Glutamatergic Neurometabolite Levels in Bipolar Disorder: A Systematic Review and Meta-analysis of Proton Magnetic Resonance Spectroscopy Studies.

Anterior cingulate cortex Bipolar disorder Glutamate Glutamate plus glutamine Glx Meta-analysis Proton magnetic resonance spectroscopy

Journal

Biological psychiatry. Cognitive neuroscience and neuroimaging
ISSN: 2451-9030
Titre abrégé: Biol Psychiatry Cogn Neurosci Neuroimaging
Pays: United States
ID NLM: 101671285

Informations de publication

Date de publication:
02 2023
Historique:
received: 18 11 2021
revised: 27 09 2022
accepted: 28 09 2022
entrez: 8 2 2023
pubmed: 9 2 2023
medline: 11 2 2023
Statut: ppublish

Résumé

The glutamatergic system is thought to play an important role in the pathophysiology of bipolar disorder (BD). While there has been an increase in proton magnetic resonance spectroscopy studies examining this neurotransmission system, the results are inconsistent. Possible reasons for the inconsistency, including clinical features such as mood state and childhood versus adulthood age, were not addressed in previous meta-analyses. This systematic review and meta-analysis of proton magnetic resonance spectroscopy studies of BD included 40 studies, with 1135 patients with BD and 964 healthy control (HC) subjects. Glutamate plus glutamine and glutamine levels in the anterior cingulate cortex of patients with BD were significantly elevated compared with those of HC subjects (standardized mean difference = 0.42, 0.48, respectively). Subgroup analyses showed that adult BD patients had significantly higher levels of glutamate plus glutamine than adult HC subjects, but this was not the case in pediatric patients. For mood states, anterior cingulate cortex glutamate plus glutamine levels were higher in patients with bipolar depression than those in HC subjects. Our results imply that glutamatergic dysfunction in the anterior cingulate cortex may be implicated in the pathophysiology of BD, which is most evident in adult BD patients and patients with bipolar depression.

Sections du résumé

BACKGROUND
The glutamatergic system is thought to play an important role in the pathophysiology of bipolar disorder (BD). While there has been an increase in proton magnetic resonance spectroscopy studies examining this neurotransmission system, the results are inconsistent. Possible reasons for the inconsistency, including clinical features such as mood state and childhood versus adulthood age, were not addressed in previous meta-analyses.
METHODS
This systematic review and meta-analysis of proton magnetic resonance spectroscopy studies of BD included 40 studies, with 1135 patients with BD and 964 healthy control (HC) subjects.
RESULTS
Glutamate plus glutamine and glutamine levels in the anterior cingulate cortex of patients with BD were significantly elevated compared with those of HC subjects (standardized mean difference = 0.42, 0.48, respectively). Subgroup analyses showed that adult BD patients had significantly higher levels of glutamate plus glutamine than adult HC subjects, but this was not the case in pediatric patients. For mood states, anterior cingulate cortex glutamate plus glutamine levels were higher in patients with bipolar depression than those in HC subjects.
CONCLUSIONS
Our results imply that glutamatergic dysfunction in the anterior cingulate cortex may be implicated in the pathophysiology of BD, which is most evident in adult BD patients and patients with bipolar depression.

Identifiants

pubmed: 36754485
pii: S2451-9022(22)00246-4
doi: 10.1016/j.bpsc.2022.09.017
pii:
doi:

Substances chimiques

Glutamine 0RH81L854J
Glutamic Acid 3KX376GY7L

Types de publication

Meta-Analysis Systematic Review Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

140-150

Informations de copyright

Copyright © 2022. Published by Elsevier Inc.

Auteurs

Hiroyasu Ino (H)

Tokyo Metropolitan Matsuzawa Hospital, Tokyo, Japan; Center for Biomedical Ethics and Law, University of Tokyo, Tokyo, Japan.

Shiori Honda (S)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.

Kohei Yamada (K)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.

Nobuyuki Horita (N)

Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Sakiko Tsugawa (S)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.

Kazunari Yoshida (K)

Tanenbaum Centre for Pharmacogenetics, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Azrieli Adult Neurodevelopmental Centre, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada.

Yoshihiro Noda (Y)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.

Jeffrey H Meyer (JH)

Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada; Research Imaging Centre, Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, Ontario, Canada; Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada.

Masaru Mimura (M)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan.

Shinichiro Nakajima (S)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan. Electronic address: shinichiro.l.nakajima@gmail.com.

Sho Moriguchi (S)

Department of Neuropsychiatry, Keio University School of Medicine, Tokyo, Japan. Electronic address: moriguchi.sho@gmail.com.

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Classifications MeSH