Choroid plexus enlargement is associated with neuroinflammation and reduction of blood brain barrier permeability in depression.


Journal

NeuroImage. Clinical
ISSN: 2213-1582
Titre abrégé: Neuroimage Clin
Pays: Netherlands
ID NLM: 101597070

Informations de publication

Date de publication:
2022
Historique:
received: 23 09 2021
revised: 08 12 2021
accepted: 21 12 2021
pubmed: 1 1 2022
medline: 4 3 2022
entrez: 31 12 2021
Statut: ppublish

Résumé

Recent studies have shown that choroid plexuses (CP) may be involved in the neuro-immune axes, playing a role in the interaction between the central and peripheral inflammation. Here we aimed to investigate CP volume alterations in depression and their associations with inflammation. 51 depressed participants (HDRS score > 13) and 25 age- and sex-matched healthy controls (HCs) from the Wellcome Trust NIMA consortium were re-analysed for the study. All the participants underwent full peripheral cytokine profiling and simultaneous [11C]PK11195 PET/structural MRI imaging for measuring neuroinflammation and CP volume respectively. We found a significantly greater CP volume in depressed subjects compared to HCs (t This result supports the hypothesis that changes in brain barriers may cause reduction in solute exchanges between blood and CSF, disturbing the brain homeostasis and ultimately contributing to inflammation in depression. Given that CP anomalies have been recently detected in other brain disorders, these results may not be specific to depression and might extend to other conditions with a peripheral inflammatory component.

Sections du résumé

BACKGROUND
Recent studies have shown that choroid plexuses (CP) may be involved in the neuro-immune axes, playing a role in the interaction between the central and peripheral inflammation. Here we aimed to investigate CP volume alterations in depression and their associations with inflammation.
METHODS
51 depressed participants (HDRS score > 13) and 25 age- and sex-matched healthy controls (HCs) from the Wellcome Trust NIMA consortium were re-analysed for the study. All the participants underwent full peripheral cytokine profiling and simultaneous [11C]PK11195 PET/structural MRI imaging for measuring neuroinflammation and CP volume respectively.
RESULTS
We found a significantly greater CP volume in depressed subjects compared to HCs (t
CONCLUSION
This result supports the hypothesis that changes in brain barriers may cause reduction in solute exchanges between blood and CSF, disturbing the brain homeostasis and ultimately contributing to inflammation in depression. Given that CP anomalies have been recently detected in other brain disorders, these results may not be specific to depression and might extend to other conditions with a peripheral inflammatory component.

Identifiants

pubmed: 34972034
pii: S2213-1582(21)00370-3
doi: 10.1016/j.nicl.2021.102926
pmc: PMC8718974
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

102926

Subventions

Organisme : Wellcome Trust
Pays : United Kingdom
Organisme : Medical Research Council
ID : MC_G0802534
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/M009041/1
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 104025
Pays : United Kingdom

Informations de copyright

Copyright © 2021 The Author(s). Published by Elsevier Inc. All rights reserved.

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Auteurs

Noha Althubaity (N)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Radiological Sciences, College of Applied Medical Science, King Saud bin Abdulaziz University for Health Sciences, Riyadh, Saudi Arabia. Electronic address: noha.althubaity@kcl.ac.uk.

Julia Schubert (J)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Daniel Martins (D)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Tayyabah Yousaf (T)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Maria A Nettis (MA)

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Valeria Mondelli (V)

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Carmine Pariante (C)

Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Neil A Harrison (NA)

Cardiff University Brain Research Imaging Centre (CUBRIC), Cardiff University, Cardiff, UK; Department of Neuroscience, Brighton and Sussex Medical School, University of Sussex, UK.

Edward T Bullmore (ET)

Department of Psychiatry, School of Clinical Medicine, University of Cambridge, UK; Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK; Immuno-Psychiatry, Immuno-Inflammation Therapeutic Area Unit, GlaxoSmithKline R&D, Stevenage, UK.

Danai Dima (D)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Psychology, School of Arts and Social Sciences, City University of London, London, UK.

Federico E Turkheimer (FE)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.

Mattia Veronese (M)

Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Department of Information Engineering, University of Padua, Padua, Italy.

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