Scientific Reports (Nov 2024)
Characterization of changes in the resting-state intrinsic network in patients with diabetic peripheral neuropathy
Abstract
Abstract Diabetic peripheral neuropathy (DPN) is the most common complication of type 2 diabetes mellitus (T2DM) and is often accompanied by a variety of cognitive and emotional deficits, but the neurologic mechanisms underlying these deficits have not been fully elucidated. Therefore, this study aimed to use independent component analysis to explore the changes in the characteristics within the intrinsic network and to reveal patterns of interactions between networks in patients with DPN. Forty-one patients with T2DM who showed DPN, 37 patients with T2DM who did not show DPN (NDPN group), and 43 healthy controls (HC) underwent a neuropsychological assessment and resting-state functional magnetic resonance imaging examinations to examine the patterns of intra- and inter-network variations in the patients with T2DM at different clinical stages (with and without DPN). The relationships of intra- and inter-network functional connectivity (FC) with clinical/cognitive variables were also examined. In comparison with the NDPN group and HC, patients with DPN showed decreased FC within the visual network and sensorimotor network (SMN). Moreover, in comparison with the HC group, patients with DPN showed decreased FC within the anterior default mode network and increased FC within the basal ganglia network. Inter-network analysis showed decreased FC between the SMN and salience network in patients with DPN relative to the NDPN and HC groups. The decreased FC within the bilateral paracentral lobule (BA 6) of SMN was associated with Color Trails Test part 1 scores (r = -0.302, P = 0.007) and disease duration (r = -0.328, P = 0.003) in all patients with T2DM. In conclusion, the results revealed that patients with DPN have abnormal FC in multiple resting-state intrinsic networks in addition to the SMN, and that decreased FC between the SMN and salience network may be involved in the neural basis of abnormal sensorimotor function in patients with DPN.
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