Introduction
Activity in neural cells is coupled with glucose metabolism. Neural function of signaling are carried out by interconnection of neurons via neuronal fibers. Diffusion-tensor imaging (DTI) is recently becoming an established technique that allows in vivo visualization of white matter fiber tracts by measuring the anisotropy of water molecular diffusion. Several studies focusing on normal aging reported significant reduction in fractional anisotropy (FA) in the corpus callosum, deep and subcortical white matter. The purpose of this study was to examine whether degradation of microstructure of fiber tracts in the elderly was associated with change in the glucose metabolism in the cerebral cortex measured with 18F-FDG-PET.
Methods
Sixteen healthy volunteers (male 11, female 5, age 73. 3±2.3 yr) participated. A 10 min emission scan was performed with a SET2400W scanner from 45 min after the injection of 211±31 MBq of 18F-FDG. MRI measurement was performed using a Symphony 1.5 T system. A volumetric T1-weighted image (T1WI) was acquired using a MPRAGE sequence. DTI was acquired using a single-shot diffusion-weighted echo planar imaging with six sets involving diffusion gradients placed along non-collinear directions (b = 1000 seconds/mm2) and another set without diffusion weighting (b = 0). A FA image was created using Dr. View/LINUX software. We placed regions of interest (ROI) using MRIcro software on the splenium and genu of the corpus callosum, the deep white matter in the right (RFr) and left (LFr) frontal lobe on each FA image. Using SPM2 software, all PET images were anatomically normalized and globally normalized. Statistical analysis was performed using FA for each ROI as a covariate, and thresholded at P < 0.05 (corrected). We also performed morphometric analysis of gray matter (GM), created by segmentation of the T1WI, to examine if there was GM atrophy that would explain correlation of 18F-FDG accumulation with FA.
Results
FA for each ROI were; 0.70±0.056 in the splenium, 0.64±0.058 in the genu, 0.27±0.032 in the RFr, and 0.26±0.032 in the LFr, respectively. There was no statistically significant correlation of FA with age. We did not found statistically significant correlation of the GM concentration with FA, as well as with age. On the other hand, we found statistically significant positive correlation of 18F-FDG accumulation in the anterolateral frontal cortex bilaterally with FA of the genu of the corpus callosum, and in the posterior prefrontal cortex bilaterally, the right anterolateral prefrontal cortex and the left superior temporal cortex, with FA of the deep white matter of the right frontal lobe. There was no age effect in FDG accumulation.
Conclusion
18F-FDG accumulation in cortical areas was correlated with FA in the genu of the corpus callosum, and in the deep white matter of the right frontal lobe, without correlation with GM atrophy. The results suggest that neuronal activity in the cortex decreases with deterioration in microstructure of the fiber tracts, which could connect those cortical neurons with others, without causing significant GM atrophy.