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Disruption of rich club organisation in cerebral small vessel disease
Cerebral small vessel disease (SVD) is an important cause of vascular cognitive impairment. Recent studies have demonstrated that structural connectivity of brain networks in SVD is disrupted. However, little is known about the extent and location of the reduced connectivity in SVD. Here they invest...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6866838/ https://www.ncbi.nlm.nih.gov/pubmed/27935154 http://dx.doi.org/10.1002/hbm.23479 |
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author | Tuladhar, Anil M. Lawrence, Andrew Norris, David. G. Barrick, Thomas R. Markus, Hugh S. de Leeuw, Frank‐Erik |
author_facet | Tuladhar, Anil M. Lawrence, Andrew Norris, David. G. Barrick, Thomas R. Markus, Hugh S. de Leeuw, Frank‐Erik |
author_sort | Tuladhar, Anil M. |
collection | PubMed |
description | Cerebral small vessel disease (SVD) is an important cause of vascular cognitive impairment. Recent studies have demonstrated that structural connectivity of brain networks in SVD is disrupted. However, little is known about the extent and location of the reduced connectivity in SVD. Here they investigate the rich club organisation—a set of highly connected and interconnected regions—and investigate whether there is preferential rich club disruption in SVD. Diffusion tensor imaging (DTI) and cognitive assessment were performed in a discovery sample of SVD patients (n = 115) and healthy control subjects (n = 50). Results were replicated in an independent dataset (49 SVD with confluent WMH cases and 108 SVD controls) with SVD patients having a similar SVD phenotype to that of the discovery cases. Rich club organisation was examined in structural networks derived from DTI followed by deterministic tractography. Structural networks in SVD patients were less dense with lower network strength and efficiency. Reduced connectivity was found in SVD, which was preferentially located in the connectivity between the rich club nodes rather than in the feeder and peripheral connections, a finding confirmed in both datasets. In discovery dataset, lower rich club connectivity was associated with lower scores on psychomotor speed (β = 0.29, P < 0.001) and executive functions (β = 0.20, P = 0.009). These results suggest that SVD is characterized by abnormal connectivity between rich club hubs in SVD and provide evidence that abnormal rich club organisation might contribute to the development of cognitive impairment in SVD. Hum Brain Mapp 38:1751–1766, 2017. © 2017 Wiley Periodicals, Inc. |
format | Online Article Text |
id | pubmed-6866838 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68668382020-06-12 Disruption of rich club organisation in cerebral small vessel disease Tuladhar, Anil M. Lawrence, Andrew Norris, David. G. Barrick, Thomas R. Markus, Hugh S. de Leeuw, Frank‐Erik Hum Brain Mapp Research Articles Cerebral small vessel disease (SVD) is an important cause of vascular cognitive impairment. Recent studies have demonstrated that structural connectivity of brain networks in SVD is disrupted. However, little is known about the extent and location of the reduced connectivity in SVD. Here they investigate the rich club organisation—a set of highly connected and interconnected regions—and investigate whether there is preferential rich club disruption in SVD. Diffusion tensor imaging (DTI) and cognitive assessment were performed in a discovery sample of SVD patients (n = 115) and healthy control subjects (n = 50). Results were replicated in an independent dataset (49 SVD with confluent WMH cases and 108 SVD controls) with SVD patients having a similar SVD phenotype to that of the discovery cases. Rich club organisation was examined in structural networks derived from DTI followed by deterministic tractography. Structural networks in SVD patients were less dense with lower network strength and efficiency. Reduced connectivity was found in SVD, which was preferentially located in the connectivity between the rich club nodes rather than in the feeder and peripheral connections, a finding confirmed in both datasets. In discovery dataset, lower rich club connectivity was associated with lower scores on psychomotor speed (β = 0.29, P < 0.001) and executive functions (β = 0.20, P = 0.009). These results suggest that SVD is characterized by abnormal connectivity between rich club hubs in SVD and provide evidence that abnormal rich club organisation might contribute to the development of cognitive impairment in SVD. Hum Brain Mapp 38:1751–1766, 2017. © 2017 Wiley Periodicals, Inc. John Wiley and Sons Inc. 2016-12-09 /pmc/articles/PMC6866838/ /pubmed/27935154 http://dx.doi.org/10.1002/hbm.23479 Text en © 2016 The Authors Human Brain Mapping Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Tuladhar, Anil M. Lawrence, Andrew Norris, David. G. Barrick, Thomas R. Markus, Hugh S. de Leeuw, Frank‐Erik Disruption of rich club organisation in cerebral small vessel disease |
title | Disruption of rich club organisation in cerebral small vessel disease |
title_full | Disruption of rich club organisation in cerebral small vessel disease |
title_fullStr | Disruption of rich club organisation in cerebral small vessel disease |
title_full_unstemmed | Disruption of rich club organisation in cerebral small vessel disease |
title_short | Disruption of rich club organisation in cerebral small vessel disease |
title_sort | disruption of rich club organisation in cerebral small vessel disease |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6866838/ https://www.ncbi.nlm.nih.gov/pubmed/27935154 http://dx.doi.org/10.1002/hbm.23479 |
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