Glutamate is the main excitatory neurotransmitter in the central nervous system. Dysfunction of the glutamatergic system plays an important and well-established role in the pathogenesis of schizophrenia. Agents with glutamatergic properties such as N-methyl-D-aspartate receptor coagonists (ie, glycine, D-cycloserine) and glycine transporter type 1 inhibitors (eg, sarcosine, bitopertin) are investigated in schizophrenia with special focus on negative and cognitive symptomatology.
In this article, we describe a case of a 34-year-old woman with diagnosis of schizophrenia with persistent moderate negative and cognitive symptoms, a participant of the Polish Sarcosine Study (PULSAR) treated with olanzapine (25 mg per day) and venlafaxine (75 mg per day).
During ten weeks of sarcosine administration (2 g per day) the patient’s activity and mood improved, but in the following 2 weeks, the patient reported decreased need for sleep, elevated mood, libido and general activity.
We describe here the second case report where sarcosine induced important affect changes when added to antidepressive and antipsychotic treatment, which supports the hypothesis of clinically important glutamate-serotonin interaction.
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Details on experience, from research paper:
During the first 10 weeks of sarcosine administration at 2 g per day, the patient reported a gradual improvement of overall activity, concentration, and mood.
After the next 2 weeks, the patient reported moderately increased mood, drive, and libido, excessive activity with talkativity, and decreased need for sleep (to 2–4 hours). The patient found these symptoms “strange” and asked for the modification of the treatment.
She described the overall impact of sarcosine as positive, and therefore it was decided to maintain the sarcosine supplementation, but the dose of venlafaxine was been reduced by half to 37.5 mg per day.
The patient declared adherence to the medication regimen. After this change, the intensity of excitation and mood elation decreased in about 1 week without secondary depressive episode. There were no external circumstances to explain hypomanic symptoms.
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Although there have been very few studies in this area, it is considered that these compounds may have beneficial effects on the symptomatology of schizophrenia, particularly on negative symptoms, affective symptoms, and disturbed cognitive functioning. The signs of excessive psychomotor agitation described in this patient have not been previously described in any patient taking sarcosine.
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The situation described here indicates a need to determine the range of sarcosine doses used in augmentation of treatment for schizophrenia. We suggest considering a more flexible use of sarcosine in the range of 1–2 g per day, particularly in combination with serotoninergic substances. Of course, flexible adjusting of the dose of selective serotonin reuptake inhibitor or other serotoninergic substances can also be considered.
In conclusion, we believe that appropriate simultaneous use of substances with glutamatergic (like Sarcosine) and serotoninergic properties may generate a synergistic antidepressive and activating effect.
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