Cortical thickness reductions associate with brain network architecture in major depressive disorder.

Connectome Cortical thickness Major depressive disorder Structural connectivity

Journal

Journal of affective disorders
ISSN: 1573-2517
Titre abrégé: J Affect Disord
Pays: Netherlands
ID NLM: 7906073

Informations de publication

Date de publication:
22 Nov 2023
Historique:
received: 01 02 2023
revised: 25 10 2023
accepted: 13 11 2023
pubmed: 25 11 2023
medline: 25 11 2023
entrez: 24 11 2023
Statut: aheadofprint

Résumé

Cortical thickness reductions in major depressive disorder are distributed across multiple regions. Research has indicated that cortical atrophy is influenced by connectome architecture on a range of neurological and psychiatric diseases. However, whether connectome architecture contributes to changes in cortical thickness in the same manner as it does in depression is unclear. This study aims to explain the distribution of cortical thickness reductions across the cortex in depression by brain connectome architecture. Here, we calculated a differential map of cortical thickness between 110 depression patients and 88 age-, gender-, and education level-matched healthy controls by using T1-weighted images and a structural network reconstructed through the diffusion tensor imaging of control group. We then used a neighborhood deformation model to explore how cortical thickness change in an area is influenced by areas structurally connected to it. We found that cortical thickness in the frontoparietal and default networks decreased in depression, regional cortical thickness changes were related to reductions in their neighbors and were mainly limited by the frontoparietal and default networks, and the epicenter was in the prefrontal lobe. Current findings suggest that connectome architecture contributes to the irregular topographic distribution of cortical thickness reductions in depression and cortical atrophy is restricted by and dependent on structural foundation.

Sections du résumé

BACKGROUND BACKGROUND
Cortical thickness reductions in major depressive disorder are distributed across multiple regions. Research has indicated that cortical atrophy is influenced by connectome architecture on a range of neurological and psychiatric diseases. However, whether connectome architecture contributes to changes in cortical thickness in the same manner as it does in depression is unclear. This study aims to explain the distribution of cortical thickness reductions across the cortex in depression by brain connectome architecture.
METHODS METHODS
Here, we calculated a differential map of cortical thickness between 110 depression patients and 88 age-, gender-, and education level-matched healthy controls by using T1-weighted images and a structural network reconstructed through the diffusion tensor imaging of control group. We then used a neighborhood deformation model to explore how cortical thickness change in an area is influenced by areas structurally connected to it.
RESULTS RESULTS
We found that cortical thickness in the frontoparietal and default networks decreased in depression, regional cortical thickness changes were related to reductions in their neighbors and were mainly limited by the frontoparietal and default networks, and the epicenter was in the prefrontal lobe.
CONCLUSION CONCLUSIONS
Current findings suggest that connectome architecture contributes to the irregular topographic distribution of cortical thickness reductions in depression and cortical atrophy is restricted by and dependent on structural foundation.

Identifiants

pubmed: 38000466
pii: S0165-0327(23)01405-2
doi: 10.1016/j.jad.2023.11.037
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

175-182

Informations de copyright

Copyright © 2023. Published by Elsevier B.V.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that there is no conflict of interests.

Auteurs

Wei Sheng (W)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Qian Cui (Q)

School of Public Affairs and Administration, University of Electronic Science and Technology of China, Chengdu, China. Electronic address: qiancui26@gmail.com.

YuanHong Guo (Y)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Qin Tang (Q)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Yun-Shuang Fan (YS)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Chong Wang (C)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Jing Guo (J)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Fengmei Lu (F)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Zongling He (Z)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China.

Huafu Chen (H)

The Clinical Hospital of Chengdu Brain Science Institute, School of Life Science and Technology, University of Electronic Science and Technology of China, Chengdu, China; MOE Key Lab for Neuroinformation, HighField Magnetic Resonance Brain Imaging Key Laboratory of Sichuan Province, University of Electronic Science and Technology of China, Chengdu, China. Electronic address: chenhf@uestc.edu.cn.

Classifications MeSH