ReviewSchizophrenia research2016
Genetic assessment of additional endophenotypes from the Consortium on the Genetics of Schizophrenia Family Study.
Review in Schizophrenia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 3 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
36 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- A Meta-analysis of the Association Between SLC6A3 Gene Polymorphisms and Schizophrenia.Journal of molecular neuroscience : MN · 2020Pooled it
- A systematic review of genome-wide association studies of antipsychotic response.Pharmacogenomics · 2019Pooled it
- Heritability of Neuropsychological Measures in Schizophrenia and Nonpsychiatric Populations: A Systematic Review and Meta-analysis.Schizophrenia bulletin · 2017Pooled it
- Design and Evaluation of Selective Positive Allosteric Modulators Targeting Kainate Receptors.ACS omega · 2026Article
- Genetic predisposition to unwanted side effects under antidepressants and antipsychotics: a molecular-genetic study of 902 patients over 6 weeks.European archives of psychiatry and clinical neuroscience · 2026Article
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.Molecular pharmacology · 2026Article
- UCM-A86 is a selective positive allosteric modulator of GluN1/GluN3 NMDA receptors.bioRxiv : the preprint server for biology · 2025Article
- Genetic determinants of antidepressant and antipsychotic drug response.European archives of psychiatry and clinical neuroscience · 2025Article
- Central role of regular firing neurons of centrolateral amygdala in affective behaviors.iScience · 2025Article
- Deep Clinical Phenotyping of Schizophrenia Spectrum Disorders Using Data-Driven Methods: Marching towards Precision Psychiatry.Journal of personalized medicine · 2023Article
- Genetic Influences on Cognitive Dysfunction in Schizophrenia.Current topics in behavioral neurosciences · 2023Article
- Modeling sex differences in humans using isogenic induced pluripotent stem cells.Stem cell reports · 2022Article
- Spironolactone alleviates schizophrenia-related reversal learning in Tcf4 transgenic mice subjected to social defeat.Schizophrenia (Heidelberg, Germany) · 2022Article
- Genes of the Glutamatergic System and Tardive Dyskinesia in Patients with Schizophrenia.Diagnostics (Basel, Switzerland) · 2022Article
- Ultrarare Loss-of-Function Mutations in the Genes Encoding the Ionotropic Glutamate Receptors of Kainate Subtypes Associated with Schizophrenia Disrupt the Interaction with PSD95.Journal of personalized medicine · 2022Article
- Integrative omics of schizophrenia: from genetic determinants to clinical classification and risk prediction.Molecular psychiatry · 2022Review
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Article
- Short-active photoperiod gestation induces psychiatry-relevant behavior in healthy mice but a resiliency to such effects are seen in mice with reduced dopamine transporter expression.Scientific reports · 2020Article
- A kainate receptor-selective RNA aptamer.The Journal of biological chemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors.
Funding
Abstract
The Consortium on the Genetics of Schizophrenia Family Study (COGS-1) has previously reported our efforts to characterize the genetic architecture of 12 primary endophenotypes for schizophrenia. We now report the characterization of 13 additional measures derived from the same endophenotype test paradigms in the COGS-1 families. Nine of the measures were found to discriminate between schizophrenia patients and controls, were significantly heritable (31 to 62%), and were sufficiently independent of previously assessed endophenotypes, demonstrating utility as additional endophenotypes. Genotyping via a custom array of 1536 SNPs from 94 candidate genes identified associations for CTNNA2, ERBB4, GRID1, GRID2, GRIK3, GRIK4, GRIN2B, NOS1AP, NRG1, and RELN across multiple endophenotypes. An experiment-wide p value of 0.003 suggested that the associations across all SNPs and endophenotypes collectively exceeded chance. Linkage analyses performed using a genome-wide SNP array further identified significant or suggestive linkage for six of the candidate endophenotypes, with several genes of interest located beneath the linkage peaks (e.g., CSMD1, DISC1, DLGAP2, GRIK2, GRIN3A, and SLC6A3). While the partial convergence of the association and linkage likely reflects differences in density of gene coverage provided by the distinct genotyping platforms, it is also likely an indication of the differential contribution of rare and common variants for some genes and methodological differences in detection ability. Still, many of the genes implicated by COGS through endophenotypes have been identified by independent studies of common, rare, and de novo variation in schizophrenia, all converging on a functional genetic network related to glutamatergic neurotransmission that warrants further investigation.
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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 OpenQuestion graph.