Manabu Kubota1, Sho Moriguchi2, Keisuke Takahata3, Shinichiro Nakajima4, Nobuyuki Horita5. 1. Department of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan; Department of Psychiatry, Kyoto University Graduate School of Medicine, 54 Shogoin-Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan. Electronic address: kubota.manabu@qst.go.jp. 2. Department of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan; Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario M5T1R8, Canada. 3. Department of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology, 4-9-1 Anagawa, Inage-ku, Chiba 263-8555, Japan; Department of Neuropsychiatry, Keio University Graduate School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. 4. Research Imaging Centre, Centre for Addiction and Mental Health, 250 College Street, Toronto, Ontario M5T1R8, Canada; Department of Neuropsychiatry, Keio University Graduate School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. 5. Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan.
Abstract
BACKGROUND: Although there is growing evidence of alterations in the neurometabolite status associated with the pathophysiology of schizophrenia, how treatments influence these metabolite levels in patients with schizophrenia remains poorly studied. METHODS: We conducted a literature search using Embase, Medline, and PsycINFO to identify proton magnetic resonance spectroscopy studies that compared neurometabolite levels before and after treatment in patients with schizophrenia. Six neurometabolites (glutamate, glutamine, glutamate + glutamine, gamma-aminobutyric acid, N-acetylaspartate, myo-inositol) and six regions of interest (frontal cortex, temporal cortex, parieto-occipital cortex, thalamus, basal ganglia, hippocampus) were investigated. RESULTS: Thirty-two studies (n = 773 at follow-up) were included in our meta-analysis. Our results demonstrated that the frontal glutamate + glutamine level was significantly decreased (14 groups; n = 292 at follow-up; effect size = -0.35, P = 0.0003; I2 = 22%) and the thalamic N-acetylaspartate level was significantly increased (7 groups; n = 184 at follow-up; effect size = 0.47, P < 0.00001; I2 = 0%) after treatment in schizophrenia patients. No significant associations were found between neurometabolite changes and age, gender, duration of illness, duration of treatment, or baseline symptom severity. CONCLUSIONS: The current results suggest that glutamatergic neurometabolite levels in the frontal cortex and neuronal integrity in the thalamus in schizophrenia might be modified following treatment.
BACKGROUND: Although there is growing evidence of alterations in the neurometabolite status associated with the pathophysiology of schizophrenia, how treatments influence these metabolite levels in patients with schizophrenia remains poorly studied. METHODS: We conducted a literature search using Embase, Medline, and PsycINFO to identify proton magnetic resonance spectroscopy studies that compared neurometabolite levels before and after treatment in patients with schizophrenia. Six neurometabolites (glutamate, glutamine, glutamate + glutamine, gamma-aminobutyric acid, N-acetylaspartate, myo-inositol) and six regions of interest (frontal cortex, temporal cortex, parieto-occipital cortex, thalamus, basal ganglia, hippocampus) were investigated. RESULTS: Thirty-two studies (n = 773 at follow-up) were included in our meta-analysis. Our results demonstrated that the frontal glutamate + glutamine level was significantly decreased (14 groups; n = 292 at follow-up; effect size = -0.35, P = 0.0003; I2 = 22%) and the thalamic N-acetylaspartate level was significantly increased (7 groups; n = 184 at follow-up; effect size = 0.47, P < 0.00001; I2 = 0%) after treatment in schizophreniapatients. No significant associations were found between neurometabolite changes and age, gender, duration of illness, duration of treatment, or baseline symptom severity. CONCLUSIONS: The current results suggest that glutamatergic neurometabolite levels in the frontal cortex and neuronal integrity in the thalamus in schizophrenia might be modified following treatment.
Authors: Uzma Zahid; Robert A McCutcheon; Faith Borgan; Sameer Jauhar; Fiona Pepper; Matthew M Nour; Maria Rogdaki; Martin Osugo; Graham K Murray; Pamela Hathway; Robin M Murray; Oliver D Howes Journal: Front Psychiatry Date: 2022-08-11 Impact factor: 5.435
Authors: Juan R Bustillo; Elizabeth G Mayer; Joel Upston; Thomas Jones; Crystal Garcia; Sulaiman Sheriff; Andrew Maudsley; Mauricio Tohen; Charles Gasparovic; Rhoshel Lenroot Journal: Front Psychiatry Date: 2021-06-07 Impact factor: 5.435