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Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease

Parkinson's disease (PD) is largely attributed to disruptions in the nigrostriatal dopamine system. These neurodegenerative changes may also have a more global effect on intrinsic brain organization at the cortical level. Functional brain connectivity between neurocognitive systems related to c...

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Autores principales: Putcha, Deepti, Ross, Robert S., Cronin-Golomb, Alice, Janes, Amy C., Stern, Chantal E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320252/
https://www.ncbi.nlm.nih.gov/pubmed/25685711
http://dx.doi.org/10.1016/j.nicl.2015.01.012
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author Putcha, Deepti
Ross, Robert S.
Cronin-Golomb, Alice
Janes, Amy C.
Stern, Chantal E.
author_facet Putcha, Deepti
Ross, Robert S.
Cronin-Golomb, Alice
Janes, Amy C.
Stern, Chantal E.
author_sort Putcha, Deepti
collection PubMed
description Parkinson's disease (PD) is largely attributed to disruptions in the nigrostriatal dopamine system. These neurodegenerative changes may also have a more global effect on intrinsic brain organization at the cortical level. Functional brain connectivity between neurocognitive systems related to cognitive processing is critical for effective neural communication, and is disrupted across neurological disorders. Three core neurocognitive networks have been established as playing a critical role in the pathophysiology of many neurological disorders: the default-mode network (DMN), the salience network (SN), and the central executive network (CEN). In healthy adults, DMN–CEN interactions are anti-correlated while SN–CEN interactions are strongly positively correlated even at rest, when individuals are not engaging in any task. These intrinsic between-network interactions at rest are necessary for efficient suppression of the DMN and activation of the CEN during a range of cognitive tasks. To identify whether these network interactions are disrupted in individuals with PD, we used resting state functional magnetic resonance imaging (rsfMRI) to compare between-network connectivity between 24 PD participants and 20 age-matched controls (MC). In comparison to the MC, individuals with PD showed significantly less SN–CEN coupling and greater DMN–CEN coupling during rest. Disease severity, an index of striatal dysfunction, was related to reduced functional coupling between the striatum and SN. These results demonstrate that individuals with PD have a dysfunctional pattern of interaction between core neurocognitive networks compared to what is found in healthy individuals, and that interaction between the SN and the striatum is even more profoundly disrupted in those with greater disease severity.
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spelling pubmed-43202522015-02-14 Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease Putcha, Deepti Ross, Robert S. Cronin-Golomb, Alice Janes, Amy C. Stern, Chantal E. Neuroimage Clin Regular Article Parkinson's disease (PD) is largely attributed to disruptions in the nigrostriatal dopamine system. These neurodegenerative changes may also have a more global effect on intrinsic brain organization at the cortical level. Functional brain connectivity between neurocognitive systems related to cognitive processing is critical for effective neural communication, and is disrupted across neurological disorders. Three core neurocognitive networks have been established as playing a critical role in the pathophysiology of many neurological disorders: the default-mode network (DMN), the salience network (SN), and the central executive network (CEN). In healthy adults, DMN–CEN interactions are anti-correlated while SN–CEN interactions are strongly positively correlated even at rest, when individuals are not engaging in any task. These intrinsic between-network interactions at rest are necessary for efficient suppression of the DMN and activation of the CEN during a range of cognitive tasks. To identify whether these network interactions are disrupted in individuals with PD, we used resting state functional magnetic resonance imaging (rsfMRI) to compare between-network connectivity between 24 PD participants and 20 age-matched controls (MC). In comparison to the MC, individuals with PD showed significantly less SN–CEN coupling and greater DMN–CEN coupling during rest. Disease severity, an index of striatal dysfunction, was related to reduced functional coupling between the striatum and SN. These results demonstrate that individuals with PD have a dysfunctional pattern of interaction between core neurocognitive networks compared to what is found in healthy individuals, and that interaction between the SN and the striatum is even more profoundly disrupted in those with greater disease severity. Elsevier 2015-01-27 /pmc/articles/PMC4320252/ /pubmed/25685711 http://dx.doi.org/10.1016/j.nicl.2015.01.012 Text en © 2015 The Authors. Published by Elsevier Inc. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Regular Article
Putcha, Deepti
Ross, Robert S.
Cronin-Golomb, Alice
Janes, Amy C.
Stern, Chantal E.
Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title_full Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title_fullStr Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title_full_unstemmed Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title_short Altered intrinsic functional coupling between core neurocognitive networks in Parkinson's disease
title_sort altered intrinsic functional coupling between core neurocognitive networks in parkinson's disease
topic Regular Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4320252/
https://www.ncbi.nlm.nih.gov/pubmed/25685711
http://dx.doi.org/10.1016/j.nicl.2015.01.012
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