Yusuke Iwata1, Shinichiro Nakajima2, Eric Plitman3, Yukiko Mihashi4, Fernando Caravaggio4, Jun Ku Chung3, Julia Kim3, Philip Gerretsen5, Masaru Mimura6, Gary Remington7, Ariel Graff-Guerrero8. 1. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada.; Department of Psychiatry, University of Toronto, 250 College Street, M5T 1R8 Toronto, Ontario, Canada; Department of Neuropsychiatry, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, 160-8582 Tokyo, Japan. 2. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada.; Department of Psychiatry, University of Toronto, 250 College Street, M5T 1R8 Toronto, Ontario, Canada; Department of Neuropsychiatry, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, 160-8582 Tokyo, Japan; Geriatric Mental Health Division, Centre for Addiction and Mental Health, 80 Workman Way, M6J 1H4 Toronto, Canada. 3. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada.; Institute of Medical Science, University of Toronto, 1 King's College Circle, M5S 1A8 Toronto, Ontario, Canada. 4. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada. 5. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada.; Department of Psychiatry, University of Toronto, 250 College Street, M5T 1R8 Toronto, Ontario, Canada; Geriatric Mental Health Division, Centre for Addiction and Mental Health, 80 Workman Way, M6J 1H4 Toronto, Canada; Campbell Research Institute, Centre for Addiction and Mental Health, 1001 Queen St. W, M6J 1H4 Toronto, Ontario, Canada. 6. Department of Neuropsychiatry, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, 160-8582 Tokyo, Japan. 7. Department of Psychiatry, University of Toronto, 250 College Street, M5T 1R8 Toronto, Ontario, Canada; Campbell Research Institute, Centre for Addiction and Mental Health, 1001 Queen St. W, M6J 1H4 Toronto, Ontario, Canada. 8. Multimodal Imaging Group, Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, M5T 1R8 Toronto, Ontario, Canada.; Department of Psychiatry, University of Toronto, 250 College Street, M5T 1R8 Toronto, Ontario, Canada; Geriatric Mental Health Division, Centre for Addiction and Mental Health, 80 Workman Way, M6J 1H4 Toronto, Canada; Campbell Research Institute, Centre for Addiction and Mental Health, 1001 Queen St. W, M6J 1H4 Toronto, Ontario, Canada. Electronic address: ariel_graff@yahoo.com.mx.
Abstract
BACKGROUND: Studies using proton magnetic resonance spectroscopy (1H-MRS) have reported altered neurometabolite levels in patients with schizophrenia. However, results are possibly confounded by the influence of antipsychotic (AP). Thus, this meta-analysis aimed to examine neurometabolite levels in AP-naïve/free patients with schizophrenia. METHODS: A literature search was conducted using Embase, Medline, and PsycINFO to identify studies that compared neurometabolite levels in AP-naïve/free patients with schizophrenia to healthy controls (HCs). Eight neurometabolites (glutamate, glutamine, glutamate + glutamine, N-acetylaspartate [NAA], choline, creatine, myo-inositol, and γ-Aminobutyric acid [GABA]) and seven regions of interest (ROI; medial prefrontal cortex, dorsolateral prefrontal cortex, frontal white matter, occipital lobe, basal ganglia, hippocampus/medial temporal lobe, and thalamus) were examined. RESULTS: Twenty-one studies (N = 1281) were included in the analysis. The results showed lower thalamic NAA levels (3 studies, n = 174, effect size = -0.56, P = 0.0005) in the patient group. No group differences were identified for other neurometabolites. CONCLUSIONS: Our findings suggest that impaired neuronal integrity in the thalamus may be a potential trait maker in the early stages of schizophrenia.
BACKGROUND: Studies using proton magnetic resonance spectroscopy (1H-MRS) have reported altered neurometabolite levels in patients with schizophrenia. However, results are possibly confounded by the influence of antipsychotic (AP). Thus, this meta-analysis aimed to examine neurometabolite levels in AP-naïve/free patients with schizophrenia. METHODS: A literature search was conducted using Embase, Medline, and PsycINFO to identify studies that compared neurometabolite levels in AP-naïve/free patients with schizophrenia to healthy controls (HCs). Eight neurometabolites (glutamate, glutamine, glutamate + glutamine, N-acetylaspartate [NAA], choline, creatine, myo-inositol, and γ-Aminobutyric acid [GABA]) and seven regions of interest (ROI; medial prefrontal cortex, dorsolateral prefrontal cortex, frontal white matter, occipital lobe, basal ganglia, hippocampus/medial temporal lobe, and thalamus) were examined. RESULTS: Twenty-one studies (N = 1281) were included in the analysis. The results showed lower thalamic NAA levels (3 studies, n = 174, effect size = -0.56, P = 0.0005) in the patient group. No group differences were identified for other neurometabolites. CONCLUSIONS: Our findings suggest that impaired neuronal integrity in the thalamus may be a potential trait maker in the early stages of schizophrenia.
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