Independent support for corticopallidal contributions to schizophrenia-related functional impairment.
Functional connectivity
Functional impairment
Globus pallidus
Salience network
Schizophrenia
fMRI
Journal
Schizophrenia research
ISSN: 1573-2509
Titre abrégé: Schizophr Res
Pays: Netherlands
ID NLM: 8804207
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
09
10
2019
revised:
02
12
2019
accepted:
15
12
2019
pubmed:
29
12
2019
medline:
22
6
2021
entrez:
29
12
2019
Statut:
ppublish
Résumé
Abnormalities between the prefrontal cortex and basal ganglia have been described by numerous studies of schizophrenia (SZ). We recently reported that individuals with first episode SZ who develop greater vocational and social impairments show lower baseline functional connectivity between the globus pallidus (GP) and regions of the intrinsic salience network. Here we extend these findings to probe the integrity of this system in individuals with chronic illness. All data were obtained from a publicly available Center of Biomedical Research Excellence dataset (http://fcon_1000. nitric.org/indi/retro/cobre.html) that included resting-state fMRI and structural scans, and an array of clinical and neuropsychological measures. Participants with SZ were divided into high- or low-functioning groups based on scores across measures of psychopathology and cognitive functioning. Corticopallidal functional connectivity was examined between low- and high-functioning individuals with SZ and matched healthy control participants. We focused on connectivity between GP structures and a priori regions of the salience network that were significant in our previous study. Exploratory voxel-wise analyses were also conducted. Lower functioning individuals with SZ demonstrated less connectivity between bilateral GP externa and nodes within the salience network, relative to healthy controls. No connectivity differences were observed between low- and high-functioning individuals with SZ. Exploratory voxel-wise analyses highlighted additional large-scale corticopallidal abnormalities in lower-functioning participants with SZ. These results confirm our previous work in a more chronic cohort of individuals with SZ. Our findings further advance corticopallidal connectivity as a biomarker of functional impairments in SZ and lay the groundwork for treatment-based studies.
Sections du résumé
BACKGROUND
Abnormalities between the prefrontal cortex and basal ganglia have been described by numerous studies of schizophrenia (SZ). We recently reported that individuals with first episode SZ who develop greater vocational and social impairments show lower baseline functional connectivity between the globus pallidus (GP) and regions of the intrinsic salience network. Here we extend these findings to probe the integrity of this system in individuals with chronic illness.
METHODS
All data were obtained from a publicly available Center of Biomedical Research Excellence dataset (http://fcon_1000.
PROJECTS
nitric.org/indi/retro/cobre.html) that included resting-state fMRI and structural scans, and an array of clinical and neuropsychological measures. Participants with SZ were divided into high- or low-functioning groups based on scores across measures of psychopathology and cognitive functioning. Corticopallidal functional connectivity was examined between low- and high-functioning individuals with SZ and matched healthy control participants. We focused on connectivity between GP structures and a priori regions of the salience network that were significant in our previous study. Exploratory voxel-wise analyses were also conducted.
RESULTS
Lower functioning individuals with SZ demonstrated less connectivity between bilateral GP externa and nodes within the salience network, relative to healthy controls. No connectivity differences were observed between low- and high-functioning individuals with SZ. Exploratory voxel-wise analyses highlighted additional large-scale corticopallidal abnormalities in lower-functioning participants with SZ.
CONCLUSIONS
These results confirm our previous work in a more chronic cohort of individuals with SZ. Our findings further advance corticopallidal connectivity as a biomarker of functional impairments in SZ and lay the groundwork for treatment-based studies.
Identifiants
pubmed: 31882276
pii: S0920-9964(19)30576-6
doi: 10.1016/j.schres.2019.12.006
pmc: PMC7239703
mid: NIHMS1547547
pii:
doi:
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
168-174Subventions
Organisme : NIMH NIH HHS
ID : K23 MH110661
Pays : United States
Organisme : NCRR NIH HHS
ID : P20 RR021938
Pays : United States
Informations de copyright
Copyright © 2019 Elsevier B.V. All rights reserved.
