Literature DB >> 8932891

Double-blind, placebo-controlled, crossover trial of glycine adjuvant therapy for treatment-resistant schizophrenia.

U Heresco-Levy1, D C Javitt, M Ermilov, C Mordel, A Horowitz, D Kelly.   

Abstract

BACKGROUND: It has been proposed that schizophrenia is associated with underactivity of brain glutamatergic neurotransmission, especially at the level of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptor. Glycine potentiates NMDA receptor-mediated neurotransmission, indicating that it may serve as an effective therapeutic agent in the treatment of schizophrenia.
METHOD: Eleven treatment-resistant patients with chronic schizophrenia completed a double-blind, placebo-controlled, six-week, randomly assigned, crossover treatment trial of 0.8 g/kg body weight/day of glycine, added to their prior antipsychotic treatment.
RESULTS: Glycine was well tolerated, resulted in significantly increased serum glycine levels and induced a mean 36 (7%) reduction in negative symptoms (P < 0.0001). Significant improvements were also induced in depressive and cognitive symptoms. The greatest reduction in negative symptoms was registered in the patients who had the lowest baseline serum glycine levels.
CONCLUSIONS: These results extend previous findings and suggest an additional approach to the pharmacotherapy of negative symptoms and cognitive deficits in schizophrenia.

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Year:  1996        PMID: 8932891     DOI: 10.1192/bjp.169.5.610

Source DB:  PubMed          Journal:  Br J Psychiatry        ISSN: 0007-1250            Impact factor:   9.319


  54 in total

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Review 5.  Recent advances in targeting the ionotropic glutamate receptors in treating schizophrenia.

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7.  Genome-wide association study of NMDA receptor coagonists in human cerebrospinal fluid and plasma.

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Review 8.  Modulation of ligand-gated ion channels by antidepressants and antipsychotics.

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9.  Treatment of schizophrenia negative symptoms: future prospects.

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10.  Effects of haloperidol, clozapine, and quetiapine on sensorimotor gating in a genetic model of reduced NMDA receptor function.

Authors:  Gary E Duncan; Sheryl S Moy; Jeffery A Lieberman; Beverly H Koller
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