Linking enlarged choroid plexus with plasma analyte and structural phenotypes in clinical high risk for psychosis: A multisite neuroimaging study.

Choroid plexus Clinical high risk for psychosis Inflammation Lateral ventricle

Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
31 Dec 2023
Historique:
received: 19 07 2023
revised: 04 12 2023
accepted: 19 12 2023
medline: 4 1 2024
pubmed: 4 1 2024
entrez: 3 1 2024
Statut: aheadofprint

Résumé

Choroid plexus (ChP) enlargement exists in first-episode and chronic psychosis, but whether enlargement occurs before psychosis onset is unknown. This study investigated whether ChP volume is enlarged in individuals with clinical high-risk (CHR) for psychosis and whether these changes are related to clinical, neuroanatomical, and plasma analytes. Clinical and neuroimaging data from the North American Prodrome Longitudinal Study 2 (NAPLS2) was used for analysis. 509 participants (169 controls, 340 CHR) were recruited. Conversion status was determined after 2-years of follow-up, with 36 psychosis converters. The lateral ventricle ChP was manually segmented from baseline scans. A subsample of 31 controls and 53 CHR had plasma analyte and neuroimaging data. Compared to controls, CHR (d = 0.23, p = 0.017) and non-converters (d = 0.22, p = 0.03) demonstrated higher ChP volumes, but not in converters. In CHR, greater ChP volume correlated with lower cortical (r = -0.22, p < 0.001), subcortical gray matter (r = -0.21, p < 0.001), and total white matter volume (r = -0.28,p < 0.001), as well as larger lateral ventricle volume (r = 0.63,p < 0.001). Greater ChP volume correlated with makers functionally associated with the lateral ventricle ChP in CHR [CCL1 (r = -0.30, p = 0.035), ICAM1 (r = 0.33, p = 0.02)], converters [IL1β (r = 0.66, p = 0.004)], and non-converters [BMP6 (r = -0.96, p < 0.001), CALB1 (r = -0.98, p < 0.001), ICAM1 (r = 0.80, p = 0.003), SELE (r = 0.59, p = 0.026), SHBG (r = 0.99, p < 0.001), TNFRSF10C (r = 0.78, p = 0.001)]. CHR and non-converters demonstrated significantly larger ChP volumes compared to controls. Enlarged ChP was associated with neuroanatomical alterations and analyte markers functionally associated with the ChP. These findings suggest that the ChP may be a key an important biomarker in CHR.

Sections du résumé

BACKGROUND BACKGROUND
Choroid plexus (ChP) enlargement exists in first-episode and chronic psychosis, but whether enlargement occurs before psychosis onset is unknown. This study investigated whether ChP volume is enlarged in individuals with clinical high-risk (CHR) for psychosis and whether these changes are related to clinical, neuroanatomical, and plasma analytes.
METHODS METHODS
Clinical and neuroimaging data from the North American Prodrome Longitudinal Study 2 (NAPLS2) was used for analysis. 509 participants (169 controls, 340 CHR) were recruited. Conversion status was determined after 2-years of follow-up, with 36 psychosis converters. The lateral ventricle ChP was manually segmented from baseline scans. A subsample of 31 controls and 53 CHR had plasma analyte and neuroimaging data.
RESULTS RESULTS
Compared to controls, CHR (d = 0.23, p = 0.017) and non-converters (d = 0.22, p = 0.03) demonstrated higher ChP volumes, but not in converters. In CHR, greater ChP volume correlated with lower cortical (r = -0.22, p < 0.001), subcortical gray matter (r = -0.21, p < 0.001), and total white matter volume (r = -0.28,p < 0.001), as well as larger lateral ventricle volume (r = 0.63,p < 0.001). Greater ChP volume correlated with makers functionally associated with the lateral ventricle ChP in CHR [CCL1 (r = -0.30, p = 0.035), ICAM1 (r = 0.33, p = 0.02)], converters [IL1β (r = 0.66, p = 0.004)], and non-converters [BMP6 (r = -0.96, p < 0.001), CALB1 (r = -0.98, p < 0.001), ICAM1 (r = 0.80, p = 0.003), SELE (r = 0.59, p = 0.026), SHBG (r = 0.99, p < 0.001), TNFRSF10C (r = 0.78, p = 0.001)].
CONCLUSIONS CONCLUSIONS
CHR and non-converters demonstrated significantly larger ChP volumes compared to controls. Enlarged ChP was associated with neuroanatomical alterations and analyte markers functionally associated with the ChP. These findings suggest that the ChP may be a key an important biomarker in CHR.

Identifiants

pubmed: 38169244
pii: S0889-1591(23)00403-8
doi: 10.1016/j.bbi.2023.12.021
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

Copyright © 2023 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Deepthi Bannai (D)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Martin Reuter (M)

German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany; A.A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Boston, MA, USA; Department of Radiology, Harvard Medical School, Boston, MA, USA.

Rachal Hegde (R)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Dung Hoang (D)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Iniya Adhan (I)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Swetha Gandu (S)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Sovannarath Pong (S)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Nick Raymond (N)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Victor Zeng (V)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Yoonho Chung (Y)

Department of Psychology, Yale University, New Haven, CT, USA.

George He (G)

Department of Psychology, Yale University, New Haven, CT, USA.

Daqiang Sun (D)

Semel Institute for Neuroscience and Human Behavior and Department of Psychology, UCLA, Los Angeles, CA, USA.

Theo G M van Erp (TGM)

Clinical Translational Neuroscience Laboratory, Department of Psychiatry and Human Behavior, UC Irvine, Irvine, CA, USA.

Jean Addington (J)

Hotchkins Brain Institute, Department of Psychiatry, University of Calgary, Calgary, AB, Canada.

Carrie E Bearden (CE)

Semel Institute for Neuroscience and Human Behavior and Department of Psychology, UCLA, Los Angeles, CA, USA.

Kristin Cadenhead (K)

Department of Psychiatry, UCSD, San Diego, CA, USA.

Barbara Cornblatt (B)

Department of Psychiatry, Zucker Hillside Hospital, Queens, NY, USA.

Daniel H Mathalon (DH)

Department of Psychiatry, UCSF, San Francisco, CA, USA.

Thomas McGlashan (T)

Department of Psychiatry, Yale University, New Haven, CT, USA.

Clark Jeffries (C)

Renaissance Computing Institute, University of North Carolina, Chapel Hill, NC, USA.

William Stone (W)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.

Ming Tsuang (M)

Department of Psychiatry, UCSD, San Diego, CA, USA.

Elaine Walker (E)

Department of Psychology, Yale University, New Haven, CT, USA.

Scott W Woods (SW)

Department of Psychiatry, Yale University, New Haven, CT, USA.

Tyrone D Cannon (TD)

Department of Psychology, Yale University, New Haven, CT, USA; Department of Psychiatry, Yale University, New Haven, CT, USA.

Diana Perkins (D)

Renaissance Computing Institute, University of North Carolina, Chapel Hill, NC, USA; Department of Psychiatry, University of North Carolina, Chapel Hill, NC, USA.

Matcheri Keshavan (M)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA.

Paulo Lizano (P)

Department of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Psychiatry, Harvard Medical School, Boston, MA, USA; Division of Translational Neuroscience, Beth Israel Deaconess Medical Center, Boston, MA, USA.

Classifications MeSH