Références
J Neurol Neurosurg Psychiatry. 2018 Jul;89(7):777-787
pubmed: 29242310
Hum Brain Mapp. 2017 Apr;38(4):1952-1964
pubmed: 28130916
Nat Rev Neurosci. 2002 Mar;3(3):201-15
pubmed: 11994752
Am J Psychiatry. 2006 Mar;163(3):418-25
pubmed: 16513862
Arch Gen Psychiatry. 1972 Dec;27(6):739-46
pubmed: 4637891
Am J Psychiatry. 2004 Mar;161(3):473-9
pubmed: 14992973
Am J Psychiatry. 2006 May;163(5):786-8
pubmed: 16648316
Neuron. 2013 Dec 18;80(6):1359-67
pubmed: 24316296
Mol Psychiatry. 2012 Jul;17(8):841-54
pubmed: 22212597
Neuroimage. 2014 Jul 15;95:287-304
pubmed: 24657353
Front Psychiatry. 2012 Jan 10;2:75
pubmed: 22291663
Lancet. 2015 Aug 22;386(9995):743-800
pubmed: 26063472
Front Neuroinform. 2011 Aug 22;5:13
pubmed: 21897815
Neuropsychopharmacology. 2014 Mar;39(4):1020-30
pubmed: 24165885
Proc Natl Acad Sci U S A. 2018 Oct 16;115(42):10792-10797
pubmed: 30275309
Curr Top Behav Neurosci. 2016;27:357-73
pubmed: 26164592
Am J Psychiatry. 1996 Mar;153(3):321-30
pubmed: 8610818
Schizophr Bull. 2013 Nov;39(6):1296-306
pubmed: 23172003
Neuroimage. 2013 Nov 15;82:208-25
pubmed: 23747457
Arch Gen Psychiatry. 1974 Nov;31(5):609-18
pubmed: 4374156
Am J Psychiatry. 2016 Jan;173(1):69-77
pubmed: 26315980
Schizophr Bull. 2020 Jan 4;46(1):184-192
pubmed: 31150557
J Neurosci. 2013 Aug 21;33(34):13639-53
pubmed: 23966686
Am J Psychiatry. 2008 Feb;165(2):203-13
pubmed: 18172019
Front Neurosci. 2016 Mar 24;10:106
pubmed: 27047328
Schizophr Bull. 2016 Jul;42 Suppl 1:S110-7
pubmed: 27460614
Nat Neurosci. 2002 Mar;5(3):267-71
pubmed: 11865311
Schizophr Bull. 1987;13(2):261-76
pubmed: 3616518
Neuron. 2008 May 8;58(3):306-24
pubmed: 18466742
Front Behav Neurosci. 2015 Feb 25;9:45
pubmed: 25762911
Neuroimage. 2012 Aug 15;62(2):782-90
pubmed: 21979382
Curr Opin Neurobiol. 2001 Apr;11(2):231-9
pubmed: 11301245
Comput Biomed Res. 1996 Jun;29(3):162-73
pubmed: 8812068
Neurosci Biobehav Rev. 2011 Jan;35(3):573-88
pubmed: 20620163
Neuropsychopharmacology. 2018 Oct;43(11):2239-2248
pubmed: 29899404
J Neurosci. 1997 Jan 1;17(1):353-62
pubmed: 8987760
Neurosci Biobehav Rev. 2015 Nov;58:186-210
pubmed: 25684727
Schizophr Res. 2017 Feb;180:58-63
pubmed: 27531067
Schizophr Bull. 2017 Oct 21;43(6):1329-1347
pubmed: 28204755
Mov Disord. 2016 Aug;31(8):1146-54
pubmed: 26900137
Nat Methods. 2011 Jun 26;8(8):665-70
pubmed: 21706013
JAMA Psychiatry. 2015 Jan;72(1):5-13
pubmed: 25372846
Emotion. 2003 Mar;3(1):97-105
pubmed: 12899321