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Major depressive disorder is a complex disease and most currently available antidepressants aiming at monoamine neurotransmission exhibit limited efficacy and cognitive effects. N-methyl-D-aspartate (NMDA), one subtype of glutamate receptors, plays an important role in learning and memory. N-methyl-D-aspartic acid (NMDA) enhancing agents, such as sarcosine (N-methylglycine), have been used as adjunctive therapy of schizophrenia. Sarcosine improved not only psychotic but also depressive symptoms in patients with schizophrenia. To confirm its antidepressant effect, the purpose of this study is to compare citalopram and sarcosine in efficacy for major depressive patients.
Major depressive disorder is a complex disease and most currently available antidepressants aiming at monoamine neurotransmission exhibit limited efficacy and cognitive effects. Novel therapies via manipulating other neurotransmission (e.g. glutamate receptor) are being developed.
NMDA enhancing agents, such as sarcosine have been demonstrated to improve negative symptoms and depressive symptoms of schizophrenic patients. The purpose of this study is to compare citalopram and sarcosine in aspects of efficacy, safety in major depressive patients.
In the study, 30 major depressive patients are recruited into the 6-week trial and randomly assigned into the two groups (20-60 mg/d citalopram, or 500 - 1500 mg/d sarcosine) with a double-blind manner. Hamilton Depression Rating Scale(21-item)and side effects are evaluated every two weeks during the trial.The efficacies of two groups are compared.
Allocation: Randomized, Control: Active Control, Endpoint Classification: Safety/Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator, Outcomes Assessor), Primary Purpose: Treatment
Major Depressive Disorder
Department of Psychiatry, China Medical University Hospital
China Medical University Hospital
Published on BioPortfolio: 2014-08-27T03:19:19-0400
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A LIVER mitochondrial matrix flavoenzyme that catalyzes the oxidation of SARCOSINE to GLYCINE and FORMALDEHYDE. Mutation in the enzyme causes sarcosinemia, a rare autosomal metabolic defect characterized by elevated levels of SARCOSINE in BLOOD and URINE.
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