Abstract
Neurovascular coupling (NVC) reflects the close connection between neural activity and cerebral blood flow (CBF) responses, providing new insights to explore the neuropathological mechanisms of various diseases. Non-dialysis patients with chronic kidney disease (CKD) exhibit cognitive decline, but the underlying pathological mechanisms are unclear. The prospective study involved 53 patients with stage 1-3a CKD (CKD1-3a), 78 patients with stage 3b-5 CKD (CKD3b-5), and 52 healthy controls (HC). Our investigation involved voxel-based assessments of both global and regional BOLD signal characteristics. Additionally, we explored the correlations between neuroimaging indices, Montreal Cognitive Assessment (MoCA) scores, and clinical laboratory findings. Compared to HC, the CKD3b-5 and CKD1-3a groups exhibited lower ALLF and ReHo in the default mode network (DMN), higher CBF in bilateral hippocampus (HIP), higher susceptibility values in bilateral caudate nucleus (CAU) and putamen (PUT), and lower susceptibility values in bilateral HIP. At the global level, the coupling coefficients were lower in CKD1-3a and CKD3b-5 groups than in HC. At the ROI level, the CBF-ALFF and CBF-ReHo coupling in HIP and basal ganglia regions were lower in CKD3b-5 groups than in the CKD1-3a group. Most importantly, susceptibility-ALFF in ANG.R may mediate the effects of phosphorus on cognitive decompensation in patients with CKD1-3a. Non-dialysis patients with CKD exhibit abnormal NCV, which is associated with the cognitive decline. Specifically, the susceptibility-ALFF may serve as a valuable biomarker for early assessment of cognitive decline in CKD, offering insights into the pathogenesis of cognitive decline in CKD.
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