Statistical maps (thresholded at TFCE-P<0.05) for increased axial/radial diffusivity and reduced FA overlaid onto the mean FA skeleton and the MNI152 template. Coronal depths are given in millimetres.
Figure 4.
Cross-sectional study of mild Alzheimer’s disease.
TBSS results for the mild-stage Alzheimer’s disease group compared to controls. Thresholded (TFCE-P<0.05) statistical maps for increased axial/radial diffusivity and reduced FA were overlaid onto the mean FA skeleton and the MNI152 template. Coronal depths are given in millimetres.
Figure 5.
Cross-sectional results in the mid-sagittal corpus callosum.
TBSS results across the sagittal midline for very mild and mild Alzheimer’s disease groups compared to controls.
Table 3.
Alzheimer’s disease skeletonised DTI parametric comparisons in different mid-sagittal callosal areas.
Table 4.
DTI group comparisons across disease stages and linear dependence on global cognition for all patients in the splenium.
Figure 6.
Cross-sectional diffusion tensor behaviour in the splenial region.
Mean subject values for skeletonised DTI parameters in the splenium as a function of cognitive status (ACE-R scores) for controls (green), very mild Alzheimer’s disease (blue) and mild Alzheimer’s disease patients (red). The error bars represent ± one group standard deviation. The vertical axes were scaled to 10 control standard deviations. The vertical lines delimit the control exclusion criteria (ACE-R<88/100) and the median split (ACE-R = 74). A least-square linear fit was displayed if Pearson’s correlation coefficient was deemed statistically significant (Table 4).
Figure 7.
Longitudinal study of Alzheimer’s disease.
Whole-brain TBSS contrast on 12-month follow-up versus baseline in the longitudinal Alzheimer’s disease cohort (TFCE-P<0.05) for increased radial diffusivity and reduced FA n.b. no significant results for λ1 or MD were found.
Figure 8.
Longitudinal results in the mid-sagittal corpus callosum.
Longitudinal TBSS results for radial diffusivity and fractional anisotropy across the midline.
Table 5.
Longitudinal DTI assessment of Alzheimer's disease in the splenium.
Figure 9.
Longitudinal tensor behaviour in the splenium.
Longitudinal pairs of mean subject skeletonised DTI parameters as a function of cognitive status (ACE-R) for Alzheimer’s disease subjects at baseline (blue) and 12 months (red).