Attenuated brain white matter functional network interactions in Parkinson's disease

Parkinson's disease (PD) is a neurodegenerative disorder characterized by extensive structural abnormalities in cortical and subcortical brain areas. However, an association between changes in the functional networks in brain white matter (BWM) and Parkinson's symptoms remains unclear. Wit...

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Bibliographic Details
Published in:Human brain mapping Vol. 43; no. 15; pp. 4567 - 4579
Main Authors: Meng, Li, Wang, Hongyu, Zou, Ting, Wang, Xuyang, Chen, Huafu, Xie, Fangfang, Li, Rong
Format: Journal Article
Language:English
Published: Hoboken, USA John Wiley & Sons, Inc 15.10.2022
Subjects:
Abnormalities
Algorithms
Brain
Brain - diagnostic imaging
Brain mapping
Causality
Clustering
Demographics
Functional magnetic resonance imaging
Granger causality analysis
Humans
interactions
Magnetic resonance imaging
Mental depression
Mental disorders
Mental Status and Dementia Tests
motor and nonmotor symptoms
Movement disorders
Nervous system
Networks
Neurodegenerative diseases
Neuroimaging
Parkinson Disease - diagnostic imaging
Parkinson's disease
Patients
Regression coefficients
Signs and symptoms
Substantia alba
White Matter - diagnostic imaging
white matter functional networks
Canada
Montreal Quebec Canada
Granger causality analysis
Parkinson's disease
motor and nonmotor symptoms
white matter functional networks
interactions
ISSN:1065-9471, 1097-0193, 1097-0193
Online Access:Get full text
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Summary:Parkinson's disease (PD) is a neurodegenerative disorder characterized by extensive structural abnormalities in cortical and subcortical brain areas. However, an association between changes in the functional networks in brain white matter (BWM) and Parkinson's symptoms remains unclear. With confirming evidence that resting‐state functional magnetic resonance imaging (rs‐fMRI) of BWM signals can effectively describe neuronal activity, this study investigated the interactions among BWM functional networks in PD relative to healthy controls (HC). Sixty‐eight patients with PD and sixty‐three HC underwent rs‐fMRI. Twelve BWM functional networks were identified by K‐means clustering algorithm, which were further classified as deep, middle, and superficial layers. Network‐level interactions were examined via coefficient Granger causality analysis. Compared with the HC, the patients with PD displayed significantly weaker functional interaction strength within the BWM networks, particularly excitatory influences from the superficial to deep networks. The patients also showed significantly weaker inhibitory influences from the deep to superficial networks. Additionally, the sum of the absolutely positive/negative regression coefficients of the tri‐layered networks in the patients was lower relative to HC (p < .05, corrected for false discovery rate). Moreover, we found the functional interactions involving the deep BWM networks negatively correlated with part III of the Unified Parkinson's Disease Rating Scales and Hamilton Depression Scales. Taken together, we demonstrated attenuated BWM interactions in PD and these abnormalities were associated with clinical motor and nonmotor symptoms. These findings may aid understanding of the neuropathology of PD and its progression throughout the nervous system from the perspective of BWM function. We found that the deep white matter functional networks associated with basal ganglia have extensive abnormal interactions with other networks in PD. Furthermore, disrupted interactions of the deep networks were significantly associated with motor and nonmotor symptoms in PD. These findings suggest that informational interactions among the white matter functional networks in PD appear interrupted relative to healthy individuals.
Bibliography:Funding information
Li Meng and Hongyu Wang contributed equally to this work.
Chengdu Science and Technology Project, Grant/Award Number: 2021‐YF05‐01211‐SN; National Natural Science Foundation of China, Grant/Award Numbers: 61906034, 62036003, 82072006, U1808204
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ISSN:1065-9471
1097-0193
1097-0193
DOI:10.1002/hbm.25973