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Glycine transporter inhibitor sarcosine changes neuronal and glial parameters in the left dorsolateral prefrontal cortex and glutamatergic parameters in the left hippocampus in stable schizophrenia

Published online by Cambridge University Press:  23 March 2020

D. Strzelecki*
Affiliation:
Central Clinical Hospital, Department of Affective and Psychotic Disorders–Medical University of Łódź, Łódź, Poland
M. Podgórski
Affiliation:
University Hospital No.1, Department of Radiology–Diagnostic Imaging–Medical University of Łódź, Łódź, Poland
O. Kałużyńska
Affiliation:
Central Clinical Hospital, Department of Affective and Psychotic Disorders–Medical University of Łódź, Łódź, Poland
M. Kotlicka-Antczak
Affiliation:
Central Clinical Hospital, Department of Affective and Psychotic Disorders–Medical University of Łódź, Łódź, Poland
O. Gawlik-Kotelnicka
Affiliation:
Central Clinical Hospital, Department of Affective and Psychotic Disorders–Medical University of Łódź, Łódź, Poland
A. Gmitrowicz
Affiliation:
Central Clinical Hospital, Department of Adolescent Psychiatry–Medical University of Łódź, Łódź, Poland
L. Stefańczyk
Affiliation:
University Hospital No.1, Department of Radiology–Diagnostic Imaging–Medical University of Łódź, Łódź, Poland
P. Grzelak
Affiliation:
University Hospital No.1, Department of Radiology–Diagnostic Imaging–Medical University of Łódź, Łódź, Poland
*
*Corresponding author.

Abstract

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Introduction

Sarcosine - glycine transporter inhibitor - increases glycine concentration around NMDA (N-methyl-D-aspartate) receptors. Function of the glutamatergic system in the prefrontal cortex and hippocampus is impaired in schizophrenia, which may lead to negative and cognitive symptomatology.

Aims

We evaluated the influence of sarcosine therapy on the concentration of metabolites (NAA, N-acetylaspartate; Glx, complex of glutamate, glutamine and γ-aminobutyric acid (GABA); mI, myo-inositol; Cr, creatine; Cho, choline) in the left dorso-lateral prefrontal cortex (DLPFC) and left hippocampus in patients with stable schizophrenia.

Methods

Fifty patients with schizophrenia, treated with constant antipsychotics doses, in stable clinical condition were randomly assigned (25 patients in each group) to administration of sarcosine (2 g) or placebo for six months. 1H-NMR spectroscopy (1.5 T) in both localisations and clinical evaluation (PANSS) was performed before and after sarcosine addition.

Results

Initially we noted no differences in metabolite concentrations between groups. In the left DLPFC, NAA/Cho, mI/Cr and mI/Cho ratios were significantly higher in the sarcosine than the placebo group after six months. In the sarcosine group, NAA/Cr, NAA/Cho, mI/Cr, mI/Cho ratios also increased compared to baseline values. In the placebo group, only the NAA/Cr ratio increased. In the left hippocampus Glx/Cr and Glx/Cho decreased in sarcosine group at the end of our study.

Conclusions

The addition of sarcosine to antipsychotic therapy for six months caused increase of neurons viability (NAA) and neurogilal activity (mI) markers in the left DLPFC and decrease of hyperglutamatergic overstimulation parameters in the left hippocampus with simultaneous improvement of clinical parameters including negative symptoms.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
EW558
Copyright
Copyright © European Psychiatric Association 2014
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