The changes in kynurenine metabolites induced by rTMS in treatment-resistant depression: A pilot study.

Cognitive dysfunction Kynurenine Metabolomics Repetitive transcranial magnetic stimulation (rTMS) Treatment-resistant depression (TRD)

Journal

Journal of psychiatric research
ISSN: 1879-1379
Titre abrégé: J Psychiatr Res
Pays: England
ID NLM: 0376331

Informations de publication

Date de publication:
06 2021
Historique:
received: 22 01 2021
revised: 28 03 2021
accepted: 04 04 2021
pubmed: 18 4 2021
medline: 6 7 2021
entrez: 17 4 2021
Statut: ppublish

Résumé

Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive brain stimulation technique that is considered a valuable and promising technique for improving depressive symptoms in treatment-resistant depression (TRD). However, the exact mechanism by which rTMS ameliorates depressive symptoms remains to be clarified. The aim of the present study was to analyzed the changes in metabolites of patients with TRD in the rTMS treatment, especially focusing on the kynurenine (KYN) pathway. Thirteen participants with TRD were enrolled in a high-frequency (10 Hz) rTMS study. Cognitive function, depressive symptoms and the concentration of plasma tryptophan (TRP) metabolites were measured at baseline and at the endpoint of rTMS treatment. rTMS treatment significantly improved depressive symptom scores and some subscales of cognitive dysfunction. The present study has demonstrated that rTMS treatment significantly increased plasma TRP levels and significantly decreased plasma serotonin levels, while plasma KYN and kynurenic acid level as well as KYN/TRP ratio remained unchanged. This is the first metabolomic study of patients with TRD undergoing rTMS treatment. To validate the present results, it is necessary to increase the number of cases including controls, use a sample of cerebrospinal fluid, and measure blood concentration over time in the course of rTMS treatment.

Sections du résumé

BACKGROUND
Repetitive transcranial magnetic stimulation (rTMS) is a noninvasive brain stimulation technique that is considered a valuable and promising technique for improving depressive symptoms in treatment-resistant depression (TRD). However, the exact mechanism by which rTMS ameliorates depressive symptoms remains to be clarified.
OBJECTIVE
The aim of the present study was to analyzed the changes in metabolites of patients with TRD in the rTMS treatment, especially focusing on the kynurenine (KYN) pathway.
METHODS
Thirteen participants with TRD were enrolled in a high-frequency (10 Hz) rTMS study. Cognitive function, depressive symptoms and the concentration of plasma tryptophan (TRP) metabolites were measured at baseline and at the endpoint of rTMS treatment.
RESULTS
rTMS treatment significantly improved depressive symptom scores and some subscales of cognitive dysfunction. The present study has demonstrated that rTMS treatment significantly increased plasma TRP levels and significantly decreased plasma serotonin levels, while plasma KYN and kynurenic acid level as well as KYN/TRP ratio remained unchanged.
CONCLUSIONS
This is the first metabolomic study of patients with TRD undergoing rTMS treatment. To validate the present results, it is necessary to increase the number of cases including controls, use a sample of cerebrospinal fluid, and measure blood concentration over time in the course of rTMS treatment.

Identifiants

pubmed: 33865168
pii: S0022-3956(21)00228-4
doi: 10.1016/j.jpsychires.2021.04.009
pii:
doi:

Substances chimiques

Kynurenine 343-65-7

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

194-199

Informations de copyright

Copyright © 2021. Published by Elsevier Ltd.

Auteurs

Hiroshi Tateishi (H)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan. Electronic address: tateishh@cc.saga-u.ac.jp.

Daiki Setoyama (D)

Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi Higashi-ku 3-1-1, Fukuoka, 812-8582, Japan.

Dongchon Kang (D)

Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University, Maidashi Higashi-ku 3-1-1, Fukuoka, 812-8582, Japan.

Jun Matsushima (J)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Ryohei Kojima (R)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Yuka Fujii (Y)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Seiji Mawatari (S)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Jun Kikuchi (J)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Yuta Sakemura (Y)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Junko Fukuchi (J)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Takumi Shiraishi (T)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Toshihiko Maekawa (T)

Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi Higashi-ku 3-1-1, Fukuoka, 812-8582, Japan.

Takahiro A Kato (TA)

Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Maidashi Higashi-ku 3-1-1, Fukuoka, 812-8582, Japan. Electronic address: takahiro@npsych.med.kyushu-u.ac.jp.

Toyoko Asami (T)

Department of Rehabilitation Medicine, Saga University Hospital, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Yoshito Mizoguchi (Y)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

Akira Monji (A)

Department of Psychiatry, Faculty of Medicine, Saga University, Nabeshima 5-1-1, Saga, 849-8501, Japan.

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