Trial reportBiological psychiatry2019
Targeted Treatment of Individuals With Psychosis Carrying a Copy Number Variant Containing a Genomic Triplication of the Glycine Decarboxylase Gene.
Trial report in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Randomized controlled trial of the glycine transporter 1 inhibitor PF-03463275 to enhance cognitive training and neuroplasticity in schizophrenia.Schizophrenia research · 2023Trial
- Toward a Pluralistic Model for the Schizophrenia Spectrum-Dopamine and Beyond.JAMA psychiatry · 2026Review
- Glycine decarboxylase as a novel regulator of N-methyl-D-aspartate receptor function: Implications for pathophysiology of schizophrenia.Neural regeneration research · 2026Article
- Lactate restores PGC1α and BDNF expression rescuing cognitive impairments in a mouse model for schizophrenia.Behavioural brain research · 2026Article
- Glycine Reverses Behavioral Deficits in a Mouse Model for Psychosis With 4 Copies of the Gldc Gene.Pharmacology research & perspectives · 2025Article
- An increased copy number of glycine decarboxylase (GLDC) associated with psychosis reduces extracellular glycine and impairs NMDA receptor function.Molecular psychiatry · 2025Article
- Advances in the Treatment of Cognitive Impairment in Schizophrenia: Targeting NMDA Receptor Pathways.International journal of molecular sciences · 2024Review
- Inverted triplications formed by iterative template switches generate structural variant diversity at genomic disorder loci.Cell genomics · 2024Article
- Review
- Preliminary studies on apparent mendelian psychotic disorders in consanguineous families.BMC psychiatry · 2022Article
- Language abnormalities in schizophrenia: binding core symptoms through contemporary empirical evidence.Schizophrenia (Heidelberg, Germany) · 2022Review
- Complex genomic rearrangements: an underestimated cause of rare diseases.Trends in genetics : TIG · 2022Review
- Deletion of Loss-of-Function-Intolerant Genes and Risk of 5 Psychiatric Disorders.JAMA psychiatry · 2022Article
- Translational Study of Copy Number Variations in Schizophrenia.International journal of molecular sciences · 2021Article
- Clan genomics: From OMIM phenotypic traits to genes and biology.American journal of medical genetics. Part A · 2021Article
- Diagnostic genetic testing for neurodevelopmental psychiatric disorders: closing the gap between recommendation and clinical implementation.Current opinion in genetics & development · 2021Review
- Copy number variation and neuropsychiatric illness.Current opinion in genetics & development · 2021Review
- Forebrain expression of serine racemase during postnatal development.Neurochemistry international · 2021Article
- Genome-Wide Association Studies of Schizophrenia and Bipolar Disorder in a Diverse Cohort of US Veterans.Schizophrenia bulletin · 2021Article
- Directly and Indirectly Targeting the Glycine Modulatory Site to Modulate NMDA Receptor Function to Address Unmet Medical Needs of Patients With Schizophrenia.Frontiers in psychiatry · 2021Review
Corrections and comments
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Authors and funding
31 authors at 14 institutions in 3 countries.
Funding
Abstract
backgroundThe increased mutational burden for rare structural genomic variants in schizophrenia and other neurodevelopmental disorders has so far not yielded therapies targeting the biological effects of specific mutations. We identified two carriers (mother and son) of a triplication of the gene encoding glycine decarboxylase, GLDC, presumably resulting in reduced availability of the N-methyl-D-aspartate receptor coagonists glycine and D-serine and N-methyl-D-aspartate receptor hypofunction. Both carriers had a diagnosis of a psychotic disorder.
methodsWe carried out two double-blind, placebo-controlled clinical trials of N-methyl-D-aspartate receptor augmentation of psychotropic drug treatment in these two individuals. Glycine was used in the first clinical trial, and D-cycloserine was used in the second one.
resultsGlycine or D-cycloserine augmentation of psychotropic drug treatment each improved psychotic and mood symptoms in placebo-controlled trials.
conclusionsThese results provide two independent proof-of-principle demonstrations of symptom relief by targeting a specific genotype and explicitly link an individual mutation to the pathophysiology of psychosis and treatment response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.