Dysregulation of kynurenine metabolism is related to proinflammatory cytokines, attention, and prefrontal cortex volume in schizophrenia.


Journal

Molecular psychiatry
ISSN: 1476-5578
Titre abrégé: Mol Psychiatry
Pays: England
ID NLM: 9607835

Informations de publication

Date de publication:
11 2020
Historique:
received: 05 10 2017
accepted: 05 03 2019
revised: 22 02 2019
pubmed: 4 4 2019
medline: 16 3 2021
entrez: 4 4 2019
Statut: ppublish

Résumé

The kynurenine pathway (KP) of tryptophan (TRP) catabolism links immune system activation with neurotransmitter signaling. The KP metabolite kynurenic acid (KYNA) is increased in the brains of people with schizophrenia. We tested the extent to which: (1) brain KP enzyme mRNAs, (2) brain KP metabolites, and (3) plasma KP metabolites differed on the basis of elevated cytokines in schizophrenia vs. control groups and the extent to which plasma KP metabolites were associated with cognition and brain volume in patients displaying elevated peripheral cytokines. KP enzyme mRNAs and metabolites were assayed in two independent postmortem brain samples from a total of 71 patients with schizophrenia and 72 controls. Plasma KP metabolites, cognition, and brain volumes were measured in an independent cohort of 96 patients with schizophrenia and 81 healthy controls. Groups were stratified based on elevated vs. normal proinflammatory cytokine mRNA levels. In the prefrontal cortex (PFC), kynurenine (KYN)/TRP ratio, KYNA levels, and mRNA for enzymes, tryptophan dioxygenase (TDO) and kynurenine aminotransferases (KATI/II), were significantly increased in the high cytokine schizophrenia subgroup. KAT mRNAs significantly correlated with mRNA for glial fibrillary acidic protein in patients. In plasma, the high cytokine schizophrenia subgroup displayed an elevated KYN/TRP ratio, which correlated inversely with attention and dorsolateral prefrontal cortex (DLPFC) volume. This study provides further evidence for the role of inflammation in a subgroup of patients with schizophrenia and suggests a molecular mechanism through which inflammation could lead to schizophrenia. Proinflammatory cytokines may elicit conversion of TRP to KYN in the periphery and increase the N-methyl-D-aspartate receptor antagonist KYNA via increased KAT mRNA and possibly more enzyme synthesis activity in brain astrocytes,  leading to DLPFC volume loss, and attention impairment in schizophrenia.

Identifiants

pubmed: 30940904
doi: 10.1038/s41380-019-0401-9
pii: 10.1038/s41380-019-0401-9
pmc: PMC7577855
doi:

Substances chimiques

Cytokines 0
Inflammation Mediators 0
Kynurenine 343-65-7
Kynurenic Acid H030S2S85J

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2860-2872

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Auteurs

Jochen Kindler (J)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia.
Neuroscience Research Australia, Randwick, NSW, 2031, Australia.
University Hospital of Child and Adolescent Psychiatry and Psychotherapy, University of Bern, 3000, Bern, Switzerland.

Chai K Lim (CK)

Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, 2109, Australia.

Cynthia Shannon Weickert (CS)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia.
Neuroscience Research Australia, Randwick, NSW, 2031, Australia.
Schizophrenia Research Institute, Randwick, NSW, 2010, Australia.

Danny Boerrigter (D)

Neuroscience Research Australia, Randwick, NSW, 2031, Australia.
Schizophrenia Research Institute, Randwick, NSW, 2010, Australia.

Cherrie Galletly (C)

Discipline of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia.
Ramsay Health Care (SA) Mental Health, Adelaide, SA, Australia.
Northern Adelaide Local Health Network, Adelaide, SA, Australia.

Dennis Liu (D)

Discipline of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia.
Northern Adelaide Local Health Network, Adelaide, SA, Australia.

Kelly R Jacobs (KR)

Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, 2109, Australia.

Ryan Balzan (R)

College of Education, Psychology, and Social Work, Flinders University, Adelaide, SA, Australia.

Jason Bruggemann (J)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia.
Neuroscience Research Australia, Randwick, NSW, 2031, Australia.

Maryanne O'Donnell (M)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia.
Kiloh Centre, Prince of Wales Hospital, Randwick, NSW, Australia.

Rhoshel Lenroot (R)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia.
Neuroscience Research Australia, Randwick, NSW, 2031, Australia.
Schizophrenia Research Institute, Randwick, NSW, 2010, Australia.

Gilles J Guillemin (GJ)

Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, 2109, Australia.

Thomas W Weickert (TW)

School of Psychiatry, University of New South Wales, Randwick, NSW, 2031, Australia. t.weickert@unsw.edu.au.
Neuroscience Research Australia, Randwick, NSW, 2031, Australia. t.weickert@unsw.edu.au.
Schizophrenia Research Institute, Randwick, NSW, 2010, Australia. t.weickert@unsw.edu.au.

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