Abstract
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Objectives: The posterior cingulate cortex, as a vital role in supporting cognition and the default mode network, showed the earliest and largest decrement in functional connectivity and energy metabolism among brain regions in Alzheimer’s disease (AD). In this study, the posterior cingulate cortex was selected as seeds to explore the global functional connectivity (gFC) , metabolism and Amyloid-β deposition in AD/MCI, as well as to further explore their association with cognitive performance.
Methods: The patient group consisted of 14 patients with AD(n=4) and MCI(n=10), 18 normal participants (age- and gender-matched) with cognitively confirmed were included in the study. The MR (T1 3D BRAVO, EPI) and PET (18F-FDG and 18F-AV45) data (37 MBq/Kg, 40 min acquisition time) were acquired simultaneously using an hybrid PET/MR system (Signa PET/MR, GE Healthcare). The gFC of the posterior cingulate region was computed through seed-based resting-state fMRI correlations through each voxel in the gray matter using DPARSF toolbox based on SPM12. The cerebellar cortex served as reference region to calculate the 18F-FDG and 18F-AV45 SUV ratio (SUVr) using PMOD software. The posterior cingulate cortex based gFC, FDG and AV45 SUVr were tested for associations with each other and with the Mini Mental Status Examination (MMSE) scores.
Results: The posterior cingulate cortex gFC in patients with AD/MCI was significantly lower in right middle Frontal gyrus and Cingulate gyrus than that in normal controls (two-sample t-test, voxel level p < 0.001, cluster level p < 0.05 gaussian random field corrected). The AD/MCI group showed significant lower FDG SUVr of posterior cingulate cortex compared to normal controls (1.562 ± 0.074 vs. 1.813 ± 0.054, p = 0.01). There was no significant difference in cortical AV45 tracer accumulation of posterior cingulate cortex between patients with AD/MCI and normal control (1.461 ± 0.091 vs. 1.593 ± 0.064, p = 0.234). In addition, a higher MMSE score was associated with larger hypermetabolism in AD/MCI (r = 0.539, p = 0.046),compared with normal control.
Conclusions: In comparison with normal controls, a decreased FDG SUVr of posterior cingulate cortex was observed in patients with AD/MCI. Hybrid PET/MR provided imaging data in the same physiological state to better understand the neuropathology. The potential of PET/MRI in exploring the pathophysiological mechanism will be carried out in future study. Fig. 1 Spatial distribution of posterior cingulate cortex global functional connectivity(A), metabolism(B), Amyloid-β deposition (C) in patients with AD/MCI and normal controls. Color bar indicate z scores. Group differences and spatial areas with reduced posterior cingulate cortex gFC in patients with AD/MCI compared with NC(A) (two-sample t-test, p < 0.05 Gaussian random field corrected). Averaged FDG metabolism(B) and Aβ deposition(C) in posterior cingulate cortex of patients with AD/MCI. [asterisk]:significantly different (p < 0.05) Fig. 2 The relationship between MMSE and posterior cingulate cortex metabolism in patients with AD/MCI.