Binding of C-Pittsburgh compound-B correlated with white matter injury in hypertensive small vessel disease.

Objective: C-Pittsburgh compound-B (C-PIB) positron emission tomography (PET) is used to visualize and quantify amyloid deposition in the brain cortex in pathological conditions such as Alzheimer's disease (AD). Intense C-PIB retention is also observed in the white matter (WM) of both healthy individuals and AD patients. However, the clinical implications of this retention in brain WM have not been clarified. We investigated the relationship between the extent of white matter lesions (WMLs) and the binding potential of C-PIB (BP) in the WM in patients with hypertensive small vessel disease. We further examined the relationship between the extent of WMLs and BP in WML and in normal-appearing white matter (NAWM).

Methods: Twenty-one hypertensive vasculopathy patients, without AD and major cerebral arterial stenosis and/or occlusion, were enrolled (9 women, 68 ± 7 years). Regions of WML and NAWM were extracted using magnetization-prepared rapid gradient-echo and fluid-attenuated inversion recovery of magnetic resonance images. Volumes of interest (VOIs) were set in the cortex-subcortex, basal ganglia, and centrum semiovale (CS). BP in the cortex-subcortex, basal ganglia, CS, WML, and NAWM were estimated on C-PIB PET using Logan graphical analysis with cerebellar regions as references. The relationships between WML volume and BP in each region were examined by linear regression analysis.

Results: BP was higher in the CS and basal ganglia than in the cortex-subcortex regions. WML volume had a significant inverse correlation with BP in the CS (Slope = -0.0042, R  = 0.44, P < 0.01). For intra WM comparison, BP in NAWM was significantly higher than that in WML. In addition, although there were no correlations between WML volume and BP in WML, WML volume was significantly correlated inversely with BP in NAWM (Slope = -0.0017, R  = 0.26, P = 0.02).

Conclusions: C-PIB could be a marker of not only cortical amyloid-β deposition but also WM injury accompanying the development of WMLs in hypertensive small vessel disease.