Increased functional connectivity of thalamic subdivisions in patients with Parkinson's disease
Date
2019-09-04
Authors
Owens-Walton, Conor
Jakabek, David
Power, Brian
Walterfang, Mark
Velakoulis, Dennis
van Westen, Danielle
Looi, Jeffrey
Shaw, Marnie
Hansson, Oskar
Journal Title
Journal ISSN
Volume Title
Publisher
Public Library of Science
Abstract
Parkinson's disease (PD) affects 2-3% of the population over the age of 65 with loss of dopaminergic neurons in the substantia nigra impacting the functioning of basal ganglia-thalamocortical circuits. The precise role played by the thalamus is unknown, despite its critical role in the functioning of the cerebral cortex, and the abnormal neuronal activity of the structure in PD. Our objective was to more clearly elucidate how functional connectivity and morphology of the thalamus are impacted in PD (n = 32) compared to Controls (n = 20). To investigate functional connectivity of the thalamus we subdivided the structure into two important regions-of-interest, the first with putative connections to the motor cortices and the second with putative connections to prefrontal cortices. We then investigated potential differences in the size and shape of the thalamus in PD, and how morphology and functional connectivity relate to clinical variables. Our data demonstrate that PD is associated with increases in functional connectivity between motor subdivisions of the thalamus and the supplementary motor area, and between prefrontal thalamic subdivisions and nuclei of the basal ganglia, anterior and dorsolateral prefrontal cortices, as well as the anterior and paracingulate gyri. These results suggest that PD is associated with increased functional connectivity of subdivisions of the thalamus which may be indicative alterations to basal ganglia-thalamocortical circuitry.
Description
Keywords
Citation
Owens-Walton C, Jakabek D, Power BD, Walterfang M, Velakoulis D, van Westen D, et al. (2019) Increased functional connectivity of thalamic subdivisions in patients with Parkinson’s disease. PLoS ONE 14(9): e0222002. https://doi. org/10.1371/journal.pone.0222002
Collections
Source
PLOS ONE (Public Library of Science)
Type
Journal article
Book Title
Entity type
Access Statement
Open Access
License Rights
Creative Commons Attribution License
Restricted until
Downloads
File
Description