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Treatment effects on neurometabolite levels in schizophrenia: A meta-analysis dataset of proton magnetic resonance spectroscopy.

ABSTRACT: This article describes a dataset for a meta-analysis that aimed to investigate the effects of treatment on the neurometabolite status in patients with schizophrenia (DOI of original article: https://doi.org/10.1016/j.schres.2020.03.069[1]). The data search was performed with MEDLINE, Embase, and PsycINFO. The neurometabolites investigated include glutamate, glutamine, glutamate?+?glutamine, gamma-aminobutyric acid, N-acetylaspartate, and myo-inositol, and the regions of interest (ROIs) include the frontal cortex, temporal cortex, parieto-occipital cortex, thalamus, basal ganglia, and hippocampus. The meta-analysis was conducted with a random-effects model, and the use of the standardized mean difference method between pre- and post-treatment of subjects for neurometabolites in each ROI of three patient groups or more. The dataset covers raw data of 39 patient groups (773 patients with schizophrenia at follow-up) with neurometabolite levels measured by magnetic resonance spectroscopy both before and after treatment. Furthermore, it contains details of clinical characteristics and treatment types for each group. Therefore, the data would be useful for a reinvestigation of treatment effects on the neurometabolite status from diverse points of view, as well as for the development of future treatment strategies for psychiatric diseases.

SUBMITTER: Kubota M

PROVIDER: S-EPMC7327820 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature

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Project description:ImportanceThe N-methyl-d-aspartic acid receptor hypofunction model of schizophrenia predicts a paradoxical increase in synaptic glutamate release. In vivo measurement of glutamatergic neurotransmission in humans is challenging, but glutamine, the principal metabolite of synaptic glutamate, can be quantified with proton magnetic resonance spectroscopy (1H-MRS). Although a few studies have measured glutamate, glutamine, and glutamine to glutamate ratio, it is not clear which of these 1H-MRS indices of glutamatergic neurotransmission is altered in schizophrenia.ObjectiveTo examine glutamine, glutamate, and glutamine to glutamate ratio in the dorsal anterior cingulate, as well as their relationships with symptoms and cognition in schizophrenia.Design, setting, and participantsCross-sectional design using 3-T 1H-MRS in participants recruited from university-based psychiatric outpatient clinics who underwent neuroimaging at an affiliated research facility. Participants were 84 patients with a DSM-IV-TR diagnosis of schizophrenia and 81 psychiatrically healthy volunteers, matched in age, sex, ethnicity, and occupational level to the head of household of family of origin.Main outcomes and measuresGlutamine, glutamate, and glutamine to glutamate ratio. Also symptoms and cognition.ResultsGlutamine was increased in the schizophrenia group (P = .01) as well as the glutamine to glutamate ratio (P = .007) but not glutamate (P = .89). Glutamine levels were positively correlated with severity of psychotic symptoms (P = .02). Choline was also increased in schizophrenia (P = .002).Conclusions and relevanceElevated glutamine, which was directly related to psychotic symptoms, is consistent with increased glutamatergic synaptic release in schizophrenia, as predicted by the N-methyl-d-aspartic acid receptor hypofunction model. Further understanding the underlying mechanism of glutamatergic dysfunction in schizophrenia may lead to new pharmacological strategies to treat psychosis.

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Treatment effects on neurometabolite levels in schizophrenia: A meta-analysis dataset of proton magnetic resonance spectroscopy.

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