Journal
NEUROPSYCHOPHARMACOLOGY
Volume 45, Issue 4, Pages 632-640Publisher
SPRINGERNATURE
DOI: 10.1038/s41386-019-0589-z
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Funding
- Japan Society for the Promotion of Science
- Japan Research Foundation for Clinical Pharmacology
- Naito Foundation
- Uehara Memorial Foundation
- Takeda Science Foundation
- Daiichi Sankyo Research Program
- Novartis Research Program
- Japan Agency for Medical Research and Development (AMED)
- Teijin Pharma Limited
- Japan Health Foundation
- Meiji Yasuda Mental Health Foundation
- Mitsui Life Social Welfare Foundation
- SENSHIN Medical Research Foundation
- Health Science Center Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Daiichi Sankyo Scholarship Donation Program
- Otsuka Pharmaceutical
- Shionogi
- Meiji-Seika Pharma
- Canada Graduate Scholarship
- Ontario Graduate Scholarship
- McGill University Healthy Brains for Healthy Lives Postdoctoral Fellowship
- Keio Research Institute
- Weston Brain Institute
- Alzheimer's Association
- Michael J. Fox Foundation
- Canadian Institutes of Health Research
- National Sciences and Engineering Research Council of Canada
- McGill University's Healthy Brains for Healthy Lives Initiative
- Eisai
- Dainippon-Sumitomo Pharma
- Mochida Pharmaceutical
- Meiji-Seika Pharmaceutical
- Novartis
- CIHR
- HLS Therapeutics
- United States National Institute of Health
- OMHF
- Consejo Nacional de Ciencia y Tecnologia
- Instituto de Ciencia y Tecnologia del DF
- Brain & Behavior Research Foundation
- Ontario Ministry of Health and Long-Term Care
- Ontario Ministry of Research and Innovation Early Research Award
- Janssen
- Asahi Kasei Pharma
- Astellas Pharmaceutical
- Daiichi Sankyo
- Eli Lilly
- GlaxoSmithKline
- Janssen Pharmaceutical
- MSD
- Novartis Pharma
- Otsuka Phacgi
- Takeda
- Tanabe Mitsubishi Pharma
- Yoshitomi Yakuhin
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Approximately 30% of patients with schizophrenia do not respond to antipsychotics and are thus considered to have treatment-resistant schizophrenia (TRS). To date, only four studies have examined glutamatergic neurometabolite levels using proton magnetic resonance spectroscopy (H-1-MRS) in patients with TRS, collectively suggesting that glutamatergic dysfunction may be implicated in the pathophysiology of TRS. Notably, the TRS patient population in these studies had mild-to-moderate illness severity, which is not entirely reflective of what is observed in clinical practice. In this present work, we compared glutamate + glutamine (Glx) levels in the dorsal anterior cingulate cortex (dACC) and caudate among patients with TRS, patients with non-TRS, and healthy controls (HCs), using 3T H-1-MRS (PRESS, TE = 35 ms). TRS criteria were defined by severe positive symptoms (i.e., >= 5 on 2 Positive and Negative Syndrome Scale (PANSS)-positive symptom items or >= 4 on 3 PANSS-positive symptom items), despite standard antipsychotic treatment. A total of 95 participants were included (29 TRS patients [PANSS = 111.2 +/- 20.4], 33 non-TRS patients [PANSS = 49.8 +/- 13.7], and 33 HCs). dACC Glx levels were higher in the TRS group vs. HCs (group effect: F[2,75] = 4.74, p = 0.011; TRS vs. HCs: p = 0.012). No group differences were identified in the caudate. There were no associations between Glx levels and clinical severity in either patient group. Our results are suggestive of greater heterogeneity in TRS relative to non-TRS with respect to dACC Glx levels, necessitating further research to determine biological subtypes of TRS.
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