Disrupted brain functional network topology and potential network reorganization in early-stage Parkinson's disease with probable REM sleep behavior disorder.

PURPOSE: Parkinson's disease with rapid eye movement sleep behavior disorder(RBD) often represents a more aggressive subtype, presenting more serious clinical manifestations even in early-stage disease. However, this subtype's specific whole-brain functional network alterations in the early stages of the disease remain unclear. Research was designed to explore the unique functional network alterations patterns in early PD with RBD and underlying abnormal neural network development mechanisms.

METHOD: We gathered resting-state fMRI data of35 healthy controls (HC), 33 early PD with probable RBD (PD + pRBD), and 32 early PD without RBD (PD-RBD). We utilized graph theory along with network-based methods to analyze the data. Research was conducted on correlations between network indicators and clinical scores.

RESULT: PD + pRBD exhibited significantly decreased local efficiency than PD-RBD (p = 0.031). Compared to HC, PD + pRBD demonstrated more severe network disruptions than PD-RBD, after FDR correction, including significantly reduced small-world properties (p = 0.003), more widespread nodal alterations (p < 0.05), and extensive functional connectivity disruptions (p < 0.05). Modular analysis revealed functional network connectivity abnormalities within and between multiple networks, characterized by concurrent reductions and abnormal enhancements in functional connectivity.

CONCLUSION

Early PD + pRBD exhibit specific and more severe neurofunctional network impairment pattern. Characterized by more significantly disrupted neurofunctional network topology and widespread functional connectivity abnormalities across multiple brain networks, with potential functional network reorganization. These functioning abnormalities may serve as imaging biomarkers for this clinically malignant subtype and provide potential neurobiological mechanism for understanding its poorer clinical phenotype.