ArticleDiabetes, metabolic syndrome and obesity : targets and therapy2025
Causal Central Network Remodeling in Diabetic Neuropathy: An Integrated MR-fMRI Study.
Article in Diabetes, metabolic syndrome and obesity : targets and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Diabetes and the Metabolic Syndrome as Drivers of Neurodegeneration: Convergent Mechanisms Linking Peripheral Neuropathy and Dementia.Annals of neurology · 2026Review
- The role of brain mechanisms in diabetic peripheral neuropathy: recent advances and comprehensive analysis.Frontiers in cellular neuroscience · 2025Review
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2 authors.
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Abstract
Purpose: Diabetic peripheral neuropathy (DPN) is traditionally viewed as a peripheral disorder, yet emerging evidence implicates central nervous system (CNS) network dysfunction in its pathogenesis, though causal mechanisms remain incompletely understood. Methods: Bidirectional two-sample Mendelian randomization (MR) analysis examined causal relationships between Resting-State Functional Magnetic Resonance Imaging (rs-fMRI) phenotypes (n=34,691) and DPN (n=96,474). For validation, amplitude of low-frequency fluctuation (ALFF) and functional connectivity (FC) analyses were conducted using rs-fMRI scans from DPN patients (n=16), diabetic controls without DPN (NDPN, n=24), and healthy controls (HC, n=20). Results: Bidirectional MR demonstrated that: (a) reduced default mode-visual network connectivity causally elevates DPN risk (OR=0.61, P=0.04); (b) DPN promotes subcortical-cerebellar hyperconnectivity (OR=1.04, P=0.01). DPN patients exhibited significantly higher age, triglyceride levels, pain scores, and cognitive impairment relative to comparison groups (all P<0.001). Neuroimaging identified increased ALFF in the left superior frontal gyrus (LSFG) (AUC=0.79, P<0.05), which correlated positively with disease duration, accompanied by decoupled FC with the lingual gyrus but enhanced FC with the precuneus. Conclusion: This study establishes DPN as a CNS-periphery integrated network disorder: genetic drivers disrupt default mode-visual integration, while compensatory subcortical-cerebellar hyperconnectivity stabilizes motor function via adaptive mechanisms. The LSFG emerges as a neuroadaptive hub, where elevated ALFF and connectivity reorganization (↓lingual gyrus/↑precuneus) reflect dynamic rebalancing between impaired basic vision and enhanced visuospatial processing. These findings redefine DPN pathogenesis beyond pure peripheral neurodegeneration, providing a theoretical foundation for early detection and circuit-targeted neuromodulation therapies.
